Gastroprotective effects of chebulagic acid against ethanol-induced gastric injury in rats

- CA exerts a gastroprotective effect against ethanol-induced injury in rats.
- CA restrains ethanol-induced oxidative stress in vivo and in vitro.
- CA attenuates ethanol-induced inflammation in gastric tissue.
- CA could contribute to increasing PGE2 and NO contents in gastric tissue.
- CA stimulates angiogenesis and wound healing.

Gastric ulcer is a major complication of gastrointestinal disease. This study focuses on the gastroprotection and potential mechanism of chebulagic acid (CA) in acute gastric ulceration induced by ethanol in rats. Specifically, in animal study, gastric ulceration was induced by ethanol, morphological features of gastric tissue were observed by ulcer score, H&E, masson and CD31 staining. CA can effectively decrease gastric injury, oxidative stress and proinflammatory cytokines. In addition, significant augment of prostaglandin E2 (PGE2) and nitric oxide (NO) was observed in the gastric tissues pretreated by CA. And CA prevented microcirculatory damage, aroused reparation of vascular architecture, and promoted collagen production, in associated with upregulated expressions of MMP-2, membrane type (MT) 1-MMP, VEGF, and transforming growth factor (TGF)-β. Taken together, these results indicated that CA had a considerable gastroprotective effect on ethanol-induced gastric injury. The underlying mechanism may be ascribed to the improvement of anti-oxidant and anti-inflammatory status as well as accelerating angiogenesis.

197