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Effect of the ethanolic extract from Humirianthera ampla administered orally on biting response caused by intrathecal injection of glutamate (175 nmol/site), trans-ACPD (50 nmol/site), NMDA (450 pmol/site), AMPA (135 pmol/site), kainate (110 pmol/site) and substance P (SP, 100 pmol/site) in mice. Each column represents the mean of 6–8 animals and vertical lines indicate the S.E.M. The asterisks denote the significance levels, when compared with untreated groups, * p < 0.05 and *** p < 0.001 by paired t -test.
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Humirianthera ampla Miers is a member of the Icacinaceae family and presents great amounts of di and triterpenoids. These chemical constituents in roots of Humirianthera ampla sustain not only the ethnopharmacological use against snake venom, but also some anti-inflammatory and analgesic properties of the plant. In this study we investigated the an...
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... by glutamate. The doses of the antagonists, agonists and other drugs were selected with basis on the literature (Santos et al., 1999, 2005; Kaster et al., 2005; Meotti et al., 2006; Pietrovski et al., 2006) or in previous results from our laboratory. To assess the participation of the opioid system, mice were pretreated intraperitoneally (i.p.) with naloxone (1 mg/kg, a non- selective opioid receptor antagonist) or naloxone methiodide (1 mg/kg, s.c., a non-selective opioid receptor antagonist not permeable into the blood-brain barrier). After 20 min the animals received EE (30 mg/kg, p.o.), morphine (2.5 mg/kg, s.c.) or vehicle (10 ml/kg, p.o.). The nociceptive response to the glutamate intraplantar injection was recorded 1 h after administration of EE or vehicle and 30 min after administration of morphine. Another group of mice was pretreated with vehicle and after 20 min, received EE, morphine or vehicle, 1, 0.5 and 1 h before glutamate injection, respectively. To investigate the role played by the l -arginine–nitric oxide pathway in the antinociception caused by EE from Humirianthera ampla , mice were pretreated with l -arginine (40 mg/kg, i.p., a nitric oxide precursor) or d -arginine (40 mg/kg, i.p., an inactive isomer of l -arginine). After 20 min the mice received the EE from Humirianthera ampla (30 mg/kg, p.o.), N -nitro- l -arginine (25 mg/kg, i.p., a nitric oxide inhibitor) or vehicle (10 ml/kg, p.o.). The nociceptive response to the glutamate intraplantar injection was recorded 1 h after administration of EE or vehicle and 30 min after administration of l -NOARG. The participation of the serotonergic system in the antinociceptive action of EE of Humirianthera ampla was investigated using WAY100635 (0.1 mg/kg, i.p., a selective 5-HT 1A receptor antagonist), ketanserin (1 mg/kg, i.p., a selective 5-HT 2A receptor antagonist), ondansetron (0.5 mg/kg, i.p., a 5-HT 3 receptor antagonist) or vehicle (10 ml/kg, i.p.). After 20 min the mice received EE (30 mg/kg, p.o.) or saline, 1 h before glutamate intraplantar injection. To investigate the role played by the adenosinergic systems in the antinociception caused by EE of Humirianthera ampla , mice were pretreated with caffeine (3 mg/kg, i.p., a non- selective adenosine receptor antagonist). After 20 min the mice received EE from Humirianthera ampla (30 mg/kg, p.o.) or vehicle (10 ml/kg, p.o.). The nociceptive response to the glutamate intraplantar injection was recorded 1 h after administration of EE or vehicle. The results are presented as mean S.E.M., except the ID50 values (i.e., the dose of EE reducing the nociceptive response by 50% relative to the control value), which are reported as geometric means accompanied by their respective 95% confidence limits. The ID50 value was determined by linear regression from individual experiments using linear regression GraphPad software (GraphPad software, San Diego, CA, USA). The statistical analyses were performed by one-way ANOVA followed by Newman–Keuls’ test or t test when appropriated. A one-way ANOVA with repeated measures was carried out for the time-course effect of the Humirianthera ampla . P -values less than 0.05 ( P < 0.05) were considered as indicative of significance. The step-down inhibitory avoidance is presented as median ± interquartile range and the data were analyzed by Kruskal–Wallis non-parametric test followed by Dunn’s post