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香草酸可增强胰岛素分泌,并可防止 HO 诱导的氧化应激对胰岛β细胞的细胞毒性。

Vanillic acid potentiates insulin secretion and prevents pancreatic β-cells cytotoxicity under HO-induced oxidative stress.

机构信息

Department of Molecular Nutrition, CSIR-Central Food Technological Research Institute (CFTRI), Mysuru, Karnataka, 570020, India.

Academy of Scientific and Innovative Research (AcSIR), Ghaziabad, 201002, India.

出版信息

Mol Biol Rep. 2023 Feb;50(2):1311-1320. doi: 10.1007/s11033-022-08046-0. Epub 2022 Dec 1.

Abstract

BACKGROUND

Oxidative stress is known to impair cellular functions and, therefore, plays a significant role in the pathophysiology of various diseases, including diabetes. The persistently elevated glucose levels may cause enhanced mitochondrial reactive oxygen species generation, which in turn can damage the pancreatic β-cells. In this study, we have investigated the effect of vanillic acid on preventing HO-induced β-cells death and retaining its insulin secretion potentiating effect in the presence of HO.

METHODS

The insulin secretion from the BRIN-BD11 cells was quantified using ELISA-based assays. The viability of the cells was assessed by estimated by the [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide] (MTT) colorimetric assay and DAPI staining. The expression levels of apoptotic and antioxidant proteins were estimated by western blot experiments.

RESULTS

Vanillic acid protected pancreatic β-cells viability and function under the HO oxidative stress condition. The Erk1/2 activation appears to play an important role in vanillic acid potentiated insulin secretion and protection of the β-cells in the presence of HO. Vanillic acid pretreated cells exhibited enhanced expression of antioxidant enzymes such as catalase and SOD-2 and reduced the expression of proapoptotic markers such as BAX and BAD. In addition, it also enhanced the expression of oxidative stress-sensitive transcription factor Nrf-2 and cell survival protein Akt.

CONCLUSION

The present study shows that vanillic acid potentiates insulin secretion and protects pancreatic β-cells from HO-induced oxidative stress.

摘要

背景

氧化应激已知会损害细胞功能,因此在各种疾病的病理生理学中起着重要作用,包括糖尿病。持续升高的葡萄糖水平可能导致线粒体活性氧产生增强,这反过来又会损害胰岛β细胞。在这项研究中,我们研究了香草酸在预防 HO 诱导的β细胞死亡以及在存在 HO 的情况下保留其增强胰岛素分泌的作用。

方法

使用基于 ELISA 的测定法来定量 BRIN-BD11 细胞的胰岛素分泌。通过[3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴化物](MTT)比色法和 DAPI 染色来评估细胞活力。通过 Western blot 实验来估计凋亡和抗氧化蛋白的表达水平。

结果

香草酸在 HO 氧化应激条件下保护胰岛β细胞的活力和功能。ERK1/2 的激活似乎在香草酸增强胰岛素分泌和保护 HO 存在下的β细胞中起着重要作用。香草酸预处理的细胞表现出抗氧化酶(如过氧化氢酶和 SOD-2)的表达增强,以及促凋亡标志物(如 BAX 和 BAD)的表达减少。此外,它还增强了氧化应激敏感转录因子 Nrf-2 和细胞存活蛋白 Akt 的表达。

结论

本研究表明,香草酸增强胰岛素分泌并保护胰岛β细胞免受 HO 诱导的氧化应激。

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