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Cardioprotective Effect of Gynostemma pentaphyllum against Streptozotocin Induced Cardiac Toxicity in Rats via Alteration of AMPK/Nrf2/HO-1 Pathway. | LitMetric

Gynostemma pentaphyllum (GP) is a plant commonly used in diabetic therapy in China. GP having potent antioxidant effect against various free radicals. The purpose of the current investigation to identify the cardioprotective effect of GP against streptozotocin (STZ)/ high fat diet (HFD) induced cardiac dysfunction in rats via alteration of AMPK/Nrf2/HO-1 pathway. Wistar rats were used for the current protocol. The rats were received the intraperitoneal injection of STZ and HFD to induce the cardiac remodelling. Blood glucose level, insulin and lipid parameters were estimated. Blood pressure and heart rate were also estimated. Cardiac parameters, antioxidant, cytokines, total protein and inflammatory mediators were analysed. The mRNA expression was detected using the RT-qPCR, respectively. GP significantly (p < 0.001) decreased the BGL and improved the insulin level. GP altered the ratio of heart/BW, liver/BW, and lung/BW. GP treatment significantly (p < 0.001) suppressed the heart rate and blood pressure (diastolic, systolic and mean pressure). GP significantly (p < 0.001) reduced the level of TC, LDL, TG, VLDL and increased the level of HDL. DCM induced rats received the GP administration exhibited reduction in the level of CK and LDH. GP significantly (p < 0.001) reduced the levels of MDA, hydrogen peroxide, peroxynitrite, ROS and increased the level of GSH, SOD, CAT and GPx. GP significantly (p < 0.001) reduced the levels of cytokines (TNF-α, IL-6, IL-1β) and inflammatory parameters (COX-2 and NFκB). GP significantly (p < 0.001) suppressed the NLRP3 and NF-κB expression. GP also boosted mitochondrial biogenesis by boosting the PGC-1α, HO-1 and Nrf2 expression in cardiac tissue. GP treatment showed the cardioprotective effects against STZ induced diabetic cardiac dysfunction via alteration of AMPK/Nrf2/HO-1 pathway.

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http://dx.doi.org/10.5650/jos.ess21281DOI Listing

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