ABSTRACT
AIM: To investigate the role and potential mechanisms of bone marrow mesenchymal stem cells (MSCs) in severe acute peritonitis (SAP). METHODS: Pancreatic acinar cells from Sprague Dawley rats were randomly divided into three groups: non-sodium deoxycholate (SDOC) group (non-SODC group), SDOC group, and a MSCs intervention group (i.e., a co-culture system of MSCs and pancreatic acinar cells + SDOC). The cell survival rate, the concentration of malonaldehyde (MDA), the density of superoxide dismutase (SOD), serum amylase (AMS) secretion rate and lactate dehydrogenase (LDH) leakage rate were detected at various time points. In a separate study, Sprague Dawley rats were randomly divided into either an SAP group or an SAP + MSCs group. Serum AMS, MDA and SOD, interleukin (IL)-6, IL-10, and tumor necrosis factor (TNF)-α levels, intestinal mucosa injury scores and proliferating cells of small intestinal mucosa were measured at various time points after injecting either MSCs or saline into rats. In both studies, the protective effect of MSCs was evaluated. RESULTS: In vitro, The cell survival rate of pancreatic acinar cells and the density of SOD were significantly reduced, and the concentration of MDA, AMS secretion rate and LDH leakage rate were significantly increased in the SDOC group compared with the MSCs intervention group and the Non-SDOC group at each time point. In vivo, Serum AMS, IL-6, TNF-α and MAD level in the SAP + MSCs group were lower than the SAP group; however serum IL-10 level was higher than the SAP group. Serum SOD level was higher than the SAP group at each time point, whereas a significant between-group difference in SOD level was only noted after 24 h. Intestinal mucosa injury scores was significantly reduced and the proliferating cells of small intestinal mucosa became obvious after injecting MSCs. CONCLUSION: MSCs can effectively relieve injury to pancreatic acinar cells and small intestinal epithelium, promote the proliferation of enteric epithelium and repair of the mucosa, attenuate systemic inflammation in rats with SAP.
