Protective effects of iridoid glycosides on acute colitis via inhibition of the inflammatory response mediated by the STAT3/NF-кB pathway

• Published in: International immunopharmacology Vol. 81; p. 106240
• Main Authors: Yuan, Jiahui, Cheng, Weipeng, Zhang, Gongye, Ma, Qiujuan, Li, Xiaomei, Zhang, Bing, Hu, Tianhui, Song, Gang
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.04.2020; Elsevier BV
• Subjects: Animal models; Animals; Anti-Inflammatory Agents - therapeutic use; Cell Line; Colitis; Colitis - chemically induced; Colitis - drug therapy; Colitis, Ulcerative - drug therapy; Colorectal carcinoma; Cornus - immunology; Cytokines; Dextran; Dextran Sulfate; Dextrans; Disease Models, Animal; Glycosides; Glycosides - therapeutic use; Health services; Herbal medicine; Humans; Inflammation; Inflammatory bowel disease; Inflammatory response; Iridoid glycosides; Iridoid Glycosides - therapeutic use; Iridoids - therapeutic use; Lipopolysaccharides; Male; Medical treatment; Medicinal plants; Medicine, Chinese Traditional; Mice; Mice, Inbred C57BL; NF-kappa B - metabolism; NF-κB protein; Phosphorylation; Signal Transduction; Sodium sulfate; Stat3 protein; STAT3 Transcription Factor - metabolism; STAT3/NF-кB; Traditional Chinese medicine; Inflammatory response; STAT3/NF-кB; Colitis; Iridoid glycosides
• ISSN: 1567-5769; 1878-1705
• DOI: 10.1016/j.intimp.2020.106240

•Morroniside and loganin was able to ameliorate intestinal barrier injury and inflammatory reaction in mice models.•The proinflammatory cytokines production was significantly reduced in morroniside and loganin-treated mice.•The possible mechanism of anti-inflammatory response may involve in the blocking of STAT3/NF-κB pathway in vivo.•Morroniside and loganin remarkably suppressed the inflammatory response via the STAT3/NF-кB pathway in vitro. Morroniside and loganin are iridoid glycosides extracted from Cornus officinalis, a plant species widely used in traditional Chinese medicine. However, the anti-inflammatory effects of morroniside and loganin in colitis are barely understood. The aim of the present study was to explore the effects of morroniside and loganin on the dextran sodium sulfate (DSS)-induced murine model of colitis and an LPS-induced colorectal cancer (CRC) cell inflammation model, and to clarify the underlying mechanisms. We found that morroniside and loganin were able to ameliorate clinical features, including disease activity index (DAI), histological inflammation score and periodic acid-Schiff staining (PAS). In the mouse model, morroniside and loganin treatment increased expression of tight junction proteins (TJs) and decreased pro-inflammatory cytokine production. Moreover, our findings showed that the expression of p-STAT3 and p-p65 were suppressed compared to the disease group. In in vitro experiments, treatment with morroniside and loganin had no obvious effects on proliferative activity in HCT116 cells and HIEC-6 cells. Expression of pro-inflammatory cytokines was inhibited by morroniside and loganin treatment in comparison with the LPS-treated group. Taken together, morroniside and loganin have beneficial effects on colitis in vivo and are anti-inflammatory in vitro. Possible mechanisms of the anti-inflammatory response may include blockade of the STAT3/NF-κB pathway.