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Dihydrotanshinone I reduces H9c2 cell damage by regulating AKT and MAPK signaling pathways

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Abstract

Cardiovascular disease is the deadliest disease in the world. Previous studies have shown that Dihydrotanshinone I (DHT) can improve cardiac function after myocardial injury. This study aimed to observe the protective effect and mechanism of DHT on H9c2 cells by establishing an oxygen–glucose deprivation/reoxygenation (OGD/R) injury model. By constructing OGD/R injury simulation of H9c2 cells in a myocardial injury model, the proliferation of H9c2 cells treated with DHT concentrations of 0.1 μmol/L were not affected at 24, 48, and 72 h. DHT can significantly reduce the apoptosis of H9c2 cells caused by OGD/R. Compared with the OGD/R group, DHT treatment significantly reduced the level of MDA and increased the level of SOD in cells. DHT treatment of cells can significantly reduce the levels of ROS and Superoxide in mitochondria in H9c2 cells caused by OGD/R and H2O2. DHT significantly reduced the phosphorylation levels of P38MAPK and ERK in H9c2 cells induced by OGD/R, and significantly increased the phosphorylation levels of AKT in H9c2 cells. DHT can significantly reduce the oxidative stress damage of H9c2 cells caused by H2O2 and OGD/R, thereby reducing the apoptosis of H9c2 cells. And this may be related to regulating the phosphorylation levels of AKT, ERK, and P38MAPK.

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Funding

This work was supported by grants from the National Natural Science Foundation of China (82174120, 81970991, 82104430, 82204831), Natural Science Foundation of Shanghai (No. 21ZR1463100), Program of Shanghai Academic Research Leader (22XD1423400) and Shanghai Sailing Program (No. 21YF1447600).

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Correspondence to Ke Ning, Bao-nian Liu or Hai-dong Guo.

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Wang, Yc., Shao, Yd., Shao, Cl. et al. Dihydrotanshinone I reduces H9c2 cell damage by regulating AKT and MAPK signaling pathways. In Vitro Cell.Dev.Biol.-Animal 60, 89–97 (2024). https://doi.org/10.1007/s11626-023-00839-2

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  • DOI: https://doi.org/10.1007/s11626-023-00839-2

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