scholarly journals Hydrogen-Rich Water Improves Cognitive Ability and Induces Antioxidative, Antiapoptotic, and Anti-Inflammatory Effects in an Acute Ischemia-Reperfusion Injury Mouse Model

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Dain Lee ◽  
Jong-Il Choi
Keyword(s):  
Cerebral Ischemia ◽  
Neurodegenerative Diseases ◽  
Reperfusion Injury ◽  
Mouse Brain ◽  
Molecular Hydrogen ◽  
Immunofluorescence Microscopy ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Hydrogen Treatment ◽  
Anti Inflammatory

Background. Cerebral ischemia and its reperfusion injury facilitate serious neurodegenerative diseases such as dementia due to cell death; however, there is currently no treatment for it. Reactive oxygen species is one of the many factors that induce and worsen the development of such diseases, and it can be targeted by hydrogen treatment. This study examined the effect of molecular hydrogen in cerebral ischemia-reperfusion injury, which is emerging as a novel therapeutic agent for various diseases. Methods. Ischemia-reperfusion injury was generated through bilateral common carotid artery occlusion in C57BL/6 mice. The test group received hydrogen-rich water orally during the test period. To confirm model establishment and the effect of hydrogen treatment, behavioural tests, biochemical assays, immunofluorescence microscopy, and cytokine assays were conducted. Results. Open field and novel object recognition tests revealed that the hydrogen-treated group had improved cognitive function and anxiety levels compared to the nontreated group, while hematoxylin and eosin stain showed abundant pyknotic cells in a model mouse brain, and this was attenuated in the hydrogen-treated mouse brain. Total antioxidant capacity and thiobarbituric acid reactive substance assays revealed that hydrogen treatment induced antioxidative effects in the mouse brain. Immunofluorescence microscopy revealed attenuated apoptosis in the striatum, cerebral cortex, and hippocampus of hydrogen-treated mice. Western blotting showed that hydrogen treatment reduced Bax and TNFα levels. Finally, cytokine assays showed that IL-2 and IL-10 levels significantly differed between the hydrogen-treated and nontreated groups. Conclusion. Hydrogen treatment could potentially be a future therapeutic strategy for ischemia and its derived neurodegenerative diseases by improving cognitive abilities and inducing antioxidative and antiapoptotic effects. Hydrogen treatment also decreased Bax and TNFα levels and induced an anti-inflammatory response via regulation of IL-2 and IL-10. These results will serve as a milestone for future studies intended to reveal the mechanism of action of molecular hydrogen in neurodegenerative diseases.

Anti-apoptotic, anti-oxidant, and anti-inflammatory effects of thalidomide on cerebral ischemia/reperfusion injury in rats

2015 ◽  
Vol 351 (1-2) ◽  
pp. 78-87 ◽  
Author(s):  
Guadalupe Palencia ◽  
Juan Ángel Núñez- Medrano ◽  
Alma Ortiz-Plata ◽  
Dolores Jiménez Farfán ◽  
Julio Sotelo ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury ◽  
Anti Oxidant ◽  
Anti Inflammatory

scholarly journals miR-155 Knockdown Protects against Cerebral Ischemia and Reperfusion Injury by Targeting MafB

2020 ◽  
Vol 2020 ◽  
pp. 1-11 ◽  
Author(s):  
Li Zhang ◽  
Chao Liu ◽  
Chao Huang ◽  
Xiaohui Xu ◽  
Junfang Teng
Keyword(s):  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Mouse Brain ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Invasion And Migration ◽  
Infarction Volume ◽  
Cox 2 ◽  
And Migration ◽  
Brain Tissues

Background. Studies have elucidated that the variable expression levels of miRNAs influence the inflammatory process in ischemic stroke. Nevertheless, the impact and potential mechanism of miR-155 in cerebral ischemia-reperfusion injury (CIRI) keep to be incompletely known. Methods. The levels of miR-155 and MafB were determined via qRT-PCR, western blot, or immunohistochemistry assays in plasma of patients with CIRI, oxygen glucose deprivation/reoxygenation (OGD/R) induced SH-SY5Y cells, and mouse models with middle cerebral artery occlusion (MCAO). The association between miR-155 and MafB was validated via dual-luciferase reporter and western blot assays. Cell viability, apoptosis, invasion, and migration were evaluated through MTT, flow cytometry, Transwell and wound healing assays. Infarction volume was measured in MCAO mouse brain tissues by TTC assay. The expression of inflammatory mediators was measured by ELISA in cells and brain tissues. Results. miR-155 level was upregulated whereas MafB was downregulated in the plasma of patients with CIRI, OGD/R-induced SH-SY5Y cells, also as mouse models with MCAO injury. Mechanistically, miR-155 directly targeted 3’UTR of MafB and restrained MafB expression in OGD/R injury SH-SY5Y cells. Downregulation of miR-155 attenuated OGD/R-induced injury through increasing proliferation, inhibiting apoptosis, enhancing invasion and migration abilities, and constraining the expression of inflammatory mediators (IL-1β, IL-6, and TNF-α) and inflammatory enzymes (iNOS and COX-2) in SH-SY5Y cells following OGD/R, while MafB inhibition reversed the protective effects. In vivo, downregulating miR-155 reduced the infarction volume in the MACO mouse brain. Furthermore, miR-155 knockdown inhibited the IL-1β, IL-6, TNF-α, iNOS, and COX-2 in the MACO mouse brain tissues. Conclusion. Our results suggest that miR-155 knockdown alleviated ischemia-reperfusion injury by targeting MafB to improve the neurological function and inhibit inflammation response, highlighting a novel therapeutic strategist for CIRI.

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