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The histopathological picture of brain cortex (A-D) and hippocampus (E-H) CA1 region in different groups. A: Sham group showing normal histologic picture of brain cortex (H&E X400). B: I/R control group showing large area of gliosis (arrow) with marked neuronal degeneration (H&E X400). C: I/R + propolis-50 group showing moderate number of degenerated and necrosed neurons (arrow) (H&E X400). D: I/R + propolis-100 group showing slight number of degenerated and necrosed neurons (arrow) (H&E X400).
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Neuroprotective impact of transforming growth factor β1 (TGF-β1) is increasingly recognized in different brain injuries. Propolis exhibits a broad spectrum of biological and pharmacological properties including neuroprotective action. The objective of the investigation was to explore the involvement of TGF-β1 signaling in the neuroprotective mechan...
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Context 1
... sham group showed normal histological picture of cerebral cortex (Fig. 5-A), and hippocampus ( Fig. 5-E). The grey matter of the cerebral cortex of I/R control group revealed areas of coagulative necrosis with inflammatory cell infiltration, massive number of degenerated and necrosed neurons with neuronophagia, multiple focal areas of gliosis, astrogliosis and microgliosis (Fig. 5-B). Whilst the cerebral ...
Context 2
... sham group showed normal histological picture of cerebral cortex (Fig. 5-A), and hippocampus ( Fig. 5-E). The grey matter of the cerebral cortex of I/R control group revealed areas of coagulative necrosis with inflammatory cell infiltration, massive number of degenerated and necrosed neurons with neuronophagia, multiple focal areas of gliosis, astrogliosis and microgliosis (Fig. 5-B). Whilst the cerebral cortex grey matter showed axonal ...
Context 3
... picture of cerebral cortex (Fig. 5-A), and hippocampus ( Fig. 5-E). The grey matter of the cerebral cortex of I/R control group revealed areas of coagulative necrosis with inflammatory cell infiltration, massive number of degenerated and necrosed neurons with neuronophagia, multiple focal areas of gliosis, astrogliosis and microgliosis (Fig. 5-B). Whilst the cerebral cortex grey matter showed axonal fragmentation and demyelination of nerve fibers. The hippocampus of the same group showed massive number of degenerated pyramidal cells (Fig. 5-F). All previous described lesions were minimal in I/ R + proposal-50 and I/R + proposal-100 groups as shown in (Fig. 5-C, D, G, H). ...
Context 4
... infiltration, massive number of degenerated and necrosed neurons with neuronophagia, multiple focal areas of gliosis, astrogliosis and microgliosis (Fig. 5-B). Whilst the cerebral cortex grey matter showed axonal fragmentation and demyelination of nerve fibers. The hippocampus of the same group showed massive number of degenerated pyramidal cells (Fig. 5-F). All previous described lesions were minimal in I/ R + proposal-50 and I/R + proposal-100 groups as shown in (Fig. 5-C, D, G, H). ...
Context 5
... and microgliosis (Fig. 5-B). Whilst the cerebral cortex grey matter showed axonal fragmentation and demyelination of nerve fibers. The hippocampus of the same group showed massive number of degenerated pyramidal cells (Fig. 5-F). All previous described lesions were minimal in I/ R + proposal-50 and I/R + proposal-100 groups as shown in (Fig. 5-C, D, G, H). ...
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Citations
... Simultaneously, VEGF-BDNF pathway could improve the cognitive dysfunction (Jeong et al., 2019). TGF-β1 also played an important role for ischemic cerebrovascular disorders (Rehab et al., 2020). Therefore, angiogenesis and neurogenesis might be a potential mechanism to improve cerebral ischemia injury. ...
