Effects of ligustrazine on inflammation and oxidative stress in rat cardiomyocytes induced by lipopolysaccharide

doi:10.12307/2023.494

Abstract

Abstract: BACKGROUND: Sepsis-induced myocardial injury is related to inflammatory response and oxidative stress injury. Previous studies have shown that ligustrazine has many functions such as anti-oxidation and maintaining calcium homeostasis.
OBJECTIVE: To investigate the effects of ligustrazine on inflammation and oxidative stress in lipopolysaccharide-induced rat cardiomyocytes.
METHODS: Rat cardiomyocytes were induced by lipopolysaccharide (1 μg/mL) to establish septic cardiomyocyte inflammatory models. Twenty-four hours after intervention with different concentrations of ligustrazine (40, 80, 160 μmol/L), the samples were collected and detected. The effects of ligustrazine on the release of lactate dehydrogenase and reactive oxygen species from H9C2 cells induced by lipopolysaccharide were detected. Apoptosis was observed by fluorescence microscope. RT-qPCR was used to detect the changes of inflammatory factors such as interleukin-1 β, tumor necrosis factor-α, and interleukin-6 as well as the expression of Toll like receptor 4 and MyD88.
RESULTS AND CONCLUSION: Compared with the normal control group, the expression of lactate dehydrogenase and reactive oxygen species in H9C2 cells increased significantly in the model group (P < 0.05) and a large number of cells were stained with propidium iodide under fluorescence microscope. The expression levels of interleukin-1β, tumor necrosis factor-α, and interleukin-6 were significantly increased (P < 0.05) and the expression of Toll like receptor 4 and MyD88 genes were significantly increased in the model group compared with the normal control group (P < 0.05). Compared with the model group, ligustrazine treatment could effectively inhibit the release of lactate dehydrogenase and reactive oxygen species, reduce the number of H9C2 cells stained by propidium iodide, downregulate the expression of interleukin-1β, tumor necrosis factor α and interleukin-6, and suppress the expression of Toll like receptor 4 and MyD88 genes (P < 0.05). To conclude, ligustrazine may reduce intracellular inflammatory factors and oxidative stress by inhibiting the expression of Toll like receptor 4/MyD88.

Key words: ligustrazine, lipopolysaccharide, H9C2, inflammation, oxidative stress

CLC Number:

Sun Fangyuan, Meng Jialei, Ma Yuhui, Geng Huan, Zhang Tao. Effects of ligustrazine on inflammation and oxidative stress in rat cardiomyocytes induced by lipopolysaccharide[J]. Chinese Journal of Tissue Engineering Research, 2023, 27(20): 3253-3258.

Figures/Tables 6

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