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a: Normal pyramidal neurons (P) with normal staining of Nissl bodies in the control group. b. Degeneration with shrinkage and strong staining of Nissl bodies (arrows) in the DLM-treated rats. c, d Little or no signs of degeneration of pyramidal neurons (P) with normal staining of Nissl bodies (arrowheads) in the CMN- and NCMN-treated groups, respectively. Cresyl violet staining, scale bar, 50 µm (a–d)
Source publication
We aimed to prove that oxidative stress is the main mechanism responsible for hippocampal neurotoxicity induced by deltamethrin (DLM). The protective role of curcumin (CMN) and nano-curcumin (NCMN) over this toxicity was studied. The rats were categorized into four groups: control, DLM, CMN and NCMN. The study continued for 30 days. Hippocampus was...
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Background
Cisplatin (CDDP) is an efficacious anticancer agent used widely in chemotherapy despite its severe side effect related to neurotoxicity. Redox imbalance and inflammatory mechanism have been implicated in the pathophysiology of CDDP-induced neurotoxicity. Herein, we investigated whether Tiliacora triandra (TT) extract could inhibit CDDP-i...
Citations
... These findings are consistent with the findings of Sarawi et al. (2021aSarawi et al. ( , 2021b, who observed that CUR-NPS improved cardiac MDA and antioxidant enzymes in copper sulfateintoxicated rats. Furthermore, many studies indicated that CUR-NPS significantly improved the oxidative stress caused by several toxic agents in both in vivo and in vitro models (El-Desoky et al., 2020;Zaki et al., 2020). CUR-NPS's antioxidant activity is attributed to its capability to counteract free radicals (Mohammed et al., 2018) as well as its ability to enhance glutathione production (Biswas et al., 2005). ...
... CPM-induced neurotoxicity is mediated through the emergence of ROS, a decline in antioxidant defense, and the inhibition of neurochemical enzymes. This further prompts inflammatory and apoptotic incidents due to its impoverished cell defense systems, since neuroinflammation and apoptosis have been established in numerous brain disorders, including CPM-induced neurotoxicity [8,38]. Caspase-3 and -9 were upregulated, which are markers of apoptosis in the brain, whereas high levels of IL-6, IL-1β, and TNF-α were found after 15 days of exposure of CPM-induced apoptosis and inflammation. ...
Cypermethrin (CPM) is the most toxic synthetic pyrethroid that has established neurotoxicity through oxidative stress and neurochemical agitation in experimental rats. The toxic effects are supposed to be mediated by modifying the sodium channels, reducing Na-K ATPase, acetylcholine esterase (AchE), and monoamine oxidase (MAO). The use of curcumin nanoparticles (NC) that have potent antioxidant, anti-inflammatory and antiapoptotic properties with improved bioavailability attenuates neurotoxicity in rat brains. To test this hypothesis, animals were divided into five groups, each having six animals. Group-I control received vehicle only, while Group-II was treated with 50 mg/kg CPM. Group-III and Group-IV received both CPM and NC 2.5 mg/kg and 5 mg/kg, respectively. Group-V received 5 mg of NC alone. The CPM and NC were given by oral route. Afterwards, brain antioxidant status was measured by assessing lipid peroxidation (LPO), 4-HNE, glutathione reduced (GSH), antioxidant enzyme catalase, and superoxide dismutase (SOD) along with neurotoxicity markers Na-K ATPase, AchE, and MAO. Inflammation and apoptosis indices were estimated by ELISA, qRT-PCR, and immunohistochemistry, while morphologic changes were examined by histopathology. Observations from the study confirmed CPM-induced neurotoxicity by altering Na-K ATPase, AchE, and MAO, and by decreasing the activity of antioxidant enzymes and GSH. Oxidative stress marker LPO and the level of inflammatory interleukins IL-6, IL-1β, and TNF-α were notably high, and elevated expressions of Bax, NF-kB, and caspase-3 and -9 were reported in CPM group. However, NC treatment against CPM offers protection by improving antioxidant status and lowering LPO, inflammation, and apoptosis. The neurotoxicity marker’s enzyme successfully attenuated after NC treatment. Therefore, this study supports the administration of NC effectively ameliorated CPM-induced neurotoxicity in experimental rats.
... We found that both curcumin and Ast prevented the decreasing trend of GSH, SOD, and CAT levels detected in D-gal and NA groups (Fig 5), suggesting that curcumin's antioxidant activity minimized the aging-associated oxidative burden in mice [69]. Our results are also in agreement with previous studies [70]. ...