At present, Stroke is still one of the leading causes of population death worldwide and leads to disability. Traditional Chinese medicine plays an important role in the prevention or treatment of stroke. l-borneol, a traditional Chinese medicine, has been used in China to treat stroke for thousands of years. However, its mechanism of action is unclear. After cerebral ischemia, promoting angiogenesis after cerebral ischemia and providing nutrition for the infarct area is an important strategy to improve the damage in the ischemic area, but it is also essential to promote neurogenesis and replenish new neurons. Here, our research shows that l-borneol can significantly improve the neurological deficits of pMCAO model rats, reduce cerebral infarction, and improve the pathological damage of cerebral ischemia. and significantly increase serum level of Ang-1 and VEGF, and significantly decrease level of ACE and Tie2 to promote angiogenesis. PCR and WB showed the same results. Immunohistochemistry also showed that l-borneol can increase the number of CD34 positive cells, further verifying that l-borneol can play a neuroprotective effect by promoting angiogenesis after cerebral ischemia injury. In addition, l-borneol can significantly promote the expression level of VEGF, BDNF and inhibit the expression levels of TGF-beta 1 and MMP9 to promote neurogenesis. The above suggests that l-borneol can promote angiogenesis coupled neurogenesis by regulating Ang1-VEGF-BDNF to play a neuroprotective effect. Molecular docking also shows that l-borneol has a very high binding rate with the above target, which further confirmed the target of l-borneol to improve cerebral ischemic injury. These results provide strong evidence for the treatment of cerebral ischemia with l-borneol and provide reference for future research.
... MCAO induction was performed as previously described (Abdel-Rahman et al., 2020). Briefly, rats were anesthetized with zoletil® (tiletamine + zolazepam), at 80 mg/kg intraperitoneal ketamine and xylazine (10 mg/kg) injection. ...
Dodonaea viscosa grows widely in Saudi Arabia, but studies evaluating its neuroprotective activity are lacking. Thus, this study aimed to isolate and identify the secondary metabolites and evaluate the neuroprotective effects of D. viscosa leaves. The isolation and identification of phytochemicals were performed using chromatographic and spectroscopic techniques. The neuroprotective potential of the extract was evaluated against focal cerebral ischaemia–reperfusion injury in rat model. Neurobehavioural deficits in the rats were evaluated, and their brains were harvested to measure infarct volume and oxidative biomarkers. Results revealed the presence of three compounds: a novel isoprenylated phenolic derivative that was elucidated as 4-hydroxy-3-(3ʹ-methyl-2ʹ-butenyl) phenyl 1-O-β-D-apiosyl-(1ʹʹʹ → 6ʹʹ)- β-D-glucopyranoside (named Viscomarfadol) and two known compounds (isorhamnetin-3-O-rutinoside and epicatechin (4–8) catechin). Pre-treatment of the rats with the extract improved neurological outcomes. It significantly reduced neurological deficits and infarct volume; significantly reduced lipid peroxidation, as evidenced by decreased malondialdehyde levels; and significantly elevated antioxidant (superoxide dismutase, catalase, and glutathione) activities. These results indicate that D. viscosa is a promising source of bioactive compounds that can improve neurological status, decrease infarct volume, and enhance antioxidant activities in rats with cerebral ischaemic injury. Thus, D. viscosa could be developed into an adjuvant therapy for ischaemic stroke and other oxidative stress-related neurodegenerative disorders. Further investigations are warranted to explore other bioactive compounds in D. viscosa and evaluate their potential neuroprotective activities.
... 29 It has been demonstrated that Prop antagonizes the damage induced by cerebral ischemia reperfusion through suppression of MDA and elevation of reduced GSH, SOD, GPO and catalase levels in the brain homogenates of rats with cerebral ischemia reperfusion injury. 30 Kaya et al., have studied the protective effect of Prop on myocardial ischemia reperfusion injury in rats and showed that Prop increases total anti-oxidant status and SOD, and decreases total oxidant status in rats. 31 da Costa et al., have reported that red Prop significantly improves oxidative stress parameters in ischemia reperfusion acute renal injury. ...
The torsion model of testis in a rat was adopted for evaluation of possible effects of propolis (Prop) on ischemia-reperfusion (IS/REP) injury. The healthy male Wistar rats (totally 24 animals) were randomized into four groups (n = 6) and animals experienced bilateral testicular torsions as follows: In sham group just, laparotomy was performed and in IS group, animals experienced a 3 hr period testicular IS. In IS/REP group, a 3 hr period of IS followed by a 3 hr period of testicular REP for left testis and a one-week testicular REP for right testis were done. In this group animals were gavaged by 1.00 mL normal saline 1 hr before the onset of IS. In IS/REP/ Prop group, the same procedures for IS/REP animals were followed as well as gavage of 1.00 mL Prop extract solution 1 hr before the onset of IS. Analyses of biochemistry, histology, inflammatory biomarkers and sperm parameters were carried out. In IS/REP/Prop group, nitric oxide synthase malondialdehyde, myeloperoxidase and 8-hydroxy-2 deoxyguanine in IS/REP/Prop group were significantly decreased and, superoxide dismutase, total glutathione, glutathione peroxidase, glutathione reductase and glutathione S-transferase were significantly increased compared to the other animals. In IS/REP/Prop group, seminiferous tubules (with normal spermatogenesis) showed all stages of spermatogenic cells with plentiful spermatozoa. Tubular deterioration and atrophy and spermatogenic cell loss in were seen in a limited extent. The mean concentrations of Interleukin-1 beta and tumor necrosis factor alpha in IS/REP/Prop were significantly decreased. Sperm quality was significantly improved by Prop in IS/REP/Prop group. It was concluded that Prop could be supportive in diminishing IS/REP injury in testicular tissue exposed to ischemia.
