[Effect of electroacupuncture at "Zusanli" (ST 36) on duodenal mast cells, NGF and NTRK1 in rats with functional dyspepsia].

• DOI: 10.13703/j.0255-2930.20211230-k0003
• Publication Date: 2022-07-12
• Authors: Jiazi Dong; Peijing Rong; Xiaotong Wang; Dan Wang; Ming-Hui Leng; Lu-Jia Xiao
• Keywords: Zusanli; Ketotifen

To observe the effect of electroacupuncture (EA) at "Zusanli" (ST 36) on duodenal mast cells, nerve growth factor (NGF) and neurotrophic tyrosine kinase receptor type 1 (NTRK1), to explore mechanism Zusanli functional dyspepsia (FD).Sixty SPF-grade 10-day-old SD rats were randomly divided into a normal group, model ketotifen group an EA 15 in each group. The FD was prepared by iodoacetamide combined with rat tail clamping method injected intraperitoneally (1 mg•kg-1•d-1) for 7 days; treated bilateral 36), disperse-dense wave, frequency 2 Hz/50 Hz intensity 0.5 mA, 20 min time, once day 14 days. gastric emptying rate small intestinal propulsion observed; morphology mucosa observed HE staining; toluidine blue staining used number degranulation cells mucosa; protein mRNA expressions NGF, NTRK1 duodenum detected Western blot real-time PCR; level interleukin-1β (IL-1β) measured ELISA.Compared decreased (P<0.01); compared increased higher than that (P<0.01). In local defects amount inflammatory cell infiltration; no obvious abnormality found other groups. Compared significantly significant degranulation; significantly, not obvious. as well IL-1β levels (P<0.01, P<0.05); expression (P<0.05, P<0.01).EA could inhibit activation regulate NGF its improve low-grade response duodenum, resulting treatment FD.目的：观察电针“足三里”对功能性消化不良（FD）大鼠十二指肠肥大细胞、神经生长因子（NGF）、神经营养因子酪氨酸激酶受体1（NTRK1）的影响，探讨电针足三里治疗FD的作用机制。方法：将60只出生10 d的SPF级幼年SD大鼠，随机分为正常组、模型组、酮替芬组、足三里组，每组15只。除正常组外，其余组大鼠均采用碘乙酰胺联合夹鼠尾法制备FD模型。酮替芬组腹腔注射酮替芬（1 mg•kg-1•d-1），连续注射7 d；足三里组于双侧“足三里”行电针干预，采用疏密波，频率2 Hz，电流强度0.5 mA，每次20 min，每天1次，连续14 d。观察各组大鼠胃排空率和小肠推进率；HE染色观察各组大鼠十二指肠组织形态；甲苯胺蓝染色观察大鼠十二指肠黏膜肥大细胞数量及脱颗粒情况；Western blot法和实时荧光定量PCR法检测大鼠十二指肠组织NGF、NTRK1蛋白及mRNA表达；ELISA法检测大鼠十二指肠组织白介素-1β（IL-1β）水平。结果：与正常组比较，模型组大鼠胃排空率和小肠推进率均降低（P<0.01）；与模型组比较，酮替芬组与足三里组大鼠胃排空率和小肠推进率均升高（P<0.01）；足三里组大鼠小肠推进率高于酮替芬组（P<0.01）。模型组大鼠十二指肠黏膜有局部缺损，有少量炎性细胞浸润；其他各组大鼠十二指肠黏膜未见明显异常。与正常组比较，模型组大鼠十二指肠黏膜肥大细胞明显增多且脱颗粒明显；与模型组比较，酮替芬组和足三里组大鼠十二指肠黏膜肥大细胞明显减少，且脱颗粒不明显。与正常组比较，模型组大鼠十二指肠组织NGF、NTRK1蛋白、mRNA表达及IL-1β水平均升高（P<0.01）；与模型组比较，酮替芬组和足三里组大鼠十二指肠组织NGF、NTRK1蛋白、mRNA表达及IL-1β水平均降低（P<0.01，P<0.05）；与酮替芬组比较，足三里组大鼠十二指肠组织NGF mRNA、NTRK1蛋白及mRNA表达均降低（P<0.05，P<0.01）。结论：电针“足三里”可能是通过抑制十二指肠肥大细胞活化，调节NGF及其受体表达，改善十二指肠低度炎性反应，从而对FD大鼠起到干预作用。.