Effects of Naomaitong Recipe on expressions of nuclear factor-κB and nitric-oxide synthases in brain tissue after focal cerebral ischemia reperfusion in aged rats

2006 ◽  
pp. 530-534
Author(s):  
Jianfeng Gao
Keyword(s):  
Nitric Oxide ◽  
Cerebral Ischemia ◽  
Brain Tissue ◽  
Focal Cerebral Ischemia ◽  
Ischemia Reperfusion ◽  
Nuclear Factor Κb ◽  
Nitric Oxide Synthases ◽  
Nuclear Factor ◽  
Aged Rats ◽  
Cerebral Ischemia Reperfusion

Protective Effect of Astragaloside on Focal Cerebral Ischemia/Reperfusion Injury in Rats

2010 ◽  
Vol 38 (03) ◽  
pp. 517-527 ◽  
Author(s):  
Yan-Yan Yin ◽  
Wei-Ping Li ◽  
Hui-Ling Gong ◽  
Fen-Fang Zhu ◽  
Wei-Zu Li ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cerebral Ischemia ◽  
Water Content ◽  
Neurological Deficit ◽  
Focal Cerebral Ischemia ◽  
Ischemia Reperfusion ◽  
Content Increase ◽  
Protective Effects ◽  
Neurological Deficit Score ◽  
Cerebral Ischemia Reperfusion

This study was to observe the neurological protective effects of astragalosides (AST) on focal cerebral ischemia-reperfusion (I/R) injury in rats and to explore its possible mechanism. Male SD rats received right middle cerebral artery occlusion for 120 min and AST (40 mg/kg) was orally administered. The rats were decapitated 1, 3, 7, and 14 days after reperfusion. The neurological deficit score, infarct volume and water content of brain were measured; the activity of superoxide dismutase (SOD), lactate dehydrogenase (LDH) and nitric oxide synthase (NOS), and the content of malondialdehyde (MDA), lactate (LD) and nitric oxide (NO) of brain tissue were detected too. The expression of inducible nitric synthase (iNOS), nerve growth factor (NGF) and tropomyosin receptor kinase A (TrkA) mRNA were measured by RT-PCR or real-time PCR. AST could significantly reduce the neurological deficit score; infract volume and water content, increase SOD and LDH activities, decrease NOS activity and MDA, LD and NO content. AST treatment could down-regulate expression of iNOS mRNA, while, NGF and TrkA mRNA were up-regulated. Our data suggest that AST have the protective effects on focal cerebral ischemia in rats at the different reperfusion time points, the mechanism may be related to the antioxidation, regulated the expressions of iNOS, NGF and TrkA mRNA.

The protective effect of ligustrazine on rats with cerebral ischemia–reperfusion injury via activating PI3K/Akt pathway

2019 ◽  
Vol 38 (10) ◽  
pp. 1168-1177 ◽  
Author(s):  
Y Ding ◽  
J Du ◽  
F Cui ◽  
L Chen ◽  
K Li
Keyword(s):  
Nitric Oxide ◽  
Cerebral Ischemia ◽  
Brain Tissue ◽  
Ischemia Reperfusion ◽  
Pi3k Inhibitor ◽  
Akt Pathway ◽  
Control Group ◽  
Dependent Manner ◽  
Cerebral Ischemia Reperfusion ◽  
Dose Dependent

