Gastroprotective effects of ginsenoside Rh4 against ethanol-induced gastric mucosal injury by inhibiting the MAPK/NF-κB signaling pathway.
Yuqing WuZhiguang DuanLinlin QuYi ZhangChenhui ZhuDaidi FanPublished in: Food & function (2023)
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.
Keyphrases
- signaling pathway
- induced apoptosis
- oxidative stress
- pi k akt
- diabetic rats
- nuclear factor
- type diabetes
- nitric oxide
- anti inflammatory
- rheumatoid arthritis
- cell cycle arrest
- epithelial mesenchymal transition
- gene expression
- insulin resistance
- toll like receptor
- metabolic syndrome
- skeletal muscle
- hydrogen peroxide
- small molecule
- lps induced
- immune response
- cell death
- ulcerative colitis
- tyrosine kinase
- electron transfer
- human health
- glycemic control
- dna methylation
- fluorescent probe
- genome wide
- heat shock protein
- nitric oxide synthase