Xinshuaining preparation protects H9c2 cells from H2O2-induced oxidative damage through the PI3K/Akt/Nrf-2 signaling pathway

Autor: Mingjun Han, Jie Lin, Yi Yang, Yumei Ding, Wenjun Ge, Haoran Fan, Ce Wang, Wen Xie
Jazyk: angličtina
Rok vydání: 2022
Předmět:
Zdroj: Clinical and Experimental Hypertension, Vol 0, Iss 0, Pp 1-9 (2022)
Druh dokumentu: article
ISSN: 1064-1963
1525-6006
10641963
DOI: 10.1080/10641963.2022.2131806
Popis: Background Cardiovascular disease (CVD) is the leading cause of death. Oxidative stress is an important pathological process of a variety of CVDs. Xinshuaining preparation has a therapeutic effect on the heart failure. However, the anti-oxidative stress role of Xinshuaining preparation in H9c2 cells is still unclear. Methods The medicated serum of Xinshuaining preparation was acquired and utilized to hatch with H2O2-induced H9c2 cells. Main components in the Xinshuaining preparation were analyzed by liquid chromatography-mass spectrometry (LC/MS). The effect of medicated serum on the cell viability, apoptosis rate, the oxidative stress indicators (SOD, GSH-Px, and MDA), mitochondrial membrane potential (MMP), and ROS level was evaluated by CCK-8, flow cytometry, commercial biochemical detection kits, and JC-1 staining. Additionally, the associated mechanism was determined by the detection of the protein levels (PI3K, phosphorylated PI3K, Akt, phosphorylated Akt, and Nrf-2) through western blot assays, which was also further assessed with the application of LY294002. Results The medicated serum of Xinshuaining preparation notably increased the H2O2-reduced, the cell viability, the concentration of SOD and GSH-Px, MMP level and the relative protein expression level of phosphorylated PI3K and Akt and Nrf-2, while dampened the H2O2-elevated the level of the cell apoptosis rate, MDA, and ROS. However, Xinshuaining preparation on the cell viability, apoptosis, and oxidative stress was notably antagonized by LY294002 pre-treatment. Conclusions The medicated serum of Xinshuaining preparation increased the cell viability and suppressed apoptosis and oxidative stress via the PI3K/Akt/Nrf-2 signaling pathway.
Databáze: Directory of Open Access Journals
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