hoc compar- isons. The oral administration of EE from Humirianthera ampla produced marked and dose-dependent attenuation of the glutamate-induced nociception. The ID 50 value (and its respective 95% confidence limits) was 19.9 (15.6–25.2) mg/kg. The peak of inhibition was 71 ± 5% at 300 mg/kg (Fig. 1A). A time- course analysis of the antinociceptive effect of EE given by p.o. route is shown in Fig. 1B. EE produced marked antinociception as early as 1 h after p.o. administration, an action that remained significant up to 10 h after the administration. Thus, the time point of 1 h was chosen for all further studies with independent groups of animals. The results depicted in Fig. 2A and B show that the EE from Humirianthera ampla (30–500 mg/kg, p.o.) caused a significant inhibition of both neurogenic (0–5 min) and inflammatory (15–30 min) phases of formalin-induced licking. However, its antinociceptive effects were significantly more pronounced against the second phase of this model of pain. The calculated mean ID 50 value (and its respective 95% confidence limits) for these effects were: >500 and 144.5 (119.3–175.1) mg/kg and the inhibitions observed were 31 ± 11 and 97 ± 2% at a dose of 500 mg/kg, for first and second phase, respectively. The results depicted in Fig. 3 show that EE from Humirianthera ampla produced marked and dose-related inhibition of the capsaicin-induced neurogenic pain in mice. The ID 50 value (and its respective 95% confidence limits) was 20.0 (17.4–23.0) mg/kg. The maximal inhibition was 80 ± 4% at a dose of 300 mg/kg. The results depicted in Fig. 4 show that EE of Humirianthera ampla (30 mg/kg) inhibited the nociceptive responses induced by spinal injections of glutamate, trans-ACPD, NMDA and substance P in mice. The inhibition values were 84 ± 2, 41 ± 10, 55 ± 8 and 53 ± 9%, respectively. In contrast, EE had no effect against AMPA- and kainate-mediated biting responses (Fig. 4). The EE from Humirianthera ampla (10–100 mg/kg) did not alter the latency response to the tail-flick test. In contrast, morphine (10 mg/kg, s.c.) caused a significant increase in the latency response (results not shown). The EE from Humirianthera ampla (30 and 500 mg/kg) did not affect the motor performance on the rota-rod task and locomotor activity in the open-field test when compared with animals that received vehicle (control group). The means ± S.E.M. on the rota-rod task were 60.0 ± 0.00; 60.0 ± 0.00 and 56.67 ± 3.33 s for the control, 30 and 500 mg/kg group, respectively. In the locomotor activity the means ± S.E.M. of crossings number were 169.5 ± 11.69; 190.5 ± 16.53 and 171.5 ± 13.51 for the control, 30 and 500 mg/kg group, respectively. The EE from Humirianthera ampla (30 mg/kg, p.o.) did not affect the acquisition or retention of the memory in rats sub- mitted to the step-down inhibitory avoidance task. Furthermore, EE at the same dose did not alter the short-term memory and long-term memory (data not shown). The results presented in Fig. 5A show that the pretreatment of mice with naloxone (1 mg/kg, i.p., a non-selective opioid receptor antagonist), given 20 min beforehand, completely reversed the antinociception of EE from Humirianthera ampla (30 mg/kg, p.o.) and morphine (2.5 mg/kg, s.c.) (Fig. 5A). The systemic treatment of mice with naloxone methiodide (1 mg/kg, s.c., a non-selective opioid receptor antagonist that is not permeable into the blood brain barrier) did not reverse the antinocicep- tion of EE against glutamate-induced pain (Fig. 5B). However, the antinociception produced by morphine was significantly reversed (Fig. 5B). The systemic pretreatment of mice with the nitric oxide precursor l -arginine (40 mg/kg, i.p.), but not with d -arginine (40 mg/kg, i.p., an inactive isomer of l -arginine), completely reversed the antinociception caused by l -NOARG (25 mg/kg, i.p., a nitric oxide inhibitor) when analyzed against glutamate- induced nociception (Fig. 6). Under the same conditions, l -arginine significantly reversed the antinociception caused by EE from Humirianthera ampla (Fig. 6). The results depicted in Fig. 7 show that the previous treatment of mice with WAY100635 (0.1 mg/kg, i.p., a selective 5-HT 1A receptor antagonist), ketanserin (1 mg/kg, i.p., a selective 5-HT 2A receptor antagonist) or ondansetron (0.5 mg/kg, i.p., a selective 5-HT receptor antagonist), significantly reversed the antinociception caused by EE (30 mg/kg, p.o.) against