The study was to investigate the effects of ligustrazine on rats with cerebral ischemia–reperfusion (I/R) injury and to explore the potential mechanism. Transient focal cerebral ischemia Wistar rat model was established through middle cerebral artery occlusion. The cerebral I/R injury rats were treated with intraperitoneal injection of ligustrazine (1, 3, and 10 mg/kg). Human amniotic epithelial cells (HAECs) were treated with ligustrazine (1, 10, 100 μM) and PI3K inhibitor wortmannin (100 μM), following oxygen–glucose deprivation (OGD) treatment. The expression levels of protein kinase B (PKB or AKT), phospho-Akt (p-Akt), endothelial nitric oxide synthase (eNOS), and phosphor-eNOS (p-eNOS) in HAECs and brains of rats were measured by Western blot. The levels of nitric oxide (NO) in HAECs were measured by Griess method using NO2−/NO3− Assay Kit. Infarct volume and neurological deficits were evaluated 24 h after reperfusion. The levels of NO, p-Akt/Akt, and p-eNOS/eNOS in HAECs were significantly reduced after OGD, but ligustrazine treatment increased the levels of those factors in a dose-dependent manner, while those increases were reversed by PI3K inhibitor wortmannin. Similarly, p-Akt/Akt and p-eNOS/eNOS in brain tissue of rats with I/R were significantly reduced compared with control group ( p < 0.05), but ligustrazine treatment increased the levels of p-Akt and p-eNOS in a dose-dependent manner ( p < 0.05), while those increases were also reversed by using wortmannin. Ligustrazine also improved the damage of rat brain tissue caused by I/R, but wortmannin reversed the improvement. Ligustrazine plays a neuroprotective role in rats with cerebral I/R injury through the activation of PI3K/Akt pathway.

scholarly journals Study of the neuroprotective effects of carnosine in an experimental model of focal cerebral ischemia/reperfusion

2018 ◽  
Vol 64 (4) ◽  
pp. 344-348 ◽  
Author(s):  
A.A. Devyatov ◽  
T.N. Fedorova ◽  
S.L. Stvolinsky ◽  
I.N. Ryzhkov ◽  
N.A. Riger ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Brain Tissue ◽  
Experimental Model ◽  
Glutathione Transferase ◽  
Focal Cerebral Ischemia ◽  
Neuroprotective Effect ◽  
Ischemia Reperfusion ◽  
Protein Carbonyls ◽  
Neuroprotective Effects ◽  
Cerebral Ischemia Reperfusion

Oxidative stress is one of the key factors in brain tissue damage in ischemia, which indicates the appropriateness of using antioxidants under these conditions. One of the promising antioxidants for the therapy of ischemic stroke is the natural dipeptide carnosine. The neuroprotective effect of dietary carnosine administration was investigated in an experimental model of focal cerebral ischemia/reperfusion in Wistar rats. Animals received carnosine with a diet at a daily dose of 150 mg/kg for 7 days before temporary occlusion of the middle cerebral artery (MCA), performed for 60 min. At 24 h after the onset of ischemia the effect of carnosine on the area of the necrotic core was evaluated in animals. In brain tissue of animals the content of malondialdehyde (MDA), protein carbonyls (PC), total antioxidant capacity (TAC), total activity of superoxide dismutase (SOD), glutathione peroxidase (GP), catalase (CAT) and glutathione transferase (GT), content of isoprostanes and cytokines were measured. Carnosine significantly reduced the infarct size. Carnosine also increased TAC and reduced the level of MDA and isoprostanes in brain tissue. Influence of carnosine on other parameters was not detected. Thus carnosine consumed prophylactically with the diet for 7 days before the induction of ischemia by means of MCA occlusion in rats provides the direct neuroprotective effect, retains high antioxidant activity of brain tissue, reduces the level of oxidative damage markers (MDA and isoprostanes) but does not have any effect on the activity of antioxidant enzyme systems and production of cytokines in brain tissue.

