Icariside II protects against cerebral ischemia–reperfusion injury in rats via nuclear factor-κB inhibition and peroxisome proliferator-activated receptor up-regulation

2016 ◽  
Vol 96 ◽  
pp. 56-61 ◽  
Author(s):  
Yuanyuan Deng ◽  
Deqing Xiong ◽  
Caixia Yin ◽  
Bo Liu ◽  
Jingshan Shi ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Nuclear Factor Κb ◽  
Peroxisome Proliferator ◽  
Nuclear Factor ◽  
Peroxisome Proliferator Activated Receptor ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury ◽  
Icariside Ii

scholarly journals Protection of Anthocyanin from Myrica rubra against Cerebral Ischemia-Reperfusion Injury via Modulation of the TLR4/NF-κB and NLRP3 Pathways

Molecules ◽  
2018 ◽  
Vol 23 (7) ◽  
pp. 1788 ◽  
Author(s):  
Hong-Xin Cui ◽  
Ji-Hong Chen ◽  
Jing-Wan Li ◽  
Fang-Rong Cheng ◽  
Ke Yuan
Keyword(s):  
Cerebral Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Nuclear Factor Κb ◽  
Total Anthocyanin ◽  
Myrica Rubra ◽  
Pyrin Domain ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury ◽  
Disease Damage

Myrica rubra (MR) is rich in anthocyanins, and it has good anti-cancer, anti-aging, antioxidant, and antiviral effects. The proportion of disability and death caused by ischemic stroke gradually increased, becoming a major disease that is harmful to human health. However, research on effects of anthocyanin from MR on cerebral ischemia-reperfusion (I/R) injury is rare. In this study, we prepared eight purified anthocyanin extracts (PAEs) from different types of MR, and examined the amounts of total anthocyanin (TA) and cyanidin-3-O-glucoside (C-3-G). After one week of PAE treatment, the cerebral infarction volume, disease damage, and contents of nitric oxide and malondialdehyde were reduced, while the level of superoxide dismutase was increased in I/R mice. Altogether, our results show that Boqi1 MR contained the most TA (22.07%) and C-3-G (21.28%), and that PAE isolated from Dongkui MR can protect the brain from I/R injury in mice, with the mechanism possibly related to the Toll-like receptor 4 (TLR4)/ nuclear factor-κB (NF-κB) and NOD-like receptor pyrin domain-containing 3 protein (NLRP3) pathways.

Diosmetin Ameliorates Cerebral Ischemia/Reperfusion Injury in PC12 Cells Through Nuclear Factor-kB (NF-kB) and Nuclear Factor Erythroid 2-Related Factor/Heme Oxygenase-1 (Nrf 2/HO-1) Pathway

2019 ◽  
Vol 17 (3) ◽  
pp. 322-328
Author(s):  
Luan Lan ◽  
Cao Lanxiu ◽  
Zhu Lei ◽  
Sun Jianhua
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Pc12 Cells ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Nuclear Factor ◽  
Oxygen Species ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury

Diosmetin, a natural flavonoid, exhibits a variety of pharmacologic activities including inhibition of inflammation and oxidation. Therefore, its potential role in the management of cerebral ischemia/reperfusion (I/R) injury remains to be examined. In this study, we explored the underlying molecular mechanisms of diosmetin effects on cerebral ischemia/reperfusion injury in vitro. The results show that hypoxia/reoxygenation treatment of PC12 cells decreased cell viability and increased apoptosis, inflammation and oxidative stress. Diosmetin improved cellular viability, decreased lactate dehydrogenase release, and inhibited apoptosis in hypoxia-/reoxygenation-treated PC12 cells. Furthermore, diosmetin effectively inhibited the NF-kB signaling pathway to attenuate the inflammatory response. Also, diosmetin inhibited reactive oxygen species generation to attenuate I/R injury-induced oxidative stress in PC12 cells probably through the activation of Nrf 2/HO-1 pathway. Therefore, diosmetin effectively protected cells from I/R injury in nerve cells by scavenging reactive oxygen species by activating Nrf 2/HO-1 pathway and inhibiting inflammation by the suppression of NF-kB signaling pathway. Diosmetin can be regarded as a potential agent for cerebral ischemia/reperfusion injury treatment.

scholarly journals Silent information regulator 1 ameliorates oxidative stress injury via PGC-1α/PPARγ-Nrf2 pathway after ischemic stroke in rat.

2020 ◽  
Author(s):  
yang zhou ◽  
Li Peng ◽  
Ning Jiang ◽  
Jingxian Wu ◽  
Yixin Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Focal Cerebral Ischemia ◽  
Ischemia Reperfusion ◽  
Peroxisome Proliferator ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury

Abstract Background Astrocytes mediate brain defense against oxidative stress-induced injury. Silent information regulator 1 (SIRT1) has anti-oxidative stress effects in many diseases and is highly expressed in astrocytes. However, the neuroprotective effects of SIRT1 on astrocytes after cerebral ischemia/reperfusion injury are unclear. Methods Here, we evaluated the effects of SIRT1 in astrocytes after cerebral ischemia/reperfusion injury using oxygen-glucose deprivation/recovery in astrocytes in vitro and middle cerebral artery occlusion in rats in vivo. Results SIRT1 knockdown reduced cell viability, increased oxidative stress, and decreased peroxisome proliferator activated receptor (PPAR)-γ coactivator (PGC)-1α, PPARγ, nuclear factor erythroid 2-related factor 2 (NRF2), heme oxygenase (HO)-1, and NAD(P)H:quinone oxidoreductase-1 (NQO1) expression. Moreover, SIRT1 knockdown also suppressed PGC-1α activity, the PGC-1α/PPARγ interaction, and the PPARγ/peroxisome proliferator-response element (PPRE) interaction. Similarly, in our in vivo experiments, SIRT1 overexpression and PGC-1α or PPARγ knockdown reduced PGC-1α, PPARγ, NRF2, HO-1, and NQO1 protein expression and blocked the PGC-1α/PPARγ interaction. SIRT1 overexpression plus PPARγ knockdown inhibited the interaction of PPARγ with PPRE. NRF2 knockdown blocked NRF2 expression and downstream proteins induced by SIRT1 overexpression. Conclusion Overall, our data indicated that SIRT1 directly mediated the PGC-1α/PPARγ pathway in response to focal cerebral ischemia/reperfusion-induced neurological deficit, providing insights into the treatment of focal cerebral ischemia/reperfusion injury.

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