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灵芝蛋白聚糖通过减轻内质网应激和调节 CHOP/JNK 通路对 INS-1 细胞抵抗 IAPP 诱导的细胞凋亡的保护作用。

Protective effects of a G. lucidum proteoglycan on INS-1 cells against IAPP-induced apoptosis via attenuating endoplasmic reticulum stress and modulating CHOP/JNK pathways.

机构信息

Department of Endocrinology, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 200437, China.

State Key Laboratory of Molecular Engineering of Polymers, Department of Macromolecular Science, Fudan University, 220 Handan Road, Shanghai 200433, China.

出版信息

Int J Biol Macromol. 2018 Jan;106:893-900. doi: 10.1016/j.ijbiomac.2017.08.089. Epub 2017 Sep 8.

Abstract

Fudan-Yueyang-G. lucidum (FYGL) is a water-soluble macromolecular proteoglycan extracted from Ganoderma lucidum which has been used for health promotion for a long time in China. The aim of this study was to investigate the protective effects of FYGL on INS-1 rat insulinoma beta cells against IAPP-induced cell apoptosis, as well as the underlying mechanisms. The results showed that apoptotic cells were significantly increased when incubated with islet amyloid polypeptide (IAPP). However, cytotoxicity of IAPP was significantly attenuated by co-incubation of the cells with FYGL. The results of RT-PCR showed that mRNA expression of caspase-3, caspase-12 and C/EBP homologous protein (CHOP) in IAPP-treated cells were inhibited by FYGL. Moreover, FYGL significantly prevented the IAPP-induced abnormal expression of inositol-requiring protein-1α (IRE1α), protein kinase RNA (PKR)-like ER kinase (PERK), activating transcription factor 6 (ATF6), as well as suppressed the activation of CHOP and c-Jun N-terminal kinase (JNK). Taken together, our results suggest that FYGL protects INS-1 pancreatic beta cells against IAPP-induced apoptosis through attenuating endoplasmic reticulum stress (ERS) and modulating CHOP/JNK pathways.

摘要

复旦 - 岳阳 - 灵芝(FYGL)是一种从灵芝中提取的水溶性大分子糖胺聚糖,在中国长期以来一直被用于促进健康。本研究旨在探讨 FYGL 对 INS-1 大鼠胰岛素瘤β细胞抵抗 IAPP 诱导的细胞凋亡的保护作用及其潜在机制。结果表明,当用胰岛淀粉样多肽(IAPP)孵育时,凋亡细胞明显增加。然而,FYGL 与细胞共孵育可显著减轻 IAPP 的细胞毒性。RT-PCR 结果表明,FYGL 抑制了 IAPP 处理细胞中 caspase-3、caspase-12 和 C/EBP 同源蛋白(CHOP)的 mRNA 表达。此外,FYGL 还显著防止了 IAPP 诱导的肌醇需求蛋白-1α(IRE1α)、蛋白激酶 RNA(PKR)样内质网激酶(PERK)、激活转录因子 6(ATF6)的异常表达,并抑制了 CHOP 和 c-Jun N-末端激酶(JNK)的激活。综上所述,我们的研究结果表明,FYGL 通过减轻内质网应激(ERS)和调节 CHOP/JNK 途径来保护 INS-1 胰腺β细胞免受 IAPP 诱导的凋亡。

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