The pancreatic β-cell death or dysfunction induced by oxidative stress plays an important effect on the development and progression of diabetes mellitus. Based on our previous findings, a natural proteoglycan extracted from Ganoderma Lucidum, named FYGL, could treat T2DM in vivo. In this study, we investigated the effects of FYGL on STZ‐induced apoptosis of INS-1 cells and its underlying mechanisms. The results showed that FYGL significantly improved the cell viability and alleviated the apoptosis in STZ‐treated INS‐1 cells. Moreover, FYGL markedly decreased the intracellular ROS accumulation and NO release, and deactivated NF-κB, JNK, and p38 MAPK signaling pathways in STZ-induced INS-1 cells. Furthermore, FYGL improved the insulin secretion through inhibiting the activation of JNK and improving the expression of Pdx-1 in INS-1 cells damaged by STZ. These results indicated that FYGL could protect pancreatic β-cells against apoptosis and dysfunction, and be used as a promising pharmacological medicine for diabetes management.

Abbreviations

T2DM: type 2 diabetes mellitus; FYGL: Fudan-Yueyang G. lucidum; ROS: reactive oxygen species; NO: reactive oxygen species; NF-κB: nuclear factor kappa beta; JNK: c-jun N-terminal kinase; MAPK: mitogen-activated protein kinase; Pdx-1: Pancreatic duodenal homeobox 1

中文翻译：

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灵芝的蛋白聚糖提取物可保护胰腺β细胞免受STZ诱导的细胞凋亡

氧化应激引起的胰腺β细胞死亡或功能异常对糖尿病的发生发展具有重要作用。根据我们之前的发现，从灵芝中提取的天然蛋白聚糖名为FYGL，可以在体内治疗T2DM 。在这项研究中，我们研究了FYGL对STZ诱导的INS-1细胞凋亡的影响及其潜在机制。结果表明，FYGL显着改善了经STZ处理的INS-1细胞的细胞活力并减轻了其凋亡。此外，FYGL明显降低了STZ诱导的INS-1细胞中细胞内ROS的积累和NO的释放，并使NF-κB，JNK和p38 MAPK信号通路失活。此外，FYGL通过抑制JNK的活化和改善STZ损伤的INS-1细胞中Pdx-1的表达来改善胰岛素分泌。这些结果表明FYGL可以保护胰腺β细胞免于凋亡和功能障碍，并被用作糖尿病治疗的有希望的药理学药物。

缩略语

T2DM：2型糖尿病；FYGL：复旦-岳阳灵芝；ROS：活性氧；NO：活性氧；NF-κB：核因子κβ；JNK：c-jun N-末端激酶；MAPK：促分裂原活化蛋白激酶；Pdx-1：胰十二指肠同源盒1