Aging-induced memory impairment is closely associated with oxidative stress. D-Galactose (D-gal) evokes severe oxidative stress and mimics normal aging in animals. Curcumin, a natural flavonoid, has potent antioxidant and anti-aging properties. There are several proteins like glutathione S-transferase A1 (GSTA1), glutathione S-transferase omega-1 (GSTO1), kelch-like ECH-associated protein 1 (KEAP1), beta-secretase 1 (BACE1), and amine oxidase [flavin-containing] A (MAOA) are commonly involved in oxidative stress and aging. This study aimed to investigate the interaction of curcumin to these proteins and their subsequent effect on aging-associated memory impairment in two robust animal models: D-Gal and normal aged (NA) mice. The aging mice model was developed by administering D-gal intraperitoneally (i.p). Mice (n = 64) were divided into the eight groups (8 mice in each group): Vehicle, Curcumin-Control, D-gal (100mg/kg; i.p), Curcumin + D-gal, Astaxanthin (Ast) + D-gal, Normal Aged (NA), Curcumin (30mg/kg Orally) + NA, Ast (20mg/kg Orally) + NA. Retention and freezing memories were assessed by passive avoidance (PA) and contextual fear conditioning (CFC). Molecular docking was performed to predict curcumin binding with potential molecular targets. Curcumin significantly increased retention time (p < 0.05) and freezing response (p < 0.05) in PA and CFC, respectively. Curcumin profoundly ameliorated the levels of glutathione, superoxide dismutase, catalase, advanced oxidation protein products, nitric oxide, and lipid peroxidation in mice hippocampi. In silico studies revealed favorable binding energies of curcumin with GSTA1, GSTO1, KEAP1, BACE1, and MAOA. Curcumin improves retention and freezing memory in D-gal and nature-induced aging mice. Curcumin ameliorates the levels of oxidative stress biomarkers in mice. Anti-aging effects of curcumin could be attributed to, at least partially, the upregulation of antioxidant enzymes through binding with GSTA1, GSTO1, KEAP1, and inhibition of oxidative damage through binding with BACE1 and MAOA.
... We found that both curcumin and Ast prevented the decreasing trend of GSH, SOD, and CAT levels detected in D-gal and NA groups (Fig 5), suggesting that curcumin's antioxidant activity minimized the aging-associated oxidative burden in mice [69]. Our results are also in agreement with previous studies [70]. ...
Aging-induced memory impairment is closely associated with oxidative stress. D-Galactose (D-gal) evokes severe oxidative stress and mimics normal aging in animals. Curcumin, a natural flavonoid, has potent antioxidant and anti-aging properties. There are several proteins like glutathione S-transferase A1 (GSTA1), glutathione S-transferase omega-1 (GSTO1), kelch-like ECH-associated protein 1 (KEAP1), beta-secretase 1 (BACE1), and amine oxidase [fla-vin-containing] A (MAOA) are commonly involved in oxidative stress and aging. This study aimed to investigate the interaction of curcumin to these proteins and their subsequent effect on aging-associated memory impairment in two robust animal models: D-Gal and normal aged (NA) mice. The aging mice model was developed by administering D-gal intraperitoneally (i.p). Mice (n = 64) were divided into the eight groups (8 mice in each group): Vehicle, Curcumin-Control, D-gal (100mg/kg; i.p), Curcumin + D-gal, Astaxanthin (Ast) + D-gal, Normal Aged (NA), Curcumin (30mg/kg Orally) + NA, Ast (20mg/kg Orally) + NA. Retention and freezing memories were assessed by passive avoidance (PA) and contextual fear conditioning (CFC). Molecular docking was performed to predict curcumin binding with potential molecular targets. Curcumin significantly increased retention time (p < 0.05) and freezing response (p < 0.05) in PA and CFC, respectively. Curcumin profoundly ameliorated the levels of glutathione, super-oxide dismutase, catalase, advanced oxidation protein products, nitric oxide, and lipid peroxi-dation in mice hippocampi. In silico studies revealed favorable binding energies of curcumin with GSTA1, GSTO1, KEAP1, BACE1, and MAOA. Curcumin improves retention and freezing memory in D-gal and nature-induced aging mice. Curcumin ameliorates the levels of oxidative stress biomarkers in mice. Anti-aging effects of curcumin could be attributed to, at least partially , the upregulation of antioxidant enzymes through binding with GSTA1, GSTO1, KEAP1, and inhibition of oxidative damage through binding with BACE1 and MAOA.
