葡萄籽原花青素通过 Nrf2 通路保护 2 型糖尿病患者的胰腺 β 细胞免受铁氧化作用的影响

IF 3.4 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Biological Trace Element Research Pub Date : 2024-12-01 Epub Date: 2024-02-17 DOI:10.1007/s12011-024-04093-9
Haiyan Li, Haowei Zhang, Tongling Wang, Liyuan Zhang, Hao Wang, Heng Lu, Ruirui Yang, Yusong Ding
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引用次数: 0

摘要

胰腺β细胞损伤是导致2型糖尿病(T2DM)的主要因素;然而,其潜在机制仍然模糊不清。本研究探讨了铁突变在胰腺β细胞损伤中的作用以及葡萄籽原花青素提取物(GSPE)的保护作用。在T2DM模型大鼠中,血糖、摄水量、尿量、HbA1c和稳态模型评估-胰岛素抵抗显著增加,而体重和胰岛素水平显著下降,表明T2DM模型的成功建立。在高糖和棕榈酸钠条件下培养 MIN6 小鼠胰岛素瘤 β 细胞以获得糖脂损伤模型,并给予 GSPE、铁前列素-1(Fer-1)或核因子红细胞 2 相关因子 2(Nrf2)小干扰(si)RNA。GSPE和Fer-1能明显改善胰腺β细胞的功能障碍并防止细胞死亡。这两种疗法都能提高超氧化物歧化酶和谷胱甘肽的活性,降低丙二醛和活性氧水平,并改善铁代谢。此外,这两种疗法还逆转了糖脂毒性导致的铁变态标志物半胱氨酸/谷氨酸转运体(XCT)和谷胱甘肽过氧化物酶 4(GPX4)的表达。GSPE 处理激活了 Nrf2 和相关蛋白的表达。当与 si-Nrf2 共同转染时,这些效应被逆转。GSPE 通过激活 Nrf2 信号通路来抑制铁突变,从而减少 T2DM 中 β 细胞的损伤和功能障碍。因此,GSPE 是治疗 T2DM 的一种潜在策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Grape Seed Proanthocyanidins Protect Pancreatic β Cells Against Ferroptosis via the Nrf2 Pathway in Type 2 Diabetes.

Pancreatic β cell damage is the primary contributor to type 2 diabetes mellitus (T2DM); however, the underlying mechanism remains nebulous. This study explored the role of ferroptosis in pancreatic β cell damage and the protective effects of grape seed proanthocyanidin extract (GSPE). In T2DM model rats, the blood glucose, water intake, urine volume, HbA1c, and homeostasis model assessment-insulin resistance were significantly increased, while the body weight and the insulin level were significantly decreased, indicating the successful establishment of the T2DM model. MIN6 mouse insulinoma β cells were cultured in high glucose and sodium palmitate conditions to obtain a glycolipid damage model, which was administered with GSPE, ferrostatin-1 (Fer-1), or nuclear factor erythroid 2-related factor 2 (Nrf2) small interfering (si) RNA. GSPE and Fer-1 treatment significantly improved pancreatic β-cell dysfunction and protected against cell death. Both treatments increased the superoxide dismutase and glutathione activity, reduced the malondialdehyde and reactive oxygen species levels, and improved iron metabolism. Furthermore, the treatments reversed the expression of ferroptosis markers cysteine/glutamate transporter (XCT) and glutathione peroxidase 4 (GPX4) caused by glycolipid toxicity. GSPE treatments activated the expression of Nrf2 and related proteins. These effects were reversed when co-transfected with si-Nrf2. GSPE inhibits ferroptosis by activating the Nrf2 signaling pathway, thus reducing β-cell damage and dysfunction in T2DM. Therefore, GSPE is a potential treatment strategy against T2DM.

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来源期刊
Biological Trace Element Research
Biological Trace Element Research 生物-内分泌学与代谢
CiteScore
8.70
自引率
10.30%
发文量
459
审稿时长
2 months
期刊介绍: Biological Trace Element Research provides a much-needed central forum for the emergent, interdisciplinary field of research on the biological, environmental, and biomedical roles of trace elements. Rather than confine itself to biochemistry, the journal emphasizes the integrative aspects of trace metal research in all appropriate fields, publishing human and animal nutritional studies devoted to the fundamental chemistry and biochemistry at issue as well as to the elucidation of the relevant aspects of preventive medicine, epidemiology, clinical chemistry, agriculture, endocrinology, animal science, pharmacology, microbiology, toxicology, virology, marine biology, sensory physiology, developmental biology, and related fields.
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