Esculentoside A Alleviates Intestinal Dysmotility in Ulcerative Colitis by Regulating HS/CSE and NO/nNOS Systems.

BACKGROUND

Ulcerative colitis (UC) is a type of inflammatory bowel disease (IBD) that commonly affects the health of many individuals. Esculentoside A (EsA), a saponin extracted from the roots of , has antioxidative and anti-inflammatory effects against various diseases. Nonetheless, its role in UC is undetermined. Hence, in this study, we examined the therapeutic effects of EsA in UC.

METHODS

Primary intestinal neuronal cells () were treated with lipopolysaccharide (LPS) to induce inflammatory injury. An UC rat model was created by the administration of dextran sulfate sodium (DSS) to rats, which were subsequently treated with different doses of EsA. The effects of EsA on intestinal motility, histological score, inflammatory response, hydrogen sulfide (HS)/cystathionine -lyase (CSE) system, NO/neuronal nitric oxide synthase (nNOS) system, and LPS-induced primary intestinal neuronal cell viability loss, proliferation inhibition, and apoptosis were detected.

RESULTS

, EsA treatment increased the number of DSS-inhibited bowel movements and body weight, improved the histological score of colitis, and inhibited the inflammatory response by reducing IL-6 and TNF- levels in rats. More importantly, EsA reduced the NO and HS levels in serum and CSE, CBS, and nNOS expressions in the colon tissue. , EsA treatment eased the viability loss, proliferation inhibition, and apoptosis of LPS-stimulated primary intestinal neuronal cells, as well as inhibited the expressions of IL-6, TNF-, CSE, CBS, and nNOS in cells.

CONCLUSION

EsA improved intestinal motility and suppressed inflammatory response in DSS-induced UC, which may be mediated by HS/CSE and NO/nNOS systems.