Banxia Xiexin Tang attenuates high glucose-induced hepatocyte injury by activating SOD2 to scavenge ROS via PGC-1α/IGFBP1.

IF 2.6 4区 生物学 Q3 BIOTECHNOLOGY & APPLIED MICROBIOLOGY
3 Biotech Pub Date : 2024-09-01 Epub Date: 2024-08-28 DOI:10.1007/s13205-024-04060-0
Xu Yang, Rensong Yue, LiangBin Zhao, Xiushen Huang, Qiyue Wang
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引用次数: 0

Abstract

This study aimed to explore the protective mechanism of Banxia Xiexin Tang (BXXXT) on liver cell damage caused by high glucose (H-G) and to clarify its molecular regulatory pathways. First, the main components in BXXXT-containing serum were analyzed by high-performance liquid chromatography (HPLC) to provide basic data for subsequent experiments. Subsequently, the effect of BXXXT on high glucose (H-G)-induced hepatocyte activity was evaluated through screening of the optimal concentration of drug-containing serum. Experimental results showed that BXXXT significantly reduced the loss of cell activity caused by high glucose. Further research focuses on the regulatory effect of BXXXT on high glucose-induced hepatocyte apoptosis, especially its effect on the PGC-1α (peroxisome proliferator-activated receptor γ coactivator-1α) pathway. Experimental results showed that BXXXT reduced high-glucose-induced hepatocyte apoptosis and exerted its protective effect by upregulating the activity of the PGC-1α pathway. BXXXT significantly increased the expression level of IGFBP1 (insulin-like growth factor-binding proteins) in hepatocytes under a high-glucose environment. It cleared mitochondrial ROS (reactive oxygen species) by enhancing SOD2 (superoxide dismutase) enzyme activity and maintained the survival of hepatocytes under a high-glucose environment. Finally, the regulation of PGC-1α by BXXXT is indeed involved in the regulation of IGFBP1 expression in hepatocytes and its downstream SOD2 effector signaling. Taken together, this study provides an in-depth explanation of the protective mechanism of BXXXT on hepatocytes in a high-glucose environment, focusing on regulating the expression of the PGC-1α pathway and IGFBP1, and reducing cell damage by scavenging ROS. This provides an experimental basis for further exploring the potential of BXXXT in the treatment of diabetes-related liver injury.

Supplementary information: The online version contains supplementary material available at 10.1007/s13205-024-04060-0.

Abstract Image

半夏泻心汤通过PGC-1α/IGFBP1激活SOD2清除ROS,从而减轻高糖诱导的肝细胞损伤。
本研究旨在探讨半夏泻心汤(BXXXT)对高血糖(H-G)所致肝细胞损伤的保护机制,并阐明其分子调控途径。首先,采用高效液相色谱法(HPLC)分析了含 BXXXT 血清中的主要成分,为后续实验提供基础数据。随后,通过筛选含药血清的最佳浓度,评估了 BXXXT 对高葡萄糖(H-G)诱导的肝细胞活性的影响。实验结果表明,BXXXT 能显著降低高糖导致的细胞活性损失。进一步研究的重点是 BXXXT 对高糖诱导的肝细胞凋亡的调控作用,尤其是其对 PGC-1α(过氧化物酶体增殖激活受体 γ 辅激活剂-1α)通路的影响。实验结果表明,BXXXT 可减少高血糖诱导的肝细胞凋亡,并通过上调 PGC-1α 通路的活性发挥其保护作用。在高糖环境下,BXXXT 能明显提高肝细胞中 IGFBP1(胰岛素样生长因子结合蛋白)的表达水平。它通过提高 SOD2(超氧化物歧化酶)酶的活性清除线粒体中的 ROS(活性氧),维持肝细胞在高糖环境下的存活。最后,BXXXT 对 PGC-1α 的调控确实参与了对肝细胞中 IGFBP1 表达及其下游 SOD2 效应信号的调控。综上所述,本研究深入解释了 BXXXT 在高糖环境下对肝细胞的保护机制,主要是调节 PGC-1α 通路和 IGFBP1 的表达,并通过清除 ROS 减少细胞损伤。这为进一步探索 BXXXT 治疗糖尿病相关肝损伤的潜力提供了实验基础:在线版本包含补充材料,可在 10.1007/s13205-024-04060-0获取。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
3 Biotech
3 Biotech Agricultural and Biological Sciences-Agricultural and Biological Sciences (miscellaneous)
CiteScore
6.00
自引率
0.00%
发文量
314
期刊介绍: 3 Biotech publishes the results of the latest research related to the study and application of biotechnology to: - Medicine and Biomedical Sciences - Agriculture - The Environment The focus on these three technology sectors recognizes that complete Biotechnology applications often require a combination of techniques. 3 Biotech not only presents the latest developments in biotechnology but also addresses the problems and benefits of integrating a variety of techniques for a particular application. 3 Biotech will appeal to scientists and engineers in both academia and industry focused on the safe and efficient application of Biotechnology to Medicine, Agriculture and the Environment.
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