glutamate-induced nociception. The systemic pretreatment of mice with caffeine (3 mg/kg, i.p., a non-selective adenosine receptor antagonist) did not significantly reverse the antinociception caused by EE from Humirianthera ampla (30 mg/kg, p.o.) against glutamate- induced nociception (results not shown). In the present study, we demonstrated that the oral treatment of mice with EE from roots of the Humirianthera ampla caused potent antinociception against the chemical agents of nociception: formalin, glutamate and capsaicin. Hence, the chemical models of nociception here employed gave us an approach about the pathways involved on the antinociception of the Humirianthera ampla. It is worth to mention that Humirianthera ampla produced antinociception against both neurogenic and inflammatory phases of formalin. However, the effect was more pronounced against the inflammatory phase. The formalin-induced nociception is a well-described model of nociception and can be consistently inhibited by typical analgesic and anti-inflammatory drugs, including morphine, indomethacin and dexamethasone (Hunskaar and Hole, 1987). Considering the inhibitory property of Humirianthera ampla on the second phase of formalin, we might suggest an anti- inflammatory action of the plant extract. In fact, the chemical constituents present in the roots of the Humirianthera ampla : diterpenoids, triterpenoids and sterols have been reported as potent anti-inflammatory agents (Hernandez-Perez et al., 1995; Fernandez et al., 2001; Yamashita et al., 2002; Spessoto et al., 2003; Liu and Lin, 2006). The EE from Humirianthera ampla strongly inhibited the nociception induced by capsaicin and glutamate. Doses from 10 and 30 mg/kg significantly inhibited the capsaicin and glutamate-induced licking, whereas doses of 100 and 500 mg/kg were necessary to inhibit the inflammatory and neurogenic phases of formalin. This suggests a straight action of Humirianthera ampla on pathways dependent on the glutamatergic and vanilloid systems. Hence, an effect of the plant extract directly on the receptors or second messengers related to these trans- ...
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... (i.p.) with naloxone (1 mg/kg, a non- selective opioid receptor antagonist) or naloxone methiodide (1 mg/kg, s.c., a non-selective opioid receptor antagonist not permeable into the blood-brain barrier). After 20 min the animals received EE (30 mg/kg, p.o.), morphine (2.5 mg/kg, s.c.) or vehicle (10 ml/kg, p.o.). The nociceptive response to the glutamate intraplantar injection was recorded 1 h after administration of EE or vehicle and 30 min after administration of morphine. Another group of mice was pretreated with vehicle and after 20 min, received EE, morphine or vehicle, 1, 0.5 and 1 h before glutamate injection, respectively. To investigate the role played by the l -arginine–nitric oxide pathway in the antinociception caused by EE from Humirianthera ampla , mice were pretreated with l -arginine (40 mg/kg, i.p., a nitric oxide precursor) or d -arginine (40 mg/kg, i.p., an inactive isomer of l -arginine). After 20 min the mice received the EE from Humirianthera ampla (30 mg/kg, p.o.), N -nitro- l -arginine (25 mg/kg, i.p., a nitric oxide inhibitor) or vehicle (10 ml/kg, p.o.). The nociceptive response to the glutamate intraplantar injection was recorded 1 h after administration of EE or vehicle and 30 min after administration of l -NOARG. The participation of the serotonergic system in the antinociceptive action of EE of Humirianthera ampla was investigated using WAY100635 (0.1 mg/kg, i.p., a selective 5-HT 1A receptor antagonist), ketanserin (1 mg/kg, i.p., a selective 5-HT 2A receptor antagonist), ondansetron (0.5 mg/kg, i.p., a 5-HT 3 receptor antagonist) or vehicle (10 ml/kg, i.p.). After 20 min the mice received EE (30 mg/kg, p.o.) or saline, 1 h before glutamate intraplantar injection. To investigate the role played by the adenosinergic systems in the antinociception caused by EE of Humirianthera ampla , mice were pretreated with caffeine (3 mg/kg, i.p., a non- selective adenosine receptor antagonist). After 20 min the mice received EE from Humirianthera ampla (30 mg/kg, p.o.) or vehicle (10 ml/kg, p.o.). The nociceptive response to the glutamate intraplantar injection was recorded 1 h after administration of EE or vehicle. The results are presented as mean S.E.M., except the ID50 values (i.e., the