| Purpose:To explore the effects and mechanism of bone marrow mesenchymal stem cells on micecardiac functionwith endotoxemia. Method:Participants were divided into the following groups:control group, endotoxemia group (LPS group), bone marrow mesenchymal stem cells group (MSCs group) and bone marrow mesenchymal stem cells treatment group (LPS+MSCs group). The HR, CO, EF AND FS of the mice was observed at the second hour,6th hours,24th hour and7th day after LPS had been injected. Apoptosis of myocardial cells and myocardial mitochondrial function were detected after LPS injection24h and7days. ELISA was used to detect the level of cytokine in myocardium and serum, and Western-blot was adopted to test thechange of signal proteins correlated with myocardium. MTT was introduced to check the growth rate of splenic cells at the24th hour and7th day as well asthe humoral immune function and phagocytosis of macrophages. Results: TheHR, CO, EF AND FS of the mice with endotoxemia declined, which recovered obviously after being treated by MSCs. Apoptosis of myocardial cells caused by LPS were inhibited by MSCs, yet declination of myocardial mitochondrial functionwasnot improved.The contents of IL-1βã€IL-6ã€TNF-aand IL-10in serum and myocardium increased after being stimulated by LPS, which declined as a result of MSCs treatment. The expression of TLR4ã€p65-NF-κB and p-p38in the mice myocardium enhanced after being stimulated by LPS, which then decreased as a result of MSCs treatment. Compared to Control group, the growth rate of splenic cells, humoral immune function and phagocytosis of the macrophages elevated, which declined after being treated by MSCs. Conclusion:MSCs inhibit the inflammatory reaction of the mice with endotoxemia, improve the cardiac function and depress the cellular immunity, humoralimmunityand phagocytosis of the macrophages enhanced by LPS stimulation, but avoid the overexpression of anti-inflammatory factorIL-10at the same time.
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