4.7 Article

Protective effect of rosmarinic acid-rich trichodesma khasianum clarke leaves against ethanol-induced gastric mucosal injury in vitro and in vivo

Journal

PHYTOMEDICINE
Volume 80, Issue -, Pages -

Publisher

ELSEVIER GMBH
DOI: 10.1016/j.phymed.2020.153382

Keywords

Anti-inflammation; Antioxidant; Gastric mucosal injury; Gut microbiota; Trichodesma khasianum clarke leaves; Rosmarinic acid

Funding

  1. Council of Agriculture, Taiwan [107AS-3.2.2-FD-Z1(3), 108AS-3.2.2-FD-Z1(1)]

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The results of this study demonstrated the remarkable gastroprotective effect of 80EETC treatment in vitro and in vivo, including suppressing inflammatory mediator protein levels, improving antiapoptotic ability and wound healing capability, promoting gastric mucosal healing, increasing gut microbiota diversity, and short-chain fatty acid production. These findings are the first to show the powerful protective effect of T. khasianum Clarke leaves against gastric mucosal injury development.
Background: Although gastropmtective drugs have been used for peptic ulcer disease prevention and treatment, side effects have been observed. Finding a safe and effective treatment strategy is important. Purpose: Edible Trichodesma khasianum (T. khasianum) Clarke leaves are considered to protect against peptic ulcers. However, scientific evidence of this effect of T. khasianum Clarke leaves remains limited. Study design/methods: In this study, we aimed to evaluate the effect of T. khasianum Clarke leaves on ethanol-induced gastric injury and gut micmbiota using RAW 264.7 cells, RGM-1 cells, and BALB/c mice, respectively. Result: The rosmarinic acid was identified as the major component of T. khasianum Clarke leaves extracted by 80% ethanol (80EETC). The results showed that 80EETC suppressed inflammatory mediator protein levels in LPS-induced RAW 264.7 cells. Additionally, heat shock protein expression, antiapoptotic ability, and wound healing migration capability were increased by 80EETC pretreatment in RGM-1 cells with the ethanol-induced injury. Remarkably, pretreatment with 80EETC (150 mg/kg b.w.) promoted gastric mucosal healing by decreasing oxidative stress, inflammatory response, pmapoptotic protein expression, and gastric mucosa damage in ethanol-induced gastric injury in mice. Crucially, no liver or kidney toxicities were observed by 80EETC oral gavage. Moreover, 80EETC increased gut microbiota diversity and short-chain fatty acid production. Conclusion: Our results illustrated the remarkable gastropmtective effect by 80EETC treatment in vitro and in vivo. These findings are the first to demonstrate the powerful protective effect of T. khasianum Clarke leaves against gastric mucosal injury development.

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