dose of EE reducing the nociceptive response by 50% relative to the control value), which are reported as geometric means accompanied by their respective 95% confidence limits. The ID50 value was determined by linear regression from individual experiments using linear regression GraphPad software (GraphPad software, San Diego, CA, USA). The statistical analyses were performed by one-way ANOVA followed by Newman–Keuls’ test or t test when appropriated. A one-way ANOVA with repeated measures was carried out for the time-course effect of the Humirianthera ampla . P -values less than 0.05 ( P < 0.05) were considered as indicative of significance. The step-down inhibitory avoidance is presented as median ± interquartile range and the data were analyzed by Kruskal–Wallis non-parametric test followed by Dunn’s post hoc compar- isons. The oral administration of EE from Humirianthera ampla produced marked and dose-dependent attenuation of the glutamate-induced nociception. The ID 50 value (and its respective 95% confidence limits) was 19.9 (15.6–25.2) mg/kg. The peak of inhibition was 71 ± 5% at 300 mg/kg (Fig. 1A). A time- course analysis of the antinociceptive effect of EE given by p.o. route is shown in Fig. 1B. EE produced marked antinociception as early as 1 h after p.o. administration, an action that remained significant up to 10 h after the administration. Thus, the time point of 1 h was chosen for all further studies with independent groups of animals. The results depicted in Fig. 2A and B show that the EE from Humirianthera ampla (30–500 mg/kg, p.o.) caused a significant inhibition of both neurogenic (0–5 min) and inflammatory (15–30 min) phases of formalin-induced licking. However, its antinociceptive effects were significantly more pronounced against the second phase of this model of pain. The calculated mean ID 50 value (and its respective 95% confidence limits) for these effects were: >500 and 144.5 (119.3–175.1) mg/kg and the inhibitions observed were 31 ± 11 and 97 ± 2% at a dose of 500 mg/kg, for first and second phase, respectively. The results depicted in Fig. 3 show that EE from Humirianthera ampla produced marked and dose-related inhibition of the capsaicin-induced neurogenic pain in mice. The ID 50 value (and its respective 95% confidence limits) was 20.0 (17.4–23.0) mg/kg. The maximal inhibition was 80 ± 4% at a dose of 300 mg/kg. The results depicted in Fig. 4 show that EE of Humirianthera ampla (30 mg/kg) inhibited the nociceptive responses induced by spinal injections of glutamate, trans-ACPD, NMDA and substance P in mice. The inhibition values were 84 ± 2, 41 ± 10, 55 ± 8 and 53 ± 9%, respectively. In contrast, EE had no effect against AMPA- and kainate-mediated biting responses (Fig. 4). The EE from Humirianthera ampla (10–100 mg/kg) did not alter the latency response to the tail-flick test. In contrast, morphine (10 mg/kg, s.c.) caused a significant increase in the latency response (results not shown). The EE from Humirianthera ampla (30 and 500 mg/kg) did not affect the motor performance on the rota-rod task and locomotor activity in the open-field test when compared with animals that received vehicle (control group). The means ± S.E.M. on the rota-rod task were 60.0 ± 0.00; 60.0 ± 0.00 and 56.67 ± 3.33 s for the control, 30 and 500 mg/kg group, respectively. In the locomotor activity the means ± S.E.M. of crossings number were 169.5 ± 11.69; 190.5 ± 16.53 and 171.5 ± 13.51 for the control, 30 and 500 mg/kg group, respectively. The EE from Humirianthera ampla (30 mg/kg, p.o.) did not affect the acquisition or retention of the memory in rats sub- mitted to the step-down inhibitory avoidance task. Furthermore, EE at the same dose did not alter the short-term memory and long-term memory (data not shown). The results presented in Fig. 5A show that the pretreatment of mice with naloxone (1 mg/kg, i.p., a non-selective opioid receptor antagonist), given 20 min beforehand, completely reversed the antinociception of EE from Humirianthera ampla (30 mg/kg, p.o.) and morphine (2.5 mg/kg, s.c.) (Fig. 5A). The systemic treatment of mice with naloxone methiodide (1 mg/kg, s.c., a non-selective opioid receptor antagonist that is not permeable into the blood brain barrier) did not reverse the antinocicep- tion of EE against glutamate-induced pain (Fig. 5B). However, the antinociception produced by morphine was significantly reversed (Fig. 5B). The