Clinical Observation on the Treatment of Chronic Atrophic Gastritis with Syndrome of Spleen Deficiency and Stasis
Obstruction by Shenqi Taohong Decoction and Its Mechanism
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Graphical Abstract
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Abstract
OBJECTIVE To study the clinical efficacy of Shenqi Taohong decoction in treating chronic atrophic gastritis with syndrome of spleen deficiency and stasis obstruction.METHODS From January 2018 to June 2019, a total of 80 patients with chronic atrophic gastritis identified as spleen deficiency and stasis obstruction syndrome were selected from the Department of Spleen, Stomach, Liver and Gallbladder, Traditional Chinese Medicine Hospital of Kunshan, and randomly divided into treatment group and control group according to random number table (40 cases in each group). The treatment group received Shenqi Taohong decoction orally, while the control group received Wei Fuchun Tablets orally. Both groups were treated continuously for 12 weeks. The Traditional Chinese medicine (TCM)syndrome score, the degree of gastric mucosal atrophy, and the expression levels of Trefoil factor2 (TFF2) and Nuclear factor-κB (NF-κB) in gastric mucosa were observed before and after treatment.RESULTS After treatment, the TCM syndrome score, the degree of gastric mucosal atrophy spreading staging and pathological integral in the 2 groups were significantly improved (P < 0.01), but the treatment group was better than the control group (P < 0.05, P < 0.01). In addition, the expression levels of TFF2 in the gastric mucosa were increased and the expression levels of NF-κB were decreased in the 2 groups (P < 0.01), but the treatment group was better than the control group (P < 0.05).CONCLUSION Shenqi Taohong decoction can effectively improve the main TCM syndromes, gastroscopic results, and pathological manifestations of chronic atrophic gastritis in the syndrome of spleen deficiency and stasis obstruction, and its mechanism may be related to increasing TFF2 expression levels and decreasing NF-κB expression levels in gastric mucosa to promote repair of damaged gastric mucosa and reduce atrophy and intestinal metaplasia of gastric mucosa.
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