Fig. 7

Schematic diagram depicting the potential therapeutic mechanism of CP-MSC to relieve SAP. During the occurrence of SAP, damaged pancreatic acinar cells release a variety of chemokines and inflammatory mediators to induce the recruitment of circulating monocytes to the pancreatic injury site and activate them into M1 macrophages, which in turn further aggravate pancreatic injury. When trypsin, damage-related molecules, and inflammatory mediators return to the liver through the portal vein, they can stimulate liver macrophages to secrete a large amount of pro-inflammatory factors, thereby further aggravating the systemic inflammatory. Therefore, liver macrophages play a “booster” role in promoting the development of local pancreatic injury to SIRS and multiple organ dysfunction. When CP-MSCs are exposed to the hyperinflammation environment of SAP, pro-inflammatory cytokines such as TNF-α stimulated CP-MSCs to secrete more TSG-6, TSG-6 regulated the polarization of macrophages from M1 to M2, and M2 macrophages secreted a large number of anti-inflammatory cytokines (such as IL-10 and IL-4) to inhibit excessive hyperinflammation and accelerate the repair of damaged pancreatic tissue