systemic pretreatment of mice with the nitric oxide precursor l -arginine (40 mg/kg, i.p.), but not with d -arginine (40 mg/kg, i.p., an inactive isomer of l -arginine), completely reversed the antinociception caused by l -NOARG (25 mg/kg, i.p., a nitric oxide inhibitor) when analyzed against glutamate- induced nociception (Fig. 6). Under the same conditions, l -arginine significantly reversed the antinociception caused by EE from Humirianthera ampla (Fig. 6). The results depicted in Fig. 7 show that the previous treatment of mice with WAY100635 (0.1 mg/kg, i.p., a selective 5-HT 1A receptor antagonist), ketanserin (1 mg/kg, i.p., a selective 5-HT 2A receptor antagonist) or ondansetron (0.5 mg/kg, i.p., a selective 5-HT receptor antagonist), significantly reversed the antinociception caused by EE (30 mg/kg, p.o.) against glutamate-induced nociception. The systemic pretreatment of mice with caffeine (3 mg/kg, i.p., a non-selective adenosine receptor antagonist) did not significantly reverse the antinociception caused by EE from Humirianthera ampla (30 mg/kg, p.o.) against glutamate- induced nociception (results not shown). In the present study, we demonstrated that the oral treatment of mice with EE from roots of the Humirianthera ampla caused potent antinociception against the chemical agents of nociception: formalin, glutamate and capsaicin. Hence, the chemical models of nociception here employed gave us an approach about the pathways involved on the antinociception of the Humirianthera ampla. It is worth to mention that Humirianthera ampla produced antinociception against both neurogenic and inflammatory phases of formalin. However, the effect was more pronounced against the inflammatory phase. The formalin-induced nociception is a well-described model of nociception and can be consistently inhibited by typical analgesic and anti-inflammatory drugs, including morphine, indomethacin and dexamethasone (Hunskaar and Hole, 1987). Considering the inhibitory property of Humirianthera ampla on the second phase of formalin, we might suggest an anti- inflammatory action of the plant extract. In fact, the chemical constituents present in the roots of the Humirianthera ampla : diterpenoids, triterpenoids and sterols have been reported as potent anti-inflammatory agents (Hernandez-Perez et al., 1995; Fernandez et al., 2001; Yamashita et al., 2002; Spessoto et al., 2003; Liu and Lin, 2006). The EE from Humirianthera ampla strongly inhibited the nociception induced by capsaicin and glutamate. Doses from 10 and 30 mg/kg significantly inhibited the capsaicin and glutamate-induced licking, whereas doses of 100 and 500 mg/kg were necessary to inhibit the inflammatory and neurogenic phases of formalin. This suggests a straight action of Humirianthera ampla on pathways dependent on the glutamatergic and vanilloid systems. Hence, an effect of the plant extract directly on the receptors or second messengers related to these trans- mitters could avoid the nociceptive response. Interestingly, the Humirianthera ampla antinociception was extended up to 10 h after the treatment, an effect that is hardly reached for analgesic clinically used. The licking response induced by formalin, capsaicin and glutamate results from a combination of peripheral input and spinal cord ...
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... results depicted in Fig. 4 show that EE of Humirianthera ampla (30 mg/kg) inhibited the nociceptive responses induced by spinal injections of glutamate, trans-ACPD, NMDA and substance P in mice. The inhibition values were 84 ± 2, 41 ± 10, 55 ± 8 and 53 ± 9%, respectively. In contrast, EE had no effect against AMPA-and kainate-mediated biting responses (Fig. 4). ...
Context 4
... depicted in Fig. 4 show that EE of Humirianthera ampla (30 mg/kg) inhibited the nociceptive responses induced by spinal injections of glutamate, trans-ACPD, NMDA and substance P in mice. The inhibition values were 84 ± 2, 41 ± 10, 55 ± 8 and 53 ± 9%, respectively. In contrast, EE had no effect against AMPA-and kainate-mediated biting responses (Fig. 4). 5 mg/kg, s.c.) against the glutamate-induced licking in mice. Each column represents the mean of 6-8 animals and vertical lines indicate the S.E.M. The symbols denote the significance levels ** p < 0.01 and *** p < 0.001 when compared with control groups; # p < 0.001 when compared with morphine or ethanolic extract treated group by ...