... We found that both curcumin and Ast prevented the decreasing trend of GSH, SOD, and CAT levels detected in D-gal and NA groups (Fig 5), suggesting that curcumin's antioxidant activity minimized the aging-associated oxidative burden in mice [69]. Our results are also in agreement with previous studies [70]. ...
Aging-induced memory impairment is closely associated with oxidative stress. D-Galactose (D-gal) evokes severe oxidative stress and mimics normal aging in animals. Curcumin, a natural flavonoid, has potent antioxidant and anti-aging properties. There are several proteins like glutathione S-transferase A1 (GSTA1), glutathione S-transferase omega-1 (GSTO1), kelch-like ECH-associated protein 1 (KEAP1), beta-secretase 1 (BACE1), and amine oxidase [fla-vin-containing] A (MAOA) are commonly involved in oxidative stress and aging. This study aimed to investigate the interaction of curcumin to these proteins and their subsequent effect on aging-associated memory impairment in two robust animal models: D-Gal and normal aged (NA) mice. The aging mice model was developed by administering D-gal intraperitoneally (i.p). Mice (n = 64) were divided into the eight groups (8 mice in each group): Vehicle, Curcumin-Control, D-gal (100mg/kg; i.p), Curcumin + D-gal, Astaxanthin (Ast) + D-gal, Normal Aged (NA), Curcumin (30mg/kg Orally) + NA, Ast (20mg/kg Orally) + NA. Retention and freezing memories were assessed by passive avoidance (PA) and contextual fear conditioning (CFC). Molecular docking was performed to predict curcumin binding with potential molecular targets. Curcumin significantly increased retention time (p < 0.05) and freezing response (p < 0.05) in PA and CFC, respectively. Curcumin profoundly ameliorated the levels of glutathione, super-oxide dismutase, catalase, advanced oxidation protein products, nitric oxide, and lipid peroxi-dation in mice hippocampi. In silico studies revealed favorable binding energies of curcumin with GSTA1, GSTO1, KEAP1, BACE1, and MAOA. Curcumin improves retention and freezing memory in D-gal and nature-induced aging mice. Curcumin ameliorates the levels of oxidative stress biomarkers in mice. Anti-aging effects of curcumin could be attributed to, at least partially , the upregulation of antioxidant enzymes through binding with GSTA1, GSTO1, KEAP1, and inhibition of oxidative damage through binding with BACE1 and MAOA.
... El-Gendy et al. [84] reported that Nrf2 protein levels significantly increased in aflatoxicated-birds supplemented with Saccharomyces cell wall. In addition, Zaki et al. [85] concluded that there was a decrease in Nrf2 protein levels with the use of curcumin and nanocurcumin compared to that of deltamethrin-treated rats, and this is what our study proves. ...
Background
The adverse effect of aflatoxin in broilers is well known. However, dietary supplementation of Saccharomyces cell wall and/or Nanocurcumin may decrease the negative effect of aflatoxin B1 because of the bio-adsorbing feature of the functional ingredients in Yeast Cell Wall and the detoxification effect of curcumin nanoparticles. The goal of this study was to see how Saccharomyces cell wall/Nanocurcumin alone or in combination with the aflatoxin-contaminated diet ameliorated the toxic effects of aflatoxin B1 on broiler development, blood and serum parameters, carcass traits, histology, immune histochemistry, liver gene expression, and aflatoxin residue in the liver and muscle tissue of broilers for 35 days. Moreover, the withdrawal time of aflatoxin was measured after feeding the aflatoxicated group an aflatoxin-free diet. Broiler chicks one day old were distributed into five groups according to Saccharomyces cell wall and/or nanocurcumin with aflatoxin supplementation. The G1 group was given a formulated diet without any supplements. The G2 group was supplemented with aflatoxin (0.25 mg/kg diet) in the formulated diet. The G3 group was supplemented with aflatoxin (0.25 mg/kg diet) and Saccharomyces cell wall (1 kg/ton diet) in the formulated diet. The G4 group was supplemented with aflatoxin (0.25 mg/kg diet) and nanocurcumin (400 mg/kg) in the formulated diet. The G5 group was supplemented with aflatoxin (0.25 mg/kg diet) and Saccharomyces cell wall (1 kg/ton diet) in combination with nanocurcumin (200 mg/kg) in the formulated diet.
