Department of Cardiovascular Medicine of The First Affiliated Hospital of Bengbu Medical College, Bengbu City, Anhui, China 233000.
Department of Cardiac Surgery of The First Affiliated Hospital of Bengbu Medical College, Bengbu City, Anhui, China 233000.
Mediators Inflamm. 2023 Apr 17;2023:3906043. doi: 10.1155/2023/3906043. eCollection 2023.
This study is aimed at exploring whether curcumin can regulate the AKT pathway, promote the transfer of Nrf2 into the nucleus, and inhibit cell pyroptosis in diabetic cardiomyopathy. Diabetic rats and cardiomyocytes were treated with curcumin to study its effect on myocardial pyroptosis. Whether curcumin can promote the transfer of Nrf2 into the nucleus through AKT pathway regulation was assessed by western blotting and immunofluorescence. The Nrf2 knockout vector and ml385 were used to block the Nrf2 pathway, and the differences between the different groups in the expression of pyroptosis protein, cell activity, and incidence of apoptosis were evaluated to verify the relationship between the effect of curcumin on pyroptosis inhibition and the Nrf2 pathway. Curcumin promoted the transfer of Nrf2 into the nucleus through the AKT pathway and increased the expression of the antioxidant factors HO-1 and GCLC. These effects reduced reactive oxygen species accumulation and mitochondrial damage in diabetic myocardium and inhibited diabetes-induced pyroptosis. However, in cardiomyocytes with a blocked Nrf2 pathway, the ability of curcumin to inhibit pyroptosis was significantly reduced, and the protective effect on the cells was lost. Curcumin can reduce the accumulation of superoxide in the myocardium through AKT/Nrf2/ARE pathway activation and inhibit pyroptosis. It also has a role in diabetic cardiomyopathy treatment. This study provides new directions for evaluating the mechanism of diabetic cardiomyopathy and treating diabetic myocardium.
本研究旨在探讨姜黄素是否可以调节 AKT 通路，促进 Nrf2 转入核内，并抑制糖尿病心肌病中的细胞焦亡。使用姜黄素处理糖尿病大鼠和心肌细胞，研究其对心肌焦亡的影响。通过 Western blot 和免疫荧光评估姜黄素是否可以通过 AKT 通路调节促进 Nrf2 转入核内。使用 Nrf2 敲除载体和 ml385 阻断 Nrf2 通路，评估不同组之间焦亡蛋白表达、细胞活性和细胞凋亡发生率的差异，以验证姜黄素抑制焦亡作用与 Nrf2 通路之间的关系。姜黄素通过 AKT 通路促进 Nrf2 转入核内，增加抗氧化因子 HO-1 和 GCLC 的表达。这些作用减少了糖尿病心肌中的活性氧积累和线粒体损伤，抑制了糖尿病诱导的焦亡。然而，在阻断 Nrf2 通路的心肌细胞中，姜黄素抑制焦亡的能力显著降低，对细胞的保护作用丧失。姜黄素通过激活 AKT/Nrf2/ARE 通路减少心肌中超氧阴离子的积累，抑制焦亡。它在糖尿病心肌病的治疗中也具有作用。本研究为评估糖尿病心肌病的机制和治疗糖尿病心肌提供了新的方向。
