Weierning, a Chinese Patent Medicine, Improves Chronic Atrophic Gastritis with Intestinal Metaplasia

Han, Lu; Lou, Zhaohuan; Huang, Jianbo; Gao, Jian‐Li; Li, Ting; Wang, Yingying; Lai, Weizhi; Niu, Zhuangwei; Zhou, Hengpu; Su, Jie; Lv, Gui‐Yuan; Zhang, Guangji

doi:10.2139/ssrn.4266866

Cited by 1 publication

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“…Then, the TUNEL staining was used to evaluate the apoptosis rate as described previously. 5 The apoptosis of cells was observed under light microscope, and the results were expressed by the average number of TUNEL positive staining cells per 200× magnification.…”

Section: Tdt-mediated Dutp Nick-end Labeling (Tunel) Stainingmentioning

confidence: 99%

“…3 Previous studies have shown that CAG is caused by a combination of factors, including helicobacter pylori infection, inadequate immune regulation and impaired energy metabolism, and that its pathogenesis is related to oxidative stress, inflammation, endothelial and mucosal dysfunction. 4,5 The current clinical treatment of CAG relies mainly on the agents used for gastric mucosal protection and symptom relief, vitamin C supplementation and proton pump inhibitors, which limit their clinical application due to their long course, aggressiveness and side effects. 6,7 Therefore, there is an urgent need for complementary and alternative treatments for CAG.…”

Section: Introductionmentioning

confidence: 99%

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Integrated Approaches Revealed the Therapeutic Mechanisms of Zuojin Pill Against Gastric Mucosa Injury in a Rat Model with Chronic Atrophic Gastritis

Chen,

He,

Wang

et al. 2024

DDDT

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Background The Zuojin Pill (ZJP) is widely used for treating chronic atrophic gastritis (CAG) in clinical practice, effectively ameliorating symptoms such as vomiting, pain, and abdominal distension in patients. However, the underlying mechanisms of ZJP in treating CAG has not been fully elucidated. Purpose This study aimed to clarify the characteristic function of ZJP in the treatment of CAG and its potential mechanism. Methods The CAG model was established by alternant administrations of ammonia solution and sodium deoxycholate, as well as an irregular diet. Therapeutic effects of ZJP on body weight, serum biochemical indexes and general condition were analyzed. HE staining and AB-PAS staining were analyzed to characterize the mucosal injury and the thickness of gastric mucosa. Furthermore, network pharmacology and molecular docking were used to predict the regulatory mechanism and main active components of ZJP in CAG treatment. RT-PCR, immunohistochemistry, immunofluorescence and Western blotting were used to measure the expression levels of apoptosis-related proteins, gastric mucosal barrier-associated proteins and PI3K/Akt signaling pathway proteins. Results The results demonstrated that ZJP significantly improved the general state of CAG rats, alleviated weight loss and gastric histological damage and reduced the serum biochemical indicators. Network pharmacology and molecular docking found that ZJP in treating CAG by inhibiting inflammation, suppressing apoptosis, and protecting the gastric mucosal barrier via the PI3K/Akt signaling pathway. Further experiments confirmed that ZJP obviously modulated the expression of key proteins involved in gastric mucosal cell apoptosis, such as Bax, Bad, Apaf-1, cleaved-caspase-3, cleaved-caspase-9, Cytochrome C, Bcl-2, and Bcl-xl. Moreover, ZJP significantly reversed the protein expression of Occludin, ZO-1, Claudin-4 and E-cadherin. Conclusion Our study revealed that ZJP treats CAG by inhibiting the PI3K/Akt signaling pathway. This research provided a scientific basis for the rational use of ZJP in clinical practice.

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Section: Tdt-mediated Dutp Nick-end Labeling (Tunel) Stainingmentioning

confidence: 99%