| 摘要 |
[Objectives] To explore the mechanism of action of Tongxieyaofang ultrafine granular powder in treating visceral hypersensitivity in rats with diarrhea-predominant irritable bowel syndrome (IBS-D) based on enteric glial cells (EGCs). [Methods] Eighty-four healthy male Wistar rats of SPF grade were selected and randomly assigned to seven groups, each comprising 12 rats: a normal control group, a model control group, a traditional Tongxieyaofang granular powder group (4.060 g/kg), three Tongxieyaofang ultrafine granular powder groups at low, medium, and high doses (1.015, 2.030, and 4.060 g/kg of raw drug, respectively), and a pinaverium bromide group (0.018 g/kg). With the exception of the normal control group, all other groups were subjected to an IBS-D visceral hypersensitivity sensitivity model in rats developed by the chronic water avoidance stress method. Three days post modeling, the rats received continuous oral gavage administration for 8 d. Following the treatment period, serum and colon tissue samples were collected from each group. The BDNF level in the serum was quantified using ELISA. Additionally, the protein expression levels of GFAP, BDNF, and TrkB in colon tissues were assessed via Western blot assay. [Results] Compared to the normal control group, the serum BDNF levels in the model control group were significantly elevated (P<0.01). In contrast, each treatment group exhibited a significant reduction in serum BDNF levels relative to the model control group (P<0.01). Furthermore, the protein expression levels of GFAP, BDNF, and TrkB in colon tissue were significantly higher in the model control group compared to the normal control group (P<0.05, P<0.01). Conversely, these protein expressions were significantly decreased in each treatment group compared to the model control group (P<0.05, P<0.01). [Conclusions] Tongxieyaofang ultrafine granular powder effectively alleviates visceral sensitivity in IBS-D rats and inhibits the activation of EGCs, speculating that its mechanism of action involves the suppression of abnormal EGC activation. |
