ABSTRACT
【Objective】 To investigate the effect of ethanol extracts of Siwei Dihuang on the apoptosis of cardiomyocytes and its mechanism. 【Methods】 The experiment set the control group， model group， model group + ethanol extracts of Siwei Dihuang-L group， model group + ethanol extracts of Siwei Dihuang-M group， model group + ethanol extracts of Siwei Dihuang-H group， model group + miR-NC group， model group + miR-26b group model group + ethanol extracts of Siwei Dihuang-M + anti-miR-NC group， and model group + ethanol extracts of Siwei Dihuang-M + anti-miR-26b group. Flow cytometry was used to detect apoptosis； lactate dehydrogenase （LDH） kit， superoxide dismutase （SOD） kit， and malondialdehyde （MDA） kit were used to detect LDH， SOD activity and MDA content， respectively. Real-time quantitative PCR （RT-qPCR） was used to detect miR-26b and MAPK mRNA levels； luciferase report experiment was conducted to detect the targeting relationship between miR-26b and MAPK. 【Results】 Compared with those in control group， the apoptosis rate of the cardiomyocytes of the model group was significantly increased， MDA content and LDH activity were significantly increased， the activity of SOD was significantly decreased， miR-26b expression was significantly decreased， but MAPK mRNA expression was significantly increased （P<0.05）. Treatment with low， medium and high concentrations of ethanol extracts of Siwei Dihuang could reduce apoptosis rate， MDA content and LDH activity， increase SOD activity and increase miR-26b expression， and decrease MAPK mRNA expression （P<0.05）. Overexpression of miR-26b inhibited high glucose-induced cardiomyocyte apoptosis and oxidative stress. Inhibition of miR-26b reversed the inhibitory effect of ethanol extracts of Siwei Dihuang on H9C2 apoptosis and oxidative stress in high glucose-induced cells. miR-26b targeted and regulated MAPK. 【Conclusion】 Ethanol extracts of Siwei Dihuang can inhibit the apoptosis and oxidative stress of H9C2 cells in high glucose， and its mechanism may be related to the upregulation of miR-26b and MAPK expressions.