Gastroprotective effects of ginsenoside Rh4 against ethanol-induced gastric mucosal injury by inhibiting the MAPK/NF-κB signaling pathway

MAPK/ERK通路 促炎细胞因子 人参皂甙 谷胱甘肽 前列腺素E2 一氧化氮 药理学 化学 肿瘤坏死因子α 氧化应激 丙二醛 超氧化物歧化酶 谷胱甘肽过氧化物酶 白细胞介素 炎症 细胞凋亡 前列腺素E 一氧化氮合酶 激酶 医学 免疫学 细胞因子 内分泌学 生物化学 人参 病理 替代医学
作者
Yuqing Wu,Zhiguang Duan,Linlin Qu,Yi Zhang,Chenhui Zhu,Daidi Fan
出处
期刊:Food & Function [The Royal Society of Chemistry]
卷期号:14 (11): 5167-5181 被引量:13
标识
DOI:10.1039/d2fo03693b
摘要

Ginsenoside Rh4, a bioactive component extracted from Panax ginseng, exhibits various pharmacological activities, such as anti-inflammatory, anti-oxidation, anti-diabetes, anti-obesity, antitumor and immunity enhancement. However, the gastroprotective effect of ginsenoside Rh4 remains unknown. The present study evaluated the gastroprotective effect and potential mechanism of ginsenoside Rh4 in an ethanol-induced gastric ulcer model. Ginsenoside Rh4 (15, 30, and 60 mg kg-1) and omeprazole (30 mg kg-1) were administered orally for 7 days. The results showed that pretreatment with ginsenoside Rh4 reduced the gastric injury area and percentage of mucosal lesions in gastric tissue. Besides, treatment with ginsenoside Rh4 increased superoxide dismutase (SOD) activity, glutathione (GSH) and nitric oxide (NO) levels, reduced the content of malonaldehyde (MDA), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β), mediated the prostaglandin E-2-cyclooxygenase-2 (PGE2-Cox-2) pathway, and mitigated inflammation and oxidative stress via blockade of proinflammatory mitogen-activated protein kinase-nuclear factor κB (MAPK/NF-κB) signaling pathways. Furthermore, ginsenoside Rh4 significantly enhanced the protein expression of B-cell lymphoma gene 2 (Bcl-2), decreased the protein expression of Bcl-2-associated X protein (Bax) and tumor necrosis factor receptor superfamily member 6 (Fas), and inhibited the number of apoptotic cells in gastric tissues. The present work demonstrated that ginsenoside Rh4 exerted a considerable gastroprotective effect against ethanol-induced gastric ulcers in rats.
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