To investigate the effects of catechins on oxidative damage, inflammation and apoptosis of rat cardiomyocytes(H9C2) induced by lipopolysaccharide (LPS), as well as the regulation of p38 mitogen-activated protein kinase (MAPK) sig naling pathway, H9C2 cells were cultured in vitro and divided into the control group which is without intervention, LPS groupwith 10 μg/mL LPS treatment, catechin with different concentrations (20, 40, 80, 160 nmol/L catechin treatment based on LPSgroup) and SB203580 group (10 μg/mL LPS+1 μmol/L SB203580 treatment), inhibitor group (10 μg/mL LPS+160 nmol/L catechin +1 μmol/L p38 MAPK pathway inhibitor SB203580 treatment) and activator group (10 μg/mL LPS+160 nmol/L catechin+10 μmol/L p38 MAPK pathway activator C16-PAF). Cell viability was measured with cell counting kit-8 (CCK-8) after 24 htreatment. The levels of interleukin-6 (IL-6) and interleukin-10 (IL-10) were detected by enzyme-linked immunosorbent assay(ELISA). Malondialdehyde (MDA) and superoxide dismutase (SOD) kits were used to detect the expression levels of oxidativestress factors MDA and SOD in cell supernatant. The apoptosis rate was determined by Hoechst 33258 staining. The expression levels of Caspase-3 and p38 MAPK pathway-related proteins were determined by Western blot. Compared with the controlgroup, the cell viability of LPS group significantly decreased (P<0.05). Compared with LPS group, the cell viability significantly increased after 160 nmol/L catechin supplementation (P<0.05). Finally, 160 nmol/L catechin group was selected as catechin group for follow-up experiment. In the follow-up experiment, compared with the control group, SOD and IL-10 contentsin LPS group significantly decreased (P<0.05), MDA and IL-6 contents, apoptosis number, Caspase-3 and P-P38 MAPK protein expression significantly increased (P<0.05)；compared with LPS group, catechin group and SB203580 group significantly reversed the changes of the above indexes (P<0.05)；compared with the catechin group, SB203580 in the inhibitor groupenhanced the changes in the above indicators, while C16-PAF in the activator group attenuated the effect of catechin on LPSinduced H9C2 cells (P<0.05). In this study, catechins can significantly inhibit the apoptosis, inflammation and oxidative stressinjury of H9C2 cells induced by LPS, and the mechanism of action may be related to the inhibition of p38 MAPK pathway signal transduction.