半夏泻心汤通过激活超氧化物歧化酶2（SOD2），经由过氧化物酶体增殖物激活受体γ共激活因子1α（PGC-1α）/胰岛素样生长因子结合蛋白1（IGFBP1）清除活性氧（ROS），减轻高糖诱导的肝细胞损伤。
Banxia Xiexin Tang attenuates high glucose-induced hepatocyte injury by activating SOD2 to scavenge ROS via PGC-1α/IGFBP1.
作者信息
Yang Xu, Yue Rensong, Zhao LiangBin, Huang Xiushen, Wang Qiyue
机构信息
Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Chengdu University of Traditional Chinese Medicine, Chengdu, China.
出版信息
3 Biotech. 2024 Sep;14(9):216. doi: 10.1007/s13205-024-04060-0. Epub 2024 Aug 28.
UNLABELLED
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.
未标注
本研究旨在探讨半夏泻心汤（BXXXT）对高糖（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BXXXT对高糖（H-G）诱导的肝细胞活性的影响。实验结果表明，BXXXT显著降低了高糖引起的细胞活性损失。进一步的研究聚焦于BXXXT对高糖诱导的肝细胞凋亡的调控作用，尤其是其对PGC-1α（过氧化物酶体增殖物激活受体γ共激活因子-1α）途径的影响。实验结果表明，BXXXT减少了高糖诱导的肝细胞凋亡，并通过上调PGC-1α途径的活性发挥其保护作用。BXXXT显著提高了高糖环境下肝细胞中IGFBP1（胰岛素样生长因子结合蛋白）的表达水平。它通过增强SOD2（超氧化物歧化酶）酶活性清除线粒体活性氧（ROS），并维持高糖环境下肝细胞的存活。最后，BXXXT对PGC-1α的调控确实参与了肝细胞中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，重点在于调节PGC-1α途径和IGFBP1的表达，并通过清除ROS减少细胞损伤。这为进一步探索BXXXT在治疗糖尿病相关肝损伤方面的潜力提供了实验依据。
补充信息
在线版本包含可在10.1007/s13205-024-04060-0获取的补充材料。
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