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

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

  • 3 Biotech. 2024 Sep;14(9):216. doi: 10.1007/s13205-024-04060-0.
Xu Yang 1 Rensong Yue 1 LiangBin Zhao 1 Xiushen Huang 2 Qiyue Wang 3
Affiliations

Affiliations

  • 1 Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China.
  • 2 Chengdu University of Traditional Chinese Medicine, Chengdu, China.
  • 3 Chengdu Jinniu Hospital of Traditional Chinese Medicine, Chengdu, China.
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.

Keywords

Banxia Xiexin Tang; Hepatocyte injury; High-glucose; IGFBP1; PGC-1α.

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