Department of Endocrine, Longhu People's Hospital,Shantou, Guangdong, China.
Department of Emergency Intensive Care Unit(EICU),First Affiliated Hospital of Medical College of Shantou University, Dongxia S Rd, Jinping Qu, Shantou Shi, Guangdong Sheng, China.
Front Biosci (Landmark Ed). 2020 Jun 1;25(11):1974-1984. doi: 10.2741/4887.
Loss of pancreatic beta-cells by apoptosis appears to play an important role in the development of insulin deficiency and the onset and/or progression of the diabetes mellitus. To this end, we report that curcumin prevents high glucose (HG) induced oxidative stress and apoptosis in mouse pancreatic beta cells. Moreover, curcumin prevents HG induced increase in expression of CHOP, decrease in PCG-1a and phosphorylation of ERK1/2 (pERK1/2) without any effect on the phosphorylation levels of p38 and JNK. Moreover, similar to curcumin, blockade of pERK1/2 reduced the HG induced apoptosis in pancreatic beta cells. Overexpression of CHOP or siRNA knockdown of PCG-1a counteracted the effect of curcumin on HG induced apoptosis and oxidative stress. These results suggest that curcumin acts through CHOP/PCG-1a and ERK1/2 signaling to block the HG induced oxidative stress and apoptosis.
细胞凋亡导致的胰岛β细胞缺失似乎在胰岛素缺乏症的发展以及糖尿病的发生和/或进展中发挥了重要作用。为此，我们报告姜黄素可预防高葡萄糖（HG）诱导的小鼠胰岛β细胞氧化应激和细胞凋亡。此外，姜黄素可预防 HG 诱导的 CHOP 表达增加、PCG-1a 减少和 ERK1/2 磷酸化（pERK1/2），而对 p38 和 JNK 的磷酸化水平没有任何影响。此外，与姜黄素相似，阻断 pERK1/2 可减少 HG 诱导的胰岛β细胞凋亡。CHOP 的过表达或 PCG-1a 的 siRNA 敲低可拮抗姜黄素对 HG 诱导的细胞凋亡和氧化应激的作用。这些结果表明，姜黄素通过 CHOP/PCG-1a 和 ERK1/2 信号通路发挥作用，以阻断 HG 诱导的氧化应激和细胞凋亡。
