Acupuncture in medicine : journal of the British Medical Acupuncture Society · 2026
Electroacupuncture at ST25 combined with metformin improves intestinal function via the JAK/STAT pathway in a rat model of diabetes.
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Qian Xu, Pei Ke, Jiang Yongwei, Xu Bin, Wu Wei
Аннотация
BACKGROUND: Metformin (Met) is a first-line pharmacological treatment for type 2 diabetes mellitus (T2DM). The potential effect of combining electroacupuncture (EA) at ST25 (Tianshu) with Met in ameliorating intestinal injury remains largely unexplored.
METHODS: We established wild-type (Control) and diabetic model groups that remained untreated (Model), received EA only (EA), received Met treatment only (Met) or received EA combined with Met (EA + Met), and compared markers of intestinal injury and insulin resistance, as well as effects on signal transducer and activator of transcription (STAT) proteins and microRNAs.
RESULTS: EA and Met treatment (alone and in combination) had positive effects on fasting plasma glucose, fasting insulin levels, Homeostatic Model Assessment-insulin resistance (HOMA-IR) indices and stool number, while fecal water content was positively impacted by EA treatment (with or without concurrent Met) but not Met alone. Hematoxylin-eosin staining demonstrated that both EA alone and EA in combination with Met appeared to repair intestinal damage in the jejunum, ileum and colon. In addition, enzyme-linked immunosorbent assay revealed that serum interleukin 10 levels were restored in all treatment groups. Furthermore, quantitative real-time polymerase chain reaction (PCR) analysis revealed that EA at ST25 resulted in the activation of STAT5A in the jejunum, as well as STAT5A, STAT5B and STAT6 in the ileum. Notably, in the EA + Met group, there was a specific enhancement of STAT2, STAT3 and STAT5B in the colon, indicating segment-specific activation within distinct regions of the intestine.
CONCLUSION: EA at ST25 may ameliorate intestinal injury via the Janus kinase (Jak)/STAT signaling pathway and is closely related to jejunal and ileal segments. These findings provide a theoretical basis for EA combined with medication.
METHODS: We established wild-type (Control) and diabetic model groups that remained untreated (Model), received EA only (EA), received Met treatment only (Met) or received EA combined with Met (EA + Met), and compared markers of intestinal injury and insulin resistance, as well as effects on signal transducer and activator of transcription (STAT) proteins and microRNAs.
RESULTS: EA and Met treatment (alone and in combination) had positive effects on fasting plasma glucose, fasting insulin levels, Homeostatic Model Assessment-insulin resistance (HOMA-IR) indices and stool number, while fecal water content was positively impacted by EA treatment (with or without concurrent Met) but not Met alone. Hematoxylin-eosin staining demonstrated that both EA alone and EA in combination with Met appeared to repair intestinal damage in the jejunum, ileum and colon. In addition, enzyme-linked immunosorbent assay revealed that serum interleukin 10 levels were restored in all treatment groups. Furthermore, quantitative real-time polymerase chain reaction (PCR) analysis revealed that EA at ST25 resulted in the activation of STAT5A in the jejunum, as well as STAT5A, STAT5B and STAT6 in the ileum. Notably, in the EA + Met group, there was a specific enhancement of STAT2, STAT3 and STAT5B in the colon, indicating segment-specific activation within distinct regions of the intestine.
CONCLUSION: EA at ST25 may ameliorate intestinal injury via the Janus kinase (Jak)/STAT signaling pathway and is closely related to jejunal and ileal segments. These findings provide a theoretical basis for EA combined with medication.