... 157,158 A well-known target is TGF-β which has a neuroprotective function in post-ischemic injury by directing protective effects on the cells during ischemic stroke. 159,160 Therefore, post-ischemic involvement of IL-10 and TGF-β is necessary to bridge the gap between the innate and adaptive immune systems during ischemic injury. ...
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a novel coronavirus, causes coronavirus disease 2019 (COVID-19) which led to neurological damage and increased mortality worldwide in its second and third waves. It is associated with systemic inflammation, myocardial infarction, neurological illness including ischemic strokes (e.g., cardiac and cerebral ischemia), and even death through multi-organ failure. At the early stage, the virus infects the lung epithelial cells and is slowly transmitted to the other organs including the gastrointestinal tract, blood vessels, kidneys, heart, and brain. The neurological effect of the virus is mainly due to hypoxia-driven reactive oxygen species (ROS) and generated cytokine storm. Internalization of SARS-CoV-2 triggers ROS production and modulation of the immunological cascade which ultimately initiates the hypercoagulable state and vascular thrombosis. Suppression of immunological machinery and inhibition of ROS play an important role in neurological disturbances. So, COVID-19 associated damage to the central nervous system, patients need special care to prevent multi-organ failure at later stages of disease progression. Here in this review, we are selectively discussing these issues and possible antioxidant-based prevention therapies for COVID-19-associated neurological damage that leads to multi-organ failure.
... This indicates that propolis has an anti-inflammatory effect [20]. Rahman et al. (2020) study on rat model of focal cerebral ischemia (ischemic reperfusion) given propolis at doses 50 and 100 mg/kgbw. The results showed improvement in neurological deficits, locomotor function and motor coordination. ...
... Propolis decreases malondialdehyde levels and increases levels of the antioxidants glutathione, superoxide dismutase, glutathione peroxidase, catalase, BDNF and dopamine levels in the brain homogenates of ischemic reperfusion rats. Propolis reduces the infarct area in the brain and increases the number of healthy cells in the cortex and hippocampus [21]. In vitro study on cytotoxicity-induced SHSY5Y neuroblastoma cell culture using H2O2. ...
... The middle cerebral artery occlusion (MCAO) was applied to rats for 2 h to induce focal cerebral I/R damage followed by reperfusion [17]. Animals were anesthetized using ketamine (100 mg/kg) and xylazine (10 mg/kg) anesthesia and were fixed in the supine position on a surgery board. ...
Oxidative stress and inflammatory reaction play critical roles in ischemia/reperfusion (I/R) injury in the brain. β-carotene (βCAR) is a naturally occurring pigment present in fruits and vegetables that expresses antioxidant and anti-inflammatory activities. This study was conducted to investigate the involvement of Bcl2/Bax and NF-κB signaling pathways in the potential protective role of βCAR against brain injury in a middle cerebral artery occlusion (MCAO) rat model. A focal brain ischemia model was created for 2 h, followed by reperfusion. Rats were given 10 and 20 mg/kg of βCAR for 7 days orally before induction of ischemia, at the start of reperfusion, and 3 days after ischemia. Scores of neurological deficit were rated 24 h after induction of ischemia. Motor coordination and spontaneous coordinate activities were assessed using rotarod and activity cage, respectively. After 2 h of the last dose, the animals were killed and their brains were extracted for further examinations. The results of the study show that βCAR diminished the score of neurological deficits and ameliorated motor coordination, balance, and locomotor activity in the I/R control group. Further, βCAR resulted in diminution of malondialdehyde (MDA) and augmentation of reduced glutathione (GSH) contents, as well as the elevation of superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) enzyme activities in the brain homogenates of I/R rats. βCAR treatment significantly reduced nuclear factor kappa B (NF-κB) brain content and myeloperoxidase (MPO) activity and ameliorated the histological alterations in the brain tissues. βCAR significantly suppressed Bcl-2-associated X protein (Bax) and caspase-3 expression, as well as upregulated B-cell lymphoma-2 (Bcl-2) expression, suggesting a neuroprotective potential via downregulating NF-kB and protecting the rat brain against the I/R-associated apoptotic injury.
