Neurogastroenterology and motility · 2026
Exploring the Mechanism of Medicated Thread Moxibustion of Zhuang Medicine in Diabetic Gastroparesis Rats Based on the Enteric Nervous System.
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Xu Hui, He Yujun, Wu Yu, Wang Zibin, Zhang Fangzhi, Fan Yushan
Аннотация
BACKGROUND: Diabetic gastroparesis (DGP) is a common complication of diabetes mellitus, for which Western medicine treatments are associated with adverse effects and limitations. Enteric nervous system (ENS) injury is a core mechanism underlying this condition. Although Medicated Thread Moxibustion of Zhuang Medicine shows significant therapeutic efficacy, the specific mechanism by which it regulates the ENS to improve DGP remains unclear.
METHODS: A DGP rat model was established by intraperitoneal injection of streptozotocin (STZ) (60 mg/kg). The experimental animals were divided into five groups: control group, model group, mosapride citrate group, non-meridian and non-acupoint group, and Yangming meridian acupoint group. The Yangming meridian acupoint group received Medicated Thread Moxibustion of Zhuang Medicine at bilateral ST21, ST30, ST36, and ST40. Blood glucose, body weight, gastric emptying rate, and small intestinal propulsion rate were measured in each group. Hematoxylin-eosin (HE) staining was used to observe the histomorphology of the antrum and duodenum. Western blotting, immunofluorescence, and immunohistochemistry were performed to detect markers of enteric neurons (PGP9.5, ChAT, and neuronal nitric oxide synthase [nNOS]) and enteric glial cells (EGCs) (S100β, glial fibrillary acidic protein [GFAP], and Glial-cell line-derived neurotrophic factor [GDNF]).
RESULTS: Following treatment with Medicated Thread Moxibustion of Zhuang Medicine at the Yangming meridian acupoints, DGP rats exhibited reduced blood glucose levels, restored body weight, increased gastric emptying rate and small intestinal propulsion rate, and ameliorated pathological damage in the gastric antrum and duodenum. Moreover, the expression levels of PGP9.5, ChAT, nNOS, S100β, GFAP, and GDNF were elevated. In addition, the glucose-lowering effect of this therapy was superior to that of mosapride citrate.
CONCLUSION: Medicated Thread Moxibustion of Zhuang Medicine at the Yangming meridian acupoints effectively restores gastrointestinal motility in DGP rats by upregulating the expression of marker proteins of enteric neurons and EGCs, thereby ameliorating the morphological damage to both cell types.
METHODS: A DGP rat model was established by intraperitoneal injection of streptozotocin (STZ) (60 mg/kg). The experimental animals were divided into five groups: control group, model group, mosapride citrate group, non-meridian and non-acupoint group, and Yangming meridian acupoint group. The Yangming meridian acupoint group received Medicated Thread Moxibustion of Zhuang Medicine at bilateral ST21, ST30, ST36, and ST40. Blood glucose, body weight, gastric emptying rate, and small intestinal propulsion rate were measured in each group. Hematoxylin-eosin (HE) staining was used to observe the histomorphology of the antrum and duodenum. Western blotting, immunofluorescence, and immunohistochemistry were performed to detect markers of enteric neurons (PGP9.5, ChAT, and neuronal nitric oxide synthase [nNOS]) and enteric glial cells (EGCs) (S100β, glial fibrillary acidic protein [GFAP], and Glial-cell line-derived neurotrophic factor [GDNF]).
RESULTS: Following treatment with Medicated Thread Moxibustion of Zhuang Medicine at the Yangming meridian acupoints, DGP rats exhibited reduced blood glucose levels, restored body weight, increased gastric emptying rate and small intestinal propulsion rate, and ameliorated pathological damage in the gastric antrum and duodenum. Moreover, the expression levels of PGP9.5, ChAT, nNOS, S100β, GFAP, and GDNF were elevated. In addition, the glucose-lowering effect of this therapy was superior to that of mosapride citrate.
CONCLUSION: Medicated Thread Moxibustion of Zhuang Medicine at the Yangming meridian acupoints effectively restores gastrointestinal motility in DGP rats by upregulating the expression of marker proteins of enteric neurons and EGCs, thereby ameliorating the morphological damage to both cell types.