Results
According to the results of this study, aflatoxin supplementation had a detrimental impact on the growth performance, blood and serum parameters, carcass traits, and aflatoxin residue in the liver and muscle tissue of broilers. In addition, aflatoxin supplementation led to a liver injury that was indicated by serum biochemistry and pathological lesions in the liver tissue. Moreover, the shortening of villi length in aflatoxicated birds resulted in a decrease in both the crypt depth ratio and the villi length ratio. The expression of CYP1A1 and Nrf2 genes in the liver tissue increased and decreased, respectively, in the aflatoxicated group. In addition, the aflatoxin residue was significantly ( P ≤ 0.05) decreased in the liver tissue of the aflatoxicated group after 2 weeks from the end of the experiment.
Conclusion
Saccharomyces cell wall alone or with nanocurcumin attenuated these negative effects and anomalies and improved all of the above-mentioned metrics.
... Consistently, it is reported that curcumin improves LTP disorders caused by lipopolysaccharide [52]. Evidence suggests that nano-curcumin is more effective than curcumin in improving impaired cognitive function [53]. A limitation in the present research was the lack of the plasma curcumin level measurement and pharmacokinetic analysis of nano-curcumin. ...
... A study by Fan et al. showed that the improving effect of nanocurcumin on spatial learning and memory is more than curcumin [38]. The beneficial effects of nano-curcumin on hippocampus-dependent cognitive function and synaptic plasticity could also be explained through its potent antioxidant effects reflected in a decreased level of malondialdehyde and increased level of glutathione, superoxide dismutase, and catalase [53]. Chronic application of curcumin leads to an increase in BDNF of the hippocampus [55]. ...
Background:
Noise pollution is one of the fundamental factors in the etiology of many disorders. Noise stress adversely affects cognitive behaviors and long-term potentiation (LTP), the candidate mechanism of learning and memory. In the present study, we examined the neuroprotective effects of nano-curcumin on behavioral and electrophysiological aspects of hippocampus-dependent memory in noise-exposed animals.
Methods:
The stressed animals received either vehicle (ST) or nano-curcumin (NANO + ST) for 2 weeks. The control groups remained either intact (CON) or received nano-curcumin (NANO + CON). The ST and NANO + ST groups were exposed to daily noise for 2 weeks. The spatial memory was assessed in the Morris water maze. The LTP was investigated through field potential recording in the CA3-CA1 pathway of the hippocampus. Serum corticosterone level was measured at the end of the experiments.
Results:
The ST group showed a lower cognitive function and suppressed LTP compared to the CON group. The nano-curcumin treatment improved the maze navigation and LTP induction compared to the ST group. While the stress exposure elevated the serum level of corticosterone in the ST animals, nano-curcumin treatment reduced it.
Conclusions:
The nano-curcumin treatment restores impaired behavioral and electrophysiological aspects of learning and memory in the noise-exposed animals. The plasma corticosterone levels may be associated with changes in cognitive behavior and synaptic plasticity.
... El-Gendy et al. [70] reported that Nrf2 protein levels signi cantly increased in a atoxicated-bird supplemented with Saccharomyces cell wall. In addition, Zaki et al. [71] concluded that there was a decrease in Nrf2 protein levels with the use of curcumin and nanocurcumin compared to that of deltamethrin-treated rats and this is what our study proves. ...
Background
The adverse effect of aflatoxin in broilers well known. However, dietary supplementation of nanocurcumin and/or Saccharomyces cell wall may decrease the bad effect of aflatoxin B1 because of their bio-adsorbing feature of the functional ingredients in Yeast Cell Wall and the detoxification effect of curcumin nanoparticles. The goal of this study was to see how nanocurcumin and/or Saccharomyces cell wall supplementation and/or aflatoxin affected broiler development, blood and serum parameters, carcass trait, histology, immune histochemistry, liver gene expression, and aflatoxin residue in the liver and muscle tissue of broilers. Broiler chicks with one day old were distributed into five groups according to nanocurcumin and/or saccharomyces cell wall with aflatoxin supplementation. The G1 group was given a formulated diet without any supplements. The G2 group was supplemented with aflatoxin (0.25 mg/kg diet) in the formulated diet. The G3 group was supplemented with aflatoxin (0.25 mg/kg diet) and Saccharomyces cell wall (1Kg/Ton diet) in the formulated diet. The G4 group was supplemented with aflatoxin (0.25 mg/kg diet) and nanocurcumin (400 mg/kg) in the formulated diet. The G5 group was supplemented with aflatoxin (0.25 mg/kg diet) and Saccharomyces cell wall (1Kg/Ton diet) with nanocurcumin (200 mg/kg) in the formulated diet.
