The level of TGF-b1, and increased the proliferation of mesothelial cells, consequently, ameliorated fibrinous deposition in adhesive bands. We also established a mechanical injury model of cultured cells in vitro. Because the basic experimental conditions employed homogenous RPMCs and was undertaken under conditions without serum, the model provided information on the direct response of RPMCs to injury. We found that MSCs could increase the early migratory capacity of RPMCs and accelerate the proliferation 6 h ahead of control group. A recent study showed that peritoneal adhesions were attenuated by enhancing the proliferation and migration of mesothelial cells. But our study avoided any potential contribution from the other cells located in the peritoneum, such as macrophages or fibroblasts. Besides, extensive evidence show that a comprehensive cytokine network play a critical role in the repair of mesothelial cells. Therefore, in vivo, the potential contributions from other cells and cytokines should be considered. This might explain for the phenomenon 
that the proliferative effect of MSCs on RPMCs in vitro did not correlate with the data obtained in vivo. The mechanisms by which MSCs exert their beneficial effects remain controversial. Studies have Lomitapide Mesylate postulated that MSCs mediate their therapeutic effects by either 3,4,5-Trimethoxyphenylacetic acid differentiating into functional reparative cells that replace injured tissues or by secreting paracrine factors that promote repair. MSCs injected intraperitoneally did not ameliorate peritoneal adhesions. Then we tracked the dynamic distribution of MSCs after their injection into rats via tail vein or peritoneum. MSCs accumulated in the lungs first and gradually accumulated in the liver and spleen; however, no apparent cells were observed in the injured peritoneum even when MSCs were injected intraperitoneally. Recent studies have found that the vast majority of MSCs injected intravenously home to the vascular endothelium of the lungs and liver, where they appear as emboli in afferent blood vessels. This distribution may be due to the size of MSCs relative to pulmonary capillaries, which may prevent the infused MSCs from passing through the pulmonary circulation. We speculated that MSCs injected into the peritoneal cavity might be absorbed through veins or lymphatic tubes and accumulated in the liver and spleen. Phagocytic response in the monocyte-macrophage system might do damage to MSCs. It is worth mentioning that allogeneic MSCs are not immunoprivileged; they may elicit a memory response leading to rapid clearance by the immune system. We injected MSCs intravenously or intraperitoneally into SCID mice 24 h after peritoneal scraping and found similar negative results in the injured peritoneum. Therefore, the acquired immune system may not influence the fate of MSCs in our rat model. One possible explanation is that ROS inhibited the cellular adhesion of engrafted MSCs. Further investigations must be performed to explain this interesting phenomenon. It has become apparent that MSCs repair injured tissues without significant engraftment or differentiation in some situations. In fact, MSCs secrete a number of cytokines and growth factors that alter the tissue microenvironment, such as TSG-6, VEGF _ENREF_38 and PDGF. One possibility is that the cells trapped in the lungs secrete soluble factors into the blood to enhance the repair of other tissues by suppressing inflammatory and immune reactions or by stimulating the propagation and differentiation of tissue-endogenous stem cells. MSCs secrete a wide spectrum of biologically active factors that can be found in CM. Some studies have suggested that pretreatment with serum-starved MSCs may maximize their protective properties. We injected serum-starved MSCsCM into rats via tail vein and found that MSCs-CM reduced adhesion formation, similar to MSCs.