Granule Dendrobii suppresses chronic atrophic gastritis induced by N-methyl-N'-nitro-N-nitrosoguanidine by modulating the gastrointestinal bacteria in rats

by Selleckchem | Jan 12 2024

Chronic atrophic gastritis (CAG) is an important stage in the transformation of the normal gastric mucosa into gastric cancer. Granule Dendrobii (GD), a proprietary Chinese medicine, has proven clinical efficacy in treating CAG. GD might promote the reversal of precancerous lesions by improving them in CAG patients. However, the mechanism of GD in CAG treatment is relatively less understood. Here, N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced CAG rats were treated with GD and its efficacy was evaluated by observing the changes in the rats' weight and the pathology of gastric tissues. The potential effect of GD on the bacteria was predicted and verified in the large and small intestines and stomachs of CAG rats using amplicon sequencing and RT-qPCR. The results showed that GD could ameliorate the symptoms of body weight loss in CAG rats. Hematoxylin-Eosin (HE) and Alcian Blue (AB) staining showed that GD significantly improved the pathological state of the gastric mucosa in CAG rats. The relative abundance (RA) of Lactobacillus and Turicibacter significantly decreased after GD intervention compared with that of the model group (P < 0.05), indicating that GD might improve CAG by regulating the RA of Lactobacillus and Turicibacter. These findings revealed that Lactobacillus and Turicibacter as bacteria agents associated with gastritis, have the potential to inhibit gastric cancer, especially Turicibacter maybe another pathogen of CAG besides Helicobacter pylori (HP), which is worthy of further study. Meanwhile, the findings provided new ideas and materials for the research and development of new CAG drugs.

Comments:

This study seems to explore the potential efficacy of Granule Dendrobii (GD), a Chinese medicine, in treating Chronic Atrophic Gastritis (CAG) and its possible mechanisms. The researchers used MNNG-induced CAG rats as a model to evaluate GD's effects on weight changes, gastric tissue pathology, and the microbiota in the stomach, large intestine, and small intestine.

The results indicate that GD intervention in CAG rats led to several positive outcomes:

1. **Improvement in Body Weight Loss**: GD treatment ameliorated the symptoms of weight loss in CAG rats, suggesting a potential positive impact on overall health.

2. **Pathological Improvement in Gastric Mucosa**: GD significantly improved the pathological state of the gastric mucosa in CAG rats, as observed through staining techniques like Hematoxylin-Eosin and Alcian Blue.

3. **Microbiota Regulation**: GD intervention led to a decrease in the relative abundance (RA) of certain bacteria, specifically Lactobacillus and Turicibacter, in the stomach. This suggests that GD might exert its effects on CAG by modulating the composition of these bacteria.

The study also proposes that Lactobacillus and Turicibacter could be associated with gastritis and might have the potential to inhibit gastric cancer. Additionally, the findings hint that Turicibacter might be another pathogen related to CAG, aside from the well-known Helicobacter pylori (HP).

Overall, the study suggests that GD could potentially be effective in treating CAG by influencing the gastric microbiota and improving gastric mucosal pathology. It also raises interesting points about specific bacteria that might play a role in CAG and potentially even gastric cancer, highlighting avenues for further research and drug development.

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