The aim of this study is to investigate the effect and mechanism of indolepropionic acid (IPA) on LPS-induced proliferation, apoptosis, and inflammatory response of peritoneal mesothelial cells. Firstly, mouse peritoneal mesothelial cells were treated with 0.1, 1.0, and 10 μmol/L IPA, respectively. After 24 h, CCK-8 method was used to detect the cytotoxicity of IPA. Next, cells were pretreated with 0.1, 1.0, and 10 μmol/L IPA for 2 h, followed by treatment of 10 mg/L LPS for 24 h. CCK-8 method was used to detect the proliferation ability of cells, and the optimal working concentration of IPA was determined. The cells were divided into 5 groups: control group, LPS group, LPS+IPA group, LPS+QNZ (a NF-κB pathway inhibitor) group, and LPS+QNZ+IPA group. CCK-8 method was used to detect cell proliferation, and flow cytometry was used to detect cell apoptosis. ELISA was used to detect the level of TNF-α in the cell supernatant, and Western blotting was used to detect the  expressions of NF-κB p65 and p-p65 in the cells. The results showed that 0.1 and 1.0 μmol/L IPA had no cytotoxicity on mouse peritoneal mesothelial cells, and the optimal working concentration of IPA was 1.0 μmol/L. Compared to those of control group, the proliferation ability of LPS group was significantly decreased (P<0.01), while the apoptosis rate, the level of TNF-α in the cell supernatant, and the phosphorylation level of NF-κB p65  in the cells were all significantly increased (P<0.01). Compared to that of the LPS group, the proliferation ability of LPS+IPA group, LPS+QNZ group, and LPS+QNZ+IPA group was significantly increased (P<0.01), while the apoptosis rate, the level of TNF-α in the cell supernatant, and the phosphorylation level of NF-κB p65  in the cells were significantly decreased (P<0.05). Therefore,LPS+QNZ+IPA combination showed the most significant effect. In summary, these results indicate that IPA promotes the proliferation of mouse peritoneal mesothelial cells induced by LPS, and inhibits cell apoptosis and inflammation. The underlying mechanism may be related to the inhibition of NF-κB pathway activation.