Results
Aflatoxin supplementation had a detrimental impact on the growth performance, blood and serum parameters, carcass trait, and aflatoxin residue in the liver and muscle tissue of broilers, according to the results of this study. In addition, aflatoxin supplementation led to a liver injury that was indicated by serum biochemistry and pathological lesions in the liver tissue. Moreover, the intestinal villi, length, and width were affected. The expression of some genes in the liver tissue was affected.
Conclusion
Saccharomyces cell wall alone or with nanocurcumin attenuated these negative effects and anomalies, and improving all of the above-mentioned metrics.
... Interestingly, FA incorporated nano- Ferulic acid-memoquin hybrids Inhibited AChE activity and Aβ fibrils formation SH-SY5Y neuroblastoma cell line [89] Ferulic acid-O-alkylamine derivatives Inhibited BuChE and Aβ aggregations Scopolamine-induced mice [90] Donepezil-ferulic acid hybrids Inhibited equineButyrylCholinEsterase (eqBuChE) selectively Chemical techniques [91] Tacrine-ferulic acid hybrid Inhibited butyrylcholinesterase activity and Aβ peptide aggregation Chemical techniques [92] Ferulic acid-based 1,3,4-oxadiazole molecular hybrids Inhibited AChE, BChE, and BACE-1 activity SH-SY5Y neuroblastoma cell line [93] Ferulic/lipoic/comenic acid-melatonin hy- Tacrine-6-ferulic acid Activated Nrf2/ARE pathway Mouse hippocampal neuronal HT22 cells [103] lipid carriers prevented cerebral ischemia/reperfusion-induced neuro-behavioral deficits and ameliorated cellular and oxidative damages in rats compared to FA alone [111,112]. Moreover, treatments, involving nano-formulations with natural antioxidants, are reported to be more effective than treatment with solely natural products possessing antioxidant activities in ameliorating oxidative alterations in both in vitro and in vivo AD models [113][114][115]. Concordantly, ferulic acid-loaded nano-emulsion (FA-NE) was prepared via the method of spontaneous nano-emulsification, and its sustained-release profile, permeability, and protective potential against ultraviolet A (UVA) induced oxidative stress were evaluated in rat skin tissue versus conventional FA in a previous study conducted by Harwans et al. [116]. ...
Alzheimer's Disease (AD) is one of the most important neurodegenerative diseases and it covers 60% of whole dementia cases. AD is a constantly progressing neurodegenerative disease as a result of the production of β-amyloid (Aβ) protein and the accumulation of hyper-phosphorylated Tau protein; it causes breakages in the synaptic bonds and neuronal deaths to a large extent. Millions of people worldwide suffer from AD because there is no definitive drug for disease prevention, treatment or slowdown. Over the last decade, multiple target applications have been developed for AD treatments. These targets include Aβ accumulations, hyper-phosphorylated Tau proteins, mitochondrial dysfunction, and oxidative stress resulting in toxicity. Various natural or semisynthetic antioxidant formulations have been shown to protect brain cells from Aβ induced toxicity and provide promising potentials for AD treatment. Ferulic acid (FA), a high-capacity antioxidant molecule, is naturally synthesized from certain plants. FA has been shown to have different substantial biological properties, such as anticancer, antidiabetic, antimicrobial, anti-inflammatory, hepatoprotective, and cardioprotective actions, etc. Furthermore, FA exerted neuroprotection via preventing Aβ-fibril formation, acting as an anti-inflammatory agent, and inhibiting free radical generation and acetylcholinesterase (AChE) enzyme activity. In this review, we present key biological roles of FA and several FA derivatives in Aβ-induced neurotoxicity, protection against free radical attacks, and enzyme inhibitions and describe them as possible therapeutic agents for the treatment of AD.
... In the present study, there was marked improvement of degenerative changes and low expression of caspase 3 in GI & GII compared to GIII. Zaki et al. (2020) reported improvement of apoptotic changes with the Cur as compared to control group. Caspase-3 is the most abundant of the recognized caspases in the brain (Kuida et al, 1999). ...
Trichinella spiralis can cause systemic inflammatory manifestations all over the body before habituating their destination in the striated muscles. Its new borne larvae (NBL) most dangerous phase go via bloodstream of different organs during migration. This study explored the anti-inflammatory, antioxidant and anti-apoptotic effects of Curcumin (Cur) and Curcumin nanoparticles (Cur-Nano) on inflammatory and pathological changes occurred in different organs in murine trichinellosis during larval migratory phase.
