Research on Molecular Mechanisms of Weiweikang and Prescription Treating Chronic Atrophic Gastritis
YU Jianin
Abstract
YU Jianin
Abstract
Objective: To study the molecular mechanisms of Weiweikang and the prescription treating chronic atrophic gastritis( CAG). Methods: 70 Wistar rats were randomly divided into normal group and making model group. The making model group rats were made CAG model with mainly intragastric administration of sodium salicylate. The remaining 50 rats which were modeled successfully were randomly divided into model group,whole formula group,Buyi group,Quxie group and Western medicine group.The groups were given saline,Weiweikang,split part I decoction,split part II decoction and the neomycin- dimensional suspension by gavage,once a day. After 30 days,the gastric mucosa pathological changes and the expression of Bcl and Bax in gastric mucosa were observed. Results: The gastric mucosa pathematology was better in the treating groups than that of the model group. There was no marked difference between the whole formula group and the normal group. Compared with normal control group whose Bcl- 2was 11. 19 ± 0. 82 and Bax was 16. 98 ± 0. 96,Bcl- 2 of model group with 18. 36 ± 1. 24 increased significantly and Bax of model group with 8. 94 ± 0. 65 decreased significantly( P 0. 01). Compared with model group,the treating groups made a significant decrease of the expression of Bcl- 2 and increase of the expression of Bax( P 0. 01). The whole formula group with Bcl- 2( 11. 93 ±1. 17) decreased significantly,compared with the Buyi group( 14. 68 ±1. 16),Quxie group( 14. 19 ±1. 64) and Western medicine group( 13. 00 ± 0. 94)( P 0. 01). The whole formula group with Bax( 14. 43 ± 0. 57) increased significantly,compared with Western medicine group( 11. 56 ± 0. 76)( P 0. 01). Conclusion: Weiweikang can significantly improve gastric mucosa of CAG rats. The molecular mechanism may be related with promotion apoptosis.
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Objective: To study the molecular mechanisms of Weiweikang and the prescription treating chronic atrophic gastritis( CAG). Methods: 70 Wistar rats were randomly divided into normal group and making model group. The making model group rats were made CAG model with mainly intragastric administration of sodium salicylate. The remaining 50 rats which were modeled successfully were randomly divided into model group,whole formula group,Buyi group,Quxie group and Western medicine group.The groups were given saline,Weiweikang,split part I decoction,split part II decoction and the neomycin- dimensional suspension by gavage,once a day. After 30 days,the gastric mucosa pathological changes and the expression of Bcl and Bax in gastric mucosa were observed. Results: The gastric mucosa pathematology was better in the treating groups than that of the model group. There was no marked difference between the whole formula group and the normal group. Compared with normal control group whose Bcl- 2was 11. 19 ± 0. 82 and Bax was 16. 98 ± 0. 96,Bcl- 2 of model group with 18. 36 ± 1. 24 increased significantly and Bax of model group with 8. 94 ± 0. 65 decreased significantly( P 0. 01). Compared with model group,the treating groups made a significant decrease of the expression of Bcl- 2 and increase of the expression of Bax( P 0. 01). The whole formula group with Bcl- 2( 11. 93 ±1. 17) decreased significantly,compared with the Buyi group( 14. 68 ±1. 16),Quxie group( 14. 19 ±1. 64) and Western medicine group( 13. 00 ± 0. 94)( P 0. 01). The whole formula group with Bax( 14. 43 ± 0. 57) increased significantly,compared with Western medicine group( 11. 56 ± 0. 76)( P 0. 01). Conclusion: Weiweikang can significantly improve gastric mucosa of CAG rats. The molecular mechanism may be related with promotion apoptosis.
Key concepts: Decoction, Medicine, Atrophic gastritis, Gastroenterology, Saline, Internal medicine, Gastric mucosa, Rat model