YANG Bin-bin, CUI Ning, WANG Shi-jun. Research on the Mechanism of Astragalus Polysaccharides on the Repair of Small Intestinal Mucosal Injury in the Rats with Dampness Stagnancy due to Spleen Deficiency Based on Wnt/β-catenin Signaling Pathway[J]. Journal of Nanjing University of traditional Chinese Medicine, 2022, 38(1): 77-82. DOI: 10.14148/j.issn.1672-0482.2022.0077
Citation: YANG Bin-bin, CUI Ning, WANG Shi-jun. Research on the Mechanism of Astragalus Polysaccharides on the Repair of Small Intestinal Mucosal Injury in the Rats with Dampness Stagnancy due to Spleen Deficiency Based on Wnt/β-catenin Signaling Pathway[J]. Journal of Nanjing University of traditional Chinese Medicine, 2022, 38(1): 77-82. DOI: 10.14148/j.issn.1672-0482.2022.0077

Research on the Mechanism of Astragalus Polysaccharides on the Repair of Small Intestinal Mucosal Injury in the Rats with Dampness Stagnancy due to Spleen Deficiency Based on Wnt/β-catenin Signaling Pathway

  •   OBJECTIVE  To explore the mechanism of Astragalus polysaccharides (APS) on the intestinal damage in rats with dampness stagnancy due to spleen deficieny, based on Wnt/β-catenin signaling pathway.
      METHODS  Sixty Wistar rats were randomly divided into six groups: control group, model group, APS high dose group, APS medium dose group, APS low dose group, Shenling Baizhu San (positive drug) group. Except for the control group, the other groups were given high-fat and low-protein feed and exhausted swimming for 8 consecutive weeks to establish a rat model of dampness stagnancy due to spleen deficiency. After successful modeling, APS groups and Shenling Baizhu group were administered the corresponding drugs, respectively, by gavage for 2 weeks. The rats were weighed every week. The propulsion rate of the small intestine of each group were measured. The levels of D-LA, DAO in serum were detected by ELISA. The protein and mRNA expressions of Wnt1, β-catenin, CyclinD1, C-MYC were detected by Western blot and qPCR.
      RESULTS  Compared with the control group, the rat body weight decreased significantly (P < 0.01), the levels of D-LA, DAO in the serum of the model group significantly increased (P < 0.01), the propulsion rate of small intestine decreased significantly (P < 0.01), the expressions of Wnt1, β-catenin, CyclinD1, C-MYC significantly increased (P < 0.01). After administration intervention, the body weight of APS high and medium dose groups was significantly higher than that of model group (P < 0.05), the levels of D-LA and DAO in APS high, medium and low dose groups were significantly lower than those of model group (P < 0.05, P < 0.01). Compared with the model group, the propotory rate of small intestine significantly increased in APS high, low dose groups (P < 0.05, P < 0.01). The protein and mRNA expressions of Wnt1, β-catenin, CyclinD1, C-MYC in APS high, medium dose groups significantly decreased (P < 0.05, P < 0.01).
      CONCLUSION  APS can repair intestinal mucosal damage by down-regulating the expressions of proteins related to the Wnt/β-catenin pathway in the small intestine tissue, which may be an important mechanism for its effects of invigorating qi, invigorating the spleen and promoting dampness.
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