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Citations
... Capsaicin-induced nociception was assayed against visnagin and morphine, individually as well as comparatively, as per Luiz et al. [23]. All the mice were divided into 5 groups. ...
Pain management has been a severe public health issue throughout the world. Acute pain if not treated at the appropriate time can lead to chronic pain that can cause psychological and social distress. Nothing can be more rewarding than treating pain successfully for a physician. However, the use of chemical NSAIDs and opiate drugs has taken a toll on the patients with their unavoidable side effects. This study intends to explore the potential to treat pain by inhibiting nociception and inflammation with a safer, non-addictive, effective, and low-cost alternative agent from a natural source, visnagin. In vivo studies have been conducted using male Swiss albino mice as models for this research. Nociception was induced using different chemical and thermal stimuli such as acetic acid, glutamate, capsaicin, and formalin. To check for the anti-inflammatory properties, carrageenan was used to induce inflammation and the activity was assayed using peritoneal cavity leukocyte infiltration analysis and pro-inflammatory cytokine level comparison with the supplementation of visnagin at three different dosages. The findings of this study revealed that the visnagin treatment effectively attenuated the acetic acid-induced writhing response, glutamate-induced paw licking numbers, capsaicin-induced pain response, and formalin-induced biphasic licking incidences in the experimental mice models. Furthermore, the visnagin treatment remarkably suppressed the carrageenan-induced inflammation in mice, which is evident from the decreased leukocytes, mononuclear, and polymorphonuclear cell numbers in the mice. The levels of cytokines such as TNF-α, IL-1β, and IL-6 were effectively reduced by the visnagin treatment in the experimental mice. The results of open field test proved that the visnagin showed a better locomotor movement in the experimental mice. These results provided evidence for the potential activity of the visnagin against inflammatory and nociceptive responses in the mice.
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... The impact of corynoline on capsaicin-provoked nociception was analyzed by the method prescribed by Luiz et al. (2007) [17]. The rodents were separated into 5 groups with 6 in each. ...
... The impact of corynoline on capsaicin-provoked nociception was analyzed by the method prescribed by Luiz et al. (2007) [17]. The rodents were separated into 5 groups with 6 in each. ...
Pain is growing to be a massive health issue across the globe. It is reported that one in every five adults tends to suffer from pain worldwide each year, regardless of age and gender. Inflammation caused by tissue damage, chemical stimulus, and foreign substances is commonly associated with pain. Inflammatory pain is mainly caused by the direct effect of inflammatory mediators on particular classes of nociceptive neurons. In the current investigation, the antinociceptive and anti-inflammatory effect of corynoline, a phytochemical compound isolated from Corydalis bungeana Turcz., has been evaluated in experimental mice. The experimental mice were divided into 5 groups of 6 animals each. The first control group was fed with water. The second, third, and fourth groups received different doses of corynoline and the fifth group of mice received positive controls. Nociception was induced with the help of acetic acid, formalin, glutamate, capsaicin, hot plate, and tail immersion in mice whereas carrageenan was used to induce inflammation. The peritoneal cavity leukocyte infiltration and pro-inflammatory mediator generation were also analyzed to confirm the anti-inflammatory effect and the natural locomotor activity was determined using an open field test. Corynoline treatment significantly suppressed the paw licking, writhing in the abdominal region, and displayed high nociceptive inhibitory reaction in a dose-related manner. Additionally, corynoline significantly reduced the carrageenan-triggered paw edema and also reduced the levels of pro-inflammatory cytokines. Thus, the antinociceptive and anti-inflammatory activity of corynoline has been successfully established.
... The effect of dieckol against the neuropathic nociception was determined by the technique of capsaicin-triggered nociceptive test described by the Luiz et al. (2007). The experimental mice was alienated into five groups with 6 mice in each. ...