... Liver-reduced glutathione content (GSH) and malondialdehyde (MDA) were determined colorimetrically as described by Abdel-Rahman et al. [19]. ...
Hepatic fibrosis causes severe morbidity and death. No viable treatment can repair fibrosis and protect the liver until now. We intended to discover the empagliflozin’s (EMPA) hepatoprotective efficacy in thioacetamide (TAA)-induced hepatotoxicity by targeting AMPK/SIRT-1 activity and reducing HIF-1α. Rats were treated orally with EMPA (3 or 6 mg/kg) with TAA (100 mg/kg, IP) thrice weekly for 6 weeks. EMPA in both doses retracted the serum GGT, ALT, AST, ammonia, triglycerides, total cholesterol, and increased serum albumin. At the same time, EMPA (3 or 6 mg/kg) replenished the hepatic content of GSH, ATP, AMP, AMPK, or SIRT-1 and mitigated the hepatic content of MDA, TNF-α, IL-6, NF-κB, or HIF-1α in a dose-dependent manner. Likewise, hepatic photomicrograph stained with hematoxylin and eosin or Masson trichrome stain of EMPA (3 or 6 mg/kg) revealed marked regression of the hepatotoxic effect of TAA with minimal injury. Similarly, in rats given EMPA (3 or 6 mg/kg), the immunohistochemically of hepatic photomicrograph revealed minimal stain of either α-SMA or caspase-3 compared to the TAA group. Therefore, we concluded that EMPA possessed an antifibrotic effect by targeting AMPK/SIRT-1 activity and inhibiting HIF-1α. The present study provided new insight into a novel treatment of liver fibrosis.Citation:
... s i-H C G 1 1 + m iR -3 8 1 -3 p a n t a g o m ir s i-H C G 1 1 + m iR -3 8 1 -3 p a n t a g o m ir s i-H C G 1 1 + m iR -3 8 1 -3 p a n t a g o m ir p53 GAPDH utes to the infarction outcome and the initiation of repair mechanisms [3]. In addition, TGF-β1 is induced with corresponding CI/R injury and played a protective role in ischemic stroke [1]. In our research, we found that MCAO promoted neuroinflammation in which both pro-inflammatory factors, TNF-α and IFN-γ, were significantly increased, while inhibition of HCG11 significantly suppressed the neuroinflammatory response. ...
... In our research, we found that MCAO promoted neuroinflammation in which both pro-inflammatory factors, TNF-α and IFN-γ, were significantly increased, while inhibition of HCG11 significantly suppressed the neuroinflammatory response. What is more, TGF-β, a pleiotropic cytokine, had a neuroprotective effect in response to hypoxia-induced central nervous system (CNS) stress in the MCAO model, whereas inhibition of HCG11 increased the protective effect on CI/RI with a further elevation of TGF-β [1]. We demonstrated that HCG11 silencing may play a neuroprotective role in inhibiting CI/R injury through oxidative stress and neuroinflammation. ...
Introduction:
Long non-coding RNA (LncRNA) plays a critical role in cerebral ischemia-reperfusion (CI/R) injury. The purpose of the current research was to investigate the regulatory role of the LncRNA human leukocyte antigen complex group 11 (HCG11) in CI/R injury and explore its potential mechanism.
Material and methods:
The rat middle cerebral artery occlusion (MCAO) model was established to simulate CI/R injury in vivo. mRNA levels of HCG11, microRNA (miR)-381-3p, tumour protein p53, and neuro-inflammatory factors were detected by quantitative reverse transcription PCR (RT-qPCR). Bederson score and Longa score were assessed for neurological deficits. Triphenyl tetrazolium chloride (TTC) staining was used to examine the cerebral infarct volume. What is more, oxidative stress was evaluated by the commercial kit. Finally, the relationship between HCG11, miR-381-3p, and p53 was verified by a dual-luciferase reporter assay.
