ArticleMedical science monitor : international medical journal of experimental and clinical research2019
Notoginsenoside R1 (NGR1) Attenuates Chronic Atrophic Gastritis in Rats.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 42 citations in OpenAlex.
- A web-based pharmacological approach to the mechanism of action of Radix Bupleuri in the treatment of chronic atrophic gastritis.Cytotechnology · 2025Article
- Berberine Alleviates 1-Methyl-3-Nitro-1-Nitrosoguanidine- Induced Chronic Atrophic Gastritis in Rats.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2025Article
- Traditional Chinese medicine for chronic atrophic gastritis: Efficacy, mechanisms and targets.World journal of gastroenterology · 2025Review
- Potential Action Mechanism of Erianin in Relieving MNNG-triggered Chronic Atrophic Gastritis.Cell biochemistry and biophysics · 2025Article
- Mechanism of Chronic Atrophic Gastritis: A 20-Year Bibliometric Analyses.Journal of inflammation research · 2025Article
- Weifuchun alleviates MNNG-induced chronic atrophic gastritis by improving the gastric and intestinal microbiota homeostasis.PloS one · 2025Article
- Effects of Granule Dendrobii on chronic atrophic gastritis induced by N-methyl-N'-nitro-N-nitrosoguanidine in rats.World journal of gastroenterology · 2022Article
- Exploration of Tuina Effect and Mechanism in Chronic Atrophic Gastritis Rats.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2022Article
- Notoginsenoside R1 relieves the myocardial infarction via activating the JAK2/STAT3 signaling pathway in vivo and in vitro.Bioengineered · 2022Article
- Notoginsenoside R1 counteracts mesenchymal stem cell-evoked oncogenesis and doxorubicin resistance in osteosarcoma cells by blocking IL-6 secretion-induced JAK2/STAT3 signaling.Investigational new drugs · 2021Article
- Chronic stress accelerates the process of gastric precancerous lesions in rats.Journal of Cancer · 2021Article
- Phytochemicals: Targeting Mitophagy to Treat Metabolic Disorders.Frontiers in cell and developmental biology · 2021Review
- Berberine Attenuates Chronic Atrophic Gastritis Induced by MNNG and Its Potential Mechanism.Frontiers in pharmacology · 2021Article
- Focus on Notoginsenoside R1 in Metabolism and Prevention Against Human Diseases.Drug design, development and therapy · 2020Review
- Weipiling ameliorates gastric precancerous lesions in Atp4aBMC complementary and alternative medicine · 2019Article
- Morroniside protects against chronic atrophic gastritis in rat via inhibiting inflammation and apoptosis.American journal of translational research · 2019Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND This study investigated the effect and mechanism of notoginsenoside R1 (NGR1) on chronic atrophic gastritis (CAG) in a rat model. MATERIAL AND METHODS To perform our investigation, a rat model of CAG was established, and then rats were treated with various doses of NGR1. After treatment, hematoxylin-eosin (HE) staining was used for histopathological observation and further scoring. Enzyme-linked immunosorbent assay (ELISA) was used to determine the contents of gastrointestinal hormones, inflammatory factors, gastric mucosal destruction factors, and gastric mucosal-protective factors. Gene and protein expressions were measured using quantitative real-time PCR and Western blot assay, respectively. RESULTS Results indicated that NGR1 relieved rat CAG. NGR1 treatment significantly increased the levels of gastrin (GAS) and somatostatin (SS) and reduced motilin (MTL) in the serum of CAG rats. The serum levels of interleukin (IL)-1β and IL-6 were significantly reduced by NGR1 treatment in CAG rats in a dose-dependent manner. Additionally, the increased levels of prostaglandin (PG)E2, nitric oxide synthase (NOS), and endothelin (ET) in CAG rats were significantly decreased by NGR1 administration. Moreover, the decreased level of secretory IgA (sIgA) and glutathione (GSH) in rats caused by MNNG was notably increased by NGR1 treatment. No significant changes were found in glutathione disulfide (GSSG) secretion. Finally, we found that the increased Bcl-2 expression and reduced Bax expression in the stomach tissues of rats caused by MNNG were eliminated by NGR1 treatment. CONCLUSIONS NGR1 exerts a protective effect on CAG, and it is a multi-target, multi-linked, comprehensive process.
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