Pain is the common indicator of inflammatory ailments and traumatic tissue injuries. The dieckol is an important therapeutic compound, which present in many seaweeds. The present research work was planned to assess the anti-inflammatory and anti-nociceptive actions of dieckol by using animal model. The anti-nociceptive action of dieckol was investigated by acetic acid triggered writhing, formalin provoked nociception, tail immersion test, hot-plate methods and the anti-inflammatory effects was explored by carrageenan triggered paw edema method. In the present investigation the administration of dieckol was remarkably suppressed and inhibited the acetic acid-provoked writhing, formalin-triggered nociception, tail immersion test, hot plate-provoked nociception in the experimental animals. The dieckol was significantly (p<0.05) inhibited the carrageenan-triggered inflammation, leukocyte infiltration and diminished the formation of pro-inflammatory regulators in the experimental animals. Altogether, the dieckol was showed a potent anti-nociceptive and anti-inflammatory activity.
... The test was performed according to the protocol of Luiz et al. (2007). Capsaicin was prepared by dissolving capsaicin with 5 % ethanol and 95% phosphate buffered saline. ...
Nanotechnology has shown rapid progress in various fields had made a remarkable change in the field of therapeutics too. The present study aims to synthesize and characterize the eco-friendly biocompatible copper oxide nanoparticles using Abies spectabilis plant extract (AS-CuONPs) and inspect its ameliorative potential against the different stimuli induced nociception and inflammatory reactions in mice. The formulated AS-CuONPs were characterized via the UV-vis spectroscopy, FT-IR, and TEM analysis. The nociception was induced by the method of acetic acid, glutamate, capsaicin, formalin, and thermal-induced techniques. The anti-inflammatory property of AS-CuONPs with carrageenan induced paw edema, peritoneal leukocyte infiltration, and carrageenan induced air pouch tests. Our result of UV-Visible spectroscopic analysis confirms the formation of AS-CuONPs and the characterization with FTIR and TEM proves the same. The result of various stimuli induced nociception models provide the evidence that formulated AS-CuONPs effectively inhibits the nociceptive responses in mice. Further the infiltration of leukocytes and inflammatory cytokines were drastically decreased by the AS-CuONPs treatment in the mice. The open field analysis confirms that the AS-CuONPs doesn’t impart any behavioral changes in mice. Over all our results confirms that AS-CuONPs is effective against different stimuli induced nociception and it act as a potent anti-inflammatory agent without rendering any side effects.
... The animals were then observed for 15 min following glutamate injection and the time spent licking or biting the injected paw was recorded as an indication of nociception. [20,21] ...
... Inhibition of glutamate induced nociception suggests that inhibition of NO release or blockade of NMDA receptors could be contributing to the analgesic effect of MECG. [20,21,28] ...
... The animals were then observed for 15 min following glutamate injection and the time spent licking or biting the injected paw was recorded as an indication of nociception. [20,21] ...
... Inhibition of glutamate induced nociception suggests that inhibition of NO release or blockade of NMDA receptors could be contributing to the analgesic effect of MECG. [20,21,28] ...
Objective: Extracts of the root of Calotropis gigantea (family: Apocynaceae) have been used as a natural therapeutic agent in traditional medicine to treat inflammation and pain. This study aims to evaluate the anti-inflammatory and analgesic activity of methanol extract of C. gigantea root (MECG). Materials and Methods: The analgesic activity of MECG was evaluated using formalin-induced pain and glutamate-induced paw licking models. Antagonism of opioid receptors using naloxone was used to determine the involvement of central pathways of pain. The acute inflammation was measured by carrageenan and dextran-induced paw edema models. Cyclooxygenase (COX) assay was carried out to determine the action of MECG on prostaglandins (PGs). Results: MECG 200 mg/kg dose was found to produce a significant (P < 0.001) and dose-dependent analgesic activity in the models used. MECG caused significant inhibition of edema in the carrageenan and dextran-induced inflammation tests. MECG was found to reduce the expression of COX, thus confirming the inhibitory action of MECG on PGs. Conclusion: The findings suggest that MECG possesses analgesic and anti-inflammatory activity mediated through peripheral and central mechanisms. The results justify its traditional use in the treatment of inflammation and pain.
... H. ampla is a member of the Icacinaceae family, popularly known as "surucucaína" or "surucuína." Studies of chemical constituents of the H. ampla's ethanolic extract revealed the presence of the di-and triterpenoids annonalide, humirianthol, acrenol, and lupeol (Luiz et al. 2007). The orchestrated action of these compounds might explain the effect of H. ampla against inflammation and pain caused by snakebite, thus validating the use of this plant by the Amazon native people for this condition. ...
