Protective effects of gastrodin pretreatment on mouse hepatic ischemia-reperfusion occurring through antioxidant and anti-apoptotic mechanisms

xlomafota13 shared this article with you from Inoreader Protective effects of gastrodin pretreatment on mouse hepatic ischemia-reperfusion occurring through antioxidant and anti-apoptotic mechanisms Via Experimental and therapeutic medicine Exp Ther Med. 2021 May;21(5):471. doi: 10.3892/etm.2021.9902. Epub 2021 Mar 8. ABSTRACT Hepatic ischemia-reperfusion injury (HIRI) often occurs following surgical procedures such as liver resection and transplantation. However, despite its clinical prominence, to the best of our knowledge, there remain no effective strategies to treat HIRI. Therefore, the aim of present study was to identify therapeutic agents that can exert beneficial effects against HIRI. The present study found that following hepatic IR modeling in mice, gastrodin (Gas) pretreatment improved the IR outcomes in terms of the serum biochemical indexes (alanine transaminase and aspartate transaminase), tissue biochemical indexes (superoxide dismutase, malondialdehyde and reduced glutathione content) and tissue pathology (H&E staining). In addition, compared with those in the IR + vehicle group, the IR + Gas group showed upregulated expression levels of nuclear eryth roid 2-related factor 2, heme oxygenase 1 and Bcl-2 as detected by western blotting and reverse transcription-quantitative PCR. The mRNA and protein expression levels of Bax and caspase-3 were downregulated in the IR + Gas group compared with the IR + vehicle group. Concurrently, no significant differences were observed in the parameters between the Sham + vehicle and the Sham + Gas groups, indicating that Gas pretreatment may not cause liver damage. In conclusion, the findings of the present study revealed that Gas pretreatment exerted a protective effect in HIRI through both antioxidant and anti-apoptotic mechanisms. PMID:33767766 | PMC:PMC7976389 | DOI:10.3892/etm.2021.9902 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.