Results:
HCG11 was elevated in MCAO rats. And it competitively bound miR-381-3p and down-regulated the expression of p53. Inhibition of HCG11 inhibited cerebral infarct volume and neurological deficits in MCAO rats, and inhibited the secretion of neuro-inflammation and the over-activation of oxidative stress, exerting the protective effect of CI/R injury. However, inhibition of miR-381-3p in rats significantly weakened the protective effect of depression of HCG11 in MCAO rats, resulting in increased cerebral infarction volume and neurological deficits, elevated neuro-inflammatory secretion, and oxidative stress activation.
Conclusions:
The present research shows that LncRNA HCG11 silencing protects against cerebral ischemia/reperfusion injury through miR-381-3p to regulate p53.
... 3 Besides, other studies have reported that inflammation is also involved in HE progression via liver-to-brain pro-inflammatory signaling pathways where astroglial cells exposed to pro-inflammatory cytokines together with ammonia showed increased expression levels of HE-implicated genes. 6 Given the crucial role of oxidative stress in the onset and progression of HE, 7 numerous reports so far have demonstrated the potential usefulness of antioxidants to decrease the development of neurological and cognitive deficits associated with HE. 8,9 Thymol (2-isopropyl-5-methylphenol) is a natural monoterpene found in high concentration in the oils of thyme from different plant species of Thymus, such as T. vulgaris, T. spicata, and T. ciliates, and Nigella sativa seeds. 10 Thymol is affirmed by the United States Food and Drug Administration as 'Generally Recognized as Safe' for dietary use; hence it is recognized to be safe with negligible toxicity. ...
In the present study, we aimed to delineate the neuroprotective potential of thymol (THY) against neurotoxicity and cognitive deterioration induced by thioacetamide (TAA) in an experimental model of hepatic encephalopathy (HE). Rats received TAA (100 mg kg-1, intraperitoneally injected, three times per week) for two weeks. THY (30 and 60 mg kg-1), and Vit E (100 mg k-1) were administered daily by oral gavage for 30 days after HE induction. Supplementation with THY significantly improved liver function, reduced serum ammonia level, and ameliorated the locomotor and cognitive deficits. THY effectively modulated the alteration in oxidative stress markers, neurotransmitters, and brain ATP content. Histopathology of liver and brain tissues showed that THY had ameliorated TAA-induced damage, astrocyte swelling and brain edema. Furthermore, THY downregulated NF-kB and upregulated GFAP protein expression. In addition, THY significantly promoted CREB and BDNF expression at both mRNA and protein levels, together with enhancing brain cAMP level. In conclusion, THY exerted hepato- and neuroprotective effects against HE by mitigating hepatotoxicity, hyperammonemia and brain ATP depletion via its antioxidant, anti-inflammatory effects in addition to activation of the CREB/BDNF signaling pathway.
... Previous research has focused on the mortality of vulnerable neurons in ischemic brain damage (Liu et al. 2017). Also, several neuroprotective methods have remained a key focus within the therapy of cerebral I/R damage (Abdel-Rahman et al. 2020). Results from a previous study reported that oxidative stress and neuronal apoptosis were associated with cerebral I/R injury (Zhang and Zhang 2020). ...
In traditional Chinese medicine, liquiritin, an active component of Glycyrrhiza uralensis Fisch . , Fabaceae, has several pharmacological effects such as anticancer, antioxidant, and neuroprotective properties. The present study aimed to explore the protective functions and molecular mechanisms underlying the effects of liquiritin on nerve injury induced by cerebral ischemia/reperfusion. SH-SY5Y cells were incubated with varying concentrations of liquiritin for different periods of time, and 3-(45)-dimethylthiahiazo(-z-y1)-35-di-phenytetrazoliumromide and lactate dehydrogenase assays were employed to determine the levels of cell viability and damage. Subsequently, cells were exposed to oxygen and glucose deprivation/reoxygenation to establish an ischemia/reperfusion injury model. The results revealed that liquiritin protected SH-SY5Y cells from oxygen and glucose deprivation/reoxygenation-induced damage by improving viability and reducing apoptosis, and oxidative stress. Liquiritin inhibited activation of the p38 mitogen-activated protein kinase (MAPK)/nuclear factor kappa B (NF-κB) signaling pathway. In addition, treatment with a p38MAPK-specific agonist reversed the protective effects of liquiritin.
Graphical abstract