Snakebite is a complex neglected health problem for which the best treatment is the – not always available – antivenom, posing a challenge to health care systems worldwide. It affects different countries and cultures which employ particular approaches for the treatment and expertise apart from the officially recommended. Ancient folk knowledge on the use of plants against snake-related accidents is well established, especially in Asia, where healers or specialists on ethnobotany propose plants for the treatment of the snake envenoming. Although folk medicine traditionally employed plants against snakebites, this is not well established in developed countries, in part due to competition with powerful pharmaceutical companies. Even so, numerous plants with antiophydic properties have been investigated, with a vast number yet to be explored. Scientists studying snake envenoming treatment over the past decades have proposed promising compounds such as coumestans from Eclipta sp. and triterpenes from Hemidesmus sp. and Combretum sp. The aim of this chapter is to review relevant publications on antiophydic plants, some with known active molecules already isolated and explored, yet with no intention of exhausting the subject.
... The glutamate-induced paw licking test was used to investigate the role of glutamatergic system in the modulation of MEMM antinociceptive action and the procedure adopted has been described by Luiz et al. (2007) with slight modifications. Rats were pre-treated orally with 10% DMSO or MEMM (100, 250, and 500 mg/kg) 60 min prior to assessment using the respective test. ...
_Melastoma malabathricum_ L., Melastomaceae, has been traditionally used to relieve diverse pain-related ailments. The objectives of the present study were to determine the antinociceptive activity of methanol extract of _M. malabathricum_ leaves (MEMM) and to elucidate the possible mechanisms of antinociception involved using various rats’ models. The extract (100, 250, and 500 mg/kg) was administered orally 60 min prior to subjection to the respective test. The _in vivo_ (acetic acid-induced abdominal constriction and formalin-induced paw licking tests) and hot plate test models of nociception were used to evaluate the extract antinociceptive activity. Further studies were carried out to determine the role of opioid and vanilloid receptors, glutamate system and nitric oxide/cyclic guanosine phosphate (NO/cGMP) pathway in modulating the extract antinociceptive activity. From the results obtained, MEMM exhibited significant (_p _< 0.05) antinociceptive activity in all the chemical- and thermal-induced nociception models. Naloxone (5 mg/kg), a non-selective opioid antagonist, failed to significantly affect the antinociceptive activity of MEMM when assessed using the abdominal constriction-, hot plate- and formalin-induced paw licking-test. MEMM antinociception was significantly (_p_ < 0.05) reversed in the capsaicin- and glutamate-induced paw licking test. Furthermore, l-arginine (a nitric oxide precursor), NG-nitro-l-arginine methyl esters (l-NAME; an inhibitor of NO synthase), methylene blue (MB; an inhibitor of cGMP), or their combination also failed to significantly (_p _< 0.05) block the MEMM antinociception. In conclusion, MEMM exerted a non-opioid/NO/cGMP-mediated antinociceptive activity at the central and peripheral levels partly via the inhibition of vanilloid receptors and glutamatergic system.
... H. ampla is a member of the Icacinaceae family, popularly known as "surucucaína" or "surucuína." Studies of chemical constituents of the H. ampla's ethanolic extract revealed the presence of the di-and triterpenoids annonalide, humirianthol, acrenol, and lupeol (Luiz et al. 2007). The orchestrated action of these compounds might explain the effect of H. ampla against inflammation and pain caused by snakebite, thus validating the use of this plant by the Amazon native people for this condition. ...
Snakebite is a complex neglected health problem for which the best treatment is the – not always available – antivenom, posing a challenge to health care systems worldwide. It affects different countries and cultures which employ particular approaches for the treatment and expertise apart from the officially recommended. Ancient folk knowledge on the use of plants against snake-related accidents is well established, especially in Asia, where healers or specialists on ethnobotany propose plants for the treatment of the snake envenoming. Although folk medicine traditionally employed plants against snakebites, this is not well established in developed countries, in part due to competition with powerful pharmaceutical companies. Even so, numerous plants with antiophydic properties have been investigated, with a vast number yet to be explored. Scientists studying snake envenoming treatment over the past decades have proposed promising compounds such as coumestans from Eclipta sp. and triterpenes from Hemidesmus sp. and Combretum sp. The aim of this chapter is to review relevant publications on antiophydic plants, some with known active molecules already isolated and explored, yet with no intention of exhausting the subject.
