Esculentoside A could attenuate apoptosis and inflammation in TNBS-induced ulcerative colitis via inhibiting the nuclear translocation of NF-κB.

Background: Esculentoside A (EsA) has had a remarkable curative effect on a variety of experimental acute and chronic inflammatory and autoimmune diseases. However, the role of EsA in the pathological process of ulcerative colitis (UC) is still unknown. Methods: Rat colonic smooth muscle cells (SMCs) were identified by immunofluorescence. The effect of EsA and/or lipopolysaccharide (LPS) on the viability, proliferation, and apoptosis of SMCs was explored via 3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide (MTT), 5-ethynyl-2'-deoxyuridine (EdU) staining, flow cytometry, and TdT-mediated dUTP nick end labeling (TUNEL) staining, respectively. The changes of apoptosis-related proteins were performed via western blotting. The expression and nuclear translocation of NF-κB were detected via western blotting, immunohistochemistry (IHC), and immunofluorescence staining, respectively. Enzyme-linked immunosorbent assay (ELISA) was used to detect the expression of IL-6 and TNF-α. Results: The EsA treatment greatly up-regulated the viability of LPS-suppressed SMCs. The LPS-induced cell apoptosis was significantly reversed by EsA treatment, which was achieved via down-regulating Bax and cleaved caspase-3 expression and up-regulating Bcl-2 expression. In addition, LPS-induced IL-6, TNF-α expression and NF-κB activation were also largely decreased when treated with EsA. Conclusions: Our data provides supportive evidence that EsA can relieve the symptoms of UC and be used as a drug candidate for the treatment of UC.