Abstract: Objective We are aimed at observing the protective effect of chrysin has on the mechanical traumatic rat heart, and explore the mechanism both in vivo and in vitro. Methods Rats were randomly divided into control group, trauma group without treatment and trauma group with injection of chrysin or solvent DMSO, there are 5 rats in each group. Recorded the changes of the left ventricular diastolic pressure. By TUNNEL staining, we assessed the apoptosis degree of cardiomyocytes. MTT assay was used to evaluate theproliferation of cells. ELISA test was administered to identify the TNF-α level. DCFH-DA was used to estimate the intracellular generation of ROS. We used confocal laser scanning microscope photoed fluorescent images to observe the cardiomyocytes to determine the changes of intracellular Ca2+ . Results Compared with control，in trauma group，+dP/dTmax, MAP, -dP/dTmax and LVDP were significantly decreased（P<0.01）,the apoptosis index apparently increased（P<0.01）；The survival rate of inflammatory cells induced by TNF-α was lower（P<0.01）；And There is a significant increase of TNF-α and ROS level.（P<0.01）.Compared with trauma group，in chrysin group，+dP/dTmax, MAP, -dP/dTmax and LVDP were significantly increased（P<0.01）,the apoptosis index apparently decreased（P<0.01）；The survival rate of inflammatory cells induced by TNF-α was higher（P<0.01）；And There is a significant decrease of TNF-α and ROS level.（P<0.01）. Conclusions Chrysin alleviates MT induced the excessive release of TNF-α,ROS and intracellular calcium overload which will reduce the apoptosis of myocardial cells and protect the heart.

Key words: chrysin, mechanical trauma, oxidative stress