Protective effect of Baicalin on lipopolysaccharide induced H9C2 cell inflammation and its mechanism

Objective To investigate the protective effect of Baicalin on inflammation induced by lipopolysaccharide in H9C2 cardiomyocytes and its possible mechanism. Methods H9C2 myocardial cells were cultured and pretreated with baicalin at the final concentration of 10, 20, 30 μmol/L for 12 hours, then stimulated with LPS at the final concentration of 1 μg/mL for 6 hours. The control group was treated with the same amount of saline to collect cell samples. CCK-8 (The Cell Counting Kit-8) was used to detect cell activity, enzyme-linked immunosorbent assay (ELISA) was used to detect the expression levels of interleukin-6 (IL-6), interleukin-1beta (IL-1β), tumor necrosis factor-alpha (TNF-α), Western blot was used to detect the protein expression levels of NF-κB p65, p-NF-κB p65, p38 MAPK, p-p38 MAPK, IκBα and p-IκBα. SPSS 23.0 statistical software was used. Independent sample t test was used for comparison between two groups, and one-way ANOVA test was used for comparison among multiple groups. Results The survival rate of myocardial cells in the control group was (93.67 +1.453)%. Compared with the control group, the survival rate of H9C2 myocardial cells induced by LPS decreased (P 0.05). Compared with LPS group, the survival rate of H9C2 myocardial cells in baicalin intervention group increased (P 0.05). Conclusions Baicalin may alleviate LPS-induced cardiomyocyte inflammation by inhibiting the activation of NF-kappa B and p38 MAPK, and improve cell survival. Key words: Baicalin; Lipopolysaccharide; Cardiomyocyte; NF-κB; P38 MAPK; Sepsis; Inflammation