N-Nitro-L-Arginine-Methyl ester Exerts Neuroprotection By Inhibiting Inflammation In Cerebral Injury Induced By Transient Ischemia/Reperfusion In Rats

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Awooda Hiba A
Keyword(s):  
Nitric Oxide ◽  
Cerebral Ischemia ◽  
Methyl Ester ◽  
Focal Cerebral Ischemia ◽  
Ischemia Reperfusion ◽  
Cerebral Injury ◽  
Cerebral Ischemia Reperfusion ◽  
Transient Focal Cerebral Ischemia ◽  
Tnf Α ◽  
Anti Inflammatory

Cerebral ischemia-reperfusion injury is a pivotal cause of deaths due to cerebrovascular accidents. Further research efforts are needed to reveal the mechanism underlying its aggravation or alleviation. We previously reported the antioxidant effect of N-Nitro-L-Arginine-Methyl Ester (L-NAME), a nonselective nitric oxide synthase (NOS) inhibitor, on rats subjected to transient focal cerebral ischemia-reperfusion (I/R). The aim of this work was to explore further neuroprotective anti-inflammatory effects of L-NAME. This study involved 30 adult male Wistar rats divided into three groups with ten rats in each: sham-operated (control), I/R group of rats subjected to 30 minutes of left common carotid artery (CCA) occlusion followed by 24-hour of reperfusion and test group infused with L-NAME intraperitoneally 15 minutes before the same I/R period. Neurological assessments were evaluated, Western blotting used to estimate Nuclear factor-kappa B (NF-қB), ELISA used to detect Tumor necrosis factor- α (TNF-α), and Nitric oxide metabolites were measured colorimetrically, as well as H&E staining to assess brain damage. Compared with the I/R group, the neurological score, infarction area, and the inflammatory biomarkers NF-қB, TNF-α, and NO were significantly decreased in L-NAME treated rats (P ≤0.001). As a conclusion from the current study, L-NAME showed potential neuroprotection through it is an anti-inflammatory effect on a rat’s model of transient focal cerebral ischemia-reperfusion.

scholarly journals Ginkgetin attenuates cerebral ischemia–reperfusion induced autophagy and cell death via modulation of the NF-κB/p53 signaling pathway

2019 ◽  
Vol 39 (9) ◽  
Author(s):  
Jianqing Pan ◽  
Xiang Li ◽  
Fei Guo ◽  
Zhigang Yang ◽  
Lingling Zhang ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Signaling Pathway ◽  
Cerebrovascular Accident ◽  
Ischemia Reperfusion ◽  
Nuclear Factor Κb ◽  
Neurological Deficits ◽  
Nuclear Factor ◽  
P53 Signaling ◽  
Cerebral Ischemia Reperfusion ◽  
P53 Signaling Pathway

Abstract Background: Cerebral ischemia–reperfusion (I/R) injury is the key to fatality in cerebrovascular accident, hence further endeavor is warranted to delineate the mechanism underlying its lethal aggravation procedure. In the present study, we aimed to elucidate the anti-autophagy and anti-apoptosis effects of ginkgetin via nuclear factor κB (NF-κB)/p53 pathway in cerebral I/R rats. Methods: Rats were administrated 2-h occlusion of right middle cerebral artery before the 24-h reperfusion followed. There were three doses of ginkgetin (25, 50, 100 mg/kg) given intraperitoneally (i.p.) after the 2-h ischemia, and Pifithrin-α (PFT-α, p53 inhibitor), SN50 (NF-κB inhibitor) and 3-methyladenine (3-MA, autophagy inhibitor) was administered 20 min before the ischemia, respectively. Results: The neurological deficits decreased significantly with the administration of ginkgetin. The concentrations of microtubule-associated protein 1 light chain 3-II and p53 were significantly decreased by PFT-α, 3-MA and ginkgetin. The concentrations of Beclin 1, damage-regulated autophagy modulator, cathepsin B and cathepsin D were significantly decreased due to the administration of PFT-α, ginkgetin and SN50. Furthermore, the concentrations of Bax and p53-upregulated modulator of apoptosis were significantly decreased with that of Bcl-2 being significantly increased by administration of SN50, PFT-α and ginkgetin. Conclusion: Ginkgetin can alleviate cerebral ischemia/reperfusion induced autophagy and apoptosis by inhibiting the NF-κB/p53 signaling pathway.

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