scholarly journals MicroRNA-424 Protects Against Focal Cerebral Ischemia and Reperfusion Injury in Mice by Suppressing Oxidative Stress

Stroke ◽  
2015 ◽  
Vol 46 (2) ◽  
pp. 513-519 ◽  
Author(s):  
Ping Liu ◽  
Haiping Zhao ◽  
Rongliang Wang ◽  
Peng Wang ◽  
Zhen Tao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Focal Cerebral Ischemia ◽  
Ischemia And Reperfusion ◽  
Ischemia And Reperfusion Injury ◽  
Cerebral Ischemia And Reperfusion

scholarly journals Long non-coding RNA TUG1 aggravates cerebral ischemia and reperfusion injury by sponging miR-493-3p/miR-410-3p

Open Medicine ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. 919-930
Author(s):  
Jinlong Du ◽  
Wenjing Li ◽  
Bing Wang
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
P38 Mapk ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Ischemia And Reperfusion ◽  
Ischemia And Reperfusion Injury ◽  
Related Factors ◽  
Cerebral Ischemia And Reperfusion

Abstract Background Cerebral ischemia and reperfusion injury (CIRI) affects bodily function by causing irreversible damage to brain cells. The diverse pathophysiological course factors hinder the research work to go deeper. Long noncoding RNA taurine-upregulated gene 1 (TUG1) has been reported to be related to CIRI. This study explored the undefined regulatory pathway of TUG1 in CIRI. Methods Quantitative real-time polymerase chain reaction was applied to test the expression of TUG1, microRNA (miR)-493-3p and miR-410-3p. The viability and apoptosis of oxygen and glucose deprivation/reoxygen (OGD/R) model cells were evaluated by cell counting kit-8 and flow cytometry assay, respectively. The determination of inflammatory factors of interleukin-6, interleukin-1β and tumor necrosis factor-α was presented by enzyme-linked immunosorbent assay. The oxidative stress was performed by measuring the generation of malondialdehyde, reactive oxygen species and the activity of superoxide dismutase. Cytotoxicity was presented by measuring the generation of lactate dehydrogenase. Western blot assay was devoted to assessing the level of apoptosis-related factors (cleaved-caspase-3 and cleaved-caspase-9) and the protein level of c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38 MAPK) pathway-related factors in neuro-2a cells treated by OGD/R. Besides, online database starBase was applied to predict the potential binding sites of TUG1 to miR-493-3p and miR-410-3p, which was further confirmed by the dual-luciferase reporter system. Results The expression of TUG1 was upregulated, while miR-493-3p or miR-410-3p was downregulated in the serum of CIRI and OGD/R model cells. Meanwhile, knockdown of TUG1 eliminated the suppression in proliferation, the promotion in apoptosis, inflammation and oxidative stress, as well as the cytotoxicity in OGD/R model cells. Interestingly, the inhibition of miR-493-3p or miR-410-3p allayed the above effects. In addition, TUG1 harbored miR-493-3p or miR-410-3p and negatively regulated their expression. Finally, the TUG1 activated JNK and p38 MAPK pathways by sponging miR-493-3p/miR-410-3p. Conclusion TUG1 motivated the development of CIRI by sponging miR-493-3p/miR-410-3p to activate JNK and p38 pathways. The novel role of TUG1 in CIRI may contribute to the advancement of CIRI treatment.

scholarly journals Neuroprotective Mechanisms of Calycosin Against Focal Cerebral Ischemia and Reperfusion Injury in Rats

2018 ◽  
Vol 45 (2) ◽  
pp. 537-546 ◽  
Author(s):  
Yong Wang ◽  
Qianyao Ren ◽  
Xing Zhang ◽  
Huiling Lu ◽  
Jian Chen
Keyword(s):  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Brca1 Gene ◽  
Ischemia And Reperfusion ◽  
Ischemia And Reperfusion Injury ◽  
Neuroprotective Effects ◽  
Cerebral Ischemia And Reperfusion ◽  
Tnf Α

Background/Aims: Emerging evidence suggests that autophagy plays important roles in the pathophysiological processes of cerebral ischemia and reperfusion injury. Calycosin, an isoflavone phytoestrogen, possesses neuroprotective effects in cerebral ischemia and reperfusion in rats. Here, we investigated the neuroprotective effects of calycosin against ischemia and reperfusion injury, as well as related probable mechanisms behind autophagy pathways. Methods: A cerebral ischemic and reperfusion injury model was established by middle cerebral artery occlusion in male Sprague-Dawley rats. Neurological scores, infarct volumes, and brain water content were assessed after 24 h reperfusion following 2 h ischemia. Additionally, the expression of the autophagy-related protein p62 and NBR1 (neighbor of BRCA1 gene 1), as well as Bcl-2, and TNF-α in rat brain tissues was measured by RT-PCR, western blotting and immunohistochemical analyses. Results: The results showed that calycosin pretreatment for 14 days markedly decreased infarct volume and brain edema, and ameliorated neurological scores in rats with focal cerebral ischemia and reperfusion. It was observed that levels of p62, NBR1 and Bcl-2 were greatly decreased, and levels of TNF-α significantly increased after ischemia and reperfusion injury. However, calycosin administration dramatically upregulated the expression of p62, NBR1 and Bcl-2, and downregulated the level of TNF-α. Conclusions: All data reveal that calycosin exerts a neuroprotective effect on cerebral ischemia and reperfusion injury, and the mechanisms maybe associated with its anti-autophagic, anti-apoptotic and anti-inflammatory action.

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