仙人掌果多糖保护胰岛 $ \beta $ 细胞免受氧化应激诱导的凋亡机制研究

文章通过网络药理学预测仙人掌果多糖(OFPPs)保护胰岛β细胞免受氧化应激损伤的可能机制，并在 $ H_{2}O_{2} $诱导的大鼠胰岛素瘤(INS-1)细胞模型中进行验证。网络药理学预测的结果表明，凋亡相关信号通路在仙人掌果多糖保护胰岛β细胞免受氧化应激损伤的机制中发挥重要作用；体外实验结果表明，其机制与调节B淋巴细胞瘤-2(Bcl-2)、Bcl-2相关X蛋白(Bax)、半胱氨酸天冬氨酸蛋白酶3(Caspase3)的表达水平有关。仙人掌果多糖可以减轻氧化应激诱导的胰岛β细胞凋亡，可能具有作为功能性食品改善糖尿病症状的潜力。

In this study, the possible mechanism of protection of pancreatic $ \beta $ cells from oxidative stress damage by Opuntia dillenii Haw. fruits polysaccharides(OFPPs) was predicted by network pharmacology and validated using an $ H_{2}O_{2} $-induced oxidative stress cell model in INS-1 cells. The results predicted by network pharmacology indicated that apoptosis-related signaling pathway played an important role in the mechanism of protection of pancreatic $ \beta $-cells from oxidative stress damage by OFPPs, and the in vitro experimental results also demonstrated that the mechanism was related to the regulation of Bax, Bcl-2 and Caspase3 expression levels. OFPPs can reduce oxidative stress-induced pancreatic $ \beta $-cell apoptosis and may have potential as functional foods to improve diabetes symptoms.