Fig. 5.

Omentum-derived ASCs protect primary isolated hepatocytes from APAP-induced toxicity. a Primary isolated hepatocytes were exposed to various concentrations of APAP for 24 h, and the intracellular ROS levels were measured by Cell ROX assay. The intracellular ROS levels increased significantly after APAP treatments at concentrations that exceeded 15 mM (a). Hepatocyte viability decreased significantly after treatment with the same APAP concentration (b). We chose 15 mM APAP for the subsequent in vitro studies. Hepatocytes were treated with APAP and co-cultured with/without omentum-derived ASCs in a transwell co-culture system. The viability of the APAP-treated hepatocytes improved significantly after 24 h of co-culture with omentum-derived ASCs, as shown by the MTT assay (b). LDH that was released into the culture medium decreased significantly after co-culture with omentum-derived ASCs (c). The GSH content of APAP-treated hepatocytes increased significantly after 24 h of co-culture with omentum-derived ASCs (d). The antioxidant enzyme (SOD, catalase, and GPx) activity also increased significantly after co-culture with omentum-derived ASCs (e, f, g). The expression of phosphorylated MAPK signaling pathway proteins (ERK/JNK) in APAP-treated hepatocytes decreased significantly after 24 h of co-culture with omentum-derived ASCs (h, i). The quantification of the phosphorylated proteins in each lane was normalized to the total protein levels. The data are expressed as the means ± SEM, n ≥ 5, *P < 0.05, **P < 0.01, and ***P < 0.001