Dong Jia-Zi, Rong Pei-Jing, Wang Xiao-Tong, Wang Dan, Leng Ming-Hui, Xiao Lu-Jia
College of Acupuncture-Moxibustion and Tuina, Liaoning University of TCM, Shenyang 110847, China; Institute of Acupuncture and Moxibustion, China Academy of Chinese Medical Sciences, Beijing 100700.
Institute of Acupuncture and Moxibustion, China Academy of Chinese Medical Sciences, Beijing 100700.
Zhongguo Zhen Jiu. 2022 Jul 12;42(7):767-72. doi: 10.13703/j.0255-2930.20211230-k0003.
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), and to explore the mechanism of electroacupuncture at Zusanli (ST 36) on functional dyspepsia (FD).
Sixty SPF-grade 10-day-old SD rats were randomly divided into a normal group, a model group, a ketotifen group and an EA group, 15 rats in each group. The FD model was prepared by iodoacetamide combined with rat tail clamping method in the model group, the ketotifen group and the EA group. The rats in the ketotifen group were injected intraperitoneally with ketotifen (1 mgkgd) for 7 days; the rats in the EA group were treated with EA at bilateral "Zusanli" (ST 36), with disperse-dense wave, frequency of 2 Hz/50 Hz and intensity of 0.5 mA, 20 min each time, once a day for 14 days. The gastric emptying rate and small intestinal propulsion rate in each group were observed; the morphology of duodenal mucosa was observed by HE staining; the toluidine blue staining was used to observe the number and degranulation of mast cells in duodenal mucosa; the protein and mRNA expressions of NGF, NTRK1 in duodenum were detected by Western blot and real-time PCR; the level of interleukin-1β (IL-1β) in duodenum was measured by ELISA.
Compared with the normal group, the gastric emptying rate and small intestinal propulsion rate in the model group were decreased (<0.01); compared with the model group, the gastric emptying rate and small intestinal propulsion rate in the ketotifen group and the EA group were increased (<0.01); the small intestinal propulsion rate in the EA group was higher than that in the ketotifen group (<0.01). In the model group, local defects in duodenal mucosa were observed with a small amount of inflammatory cell infiltration; no obvious abnormality was found in duodenal mucosa of the other groups. Compared with the normal group, the mast cells of duodenal mucosa in the model group were increased significantly with significant degranulation; compared with the model group, the mast cells of duodenal mucosa in the ketotifen group and the EA group were decreased significantly, and the degranulation was not obvious. Compared with the normal group, the protein and mRNA expressions of NGF, NTRK1 as well as the level of IL-1β in duodenum in the model group were increased (<0.01); compared with the model group, the protein and mRNA expressions of NGF, NTRK1 as well as the levels of IL-1β in duodenum in the ketotifen group and the EA group were decreased (<0.01, <0.05); compared with the ketotifen group, the mRNA expression of NGF, as well as the protein and mRNA expressions of NTRK1 in duodenum in the EA group were decreased (<0.05, <0.01).
EA at "Zusanli" (ST 36) could inhibit the activation of duodenal mast cells and regulate the expressions of NGF and its receptor to improve the low-grade inflammatory response of duodenum, resulting in treatment effect on FD.
观察电针“足三里”（ST 36）对十二指肠肥大细胞、神经生长因子（NGF）及神经营养性酪氨酸激酶受体1型（NTRK1）的影响，探讨电针足三里（ST 36）治疗功能性消化不良（FD）的机制。
将60只10日龄SPF级SD大鼠随机分为正常组、模型组、酮替芬组和电针组，每组15只。模型组、酮替芬组和电针组采用碘乙酰胺联合夹尾法制备FD模型。酮替芬组大鼠腹腔注射酮替芬（1 mg·kg-1·d-1），连续7天；电针组大鼠取双侧“足三里”（ST 36）进行电针治疗，采用疏密波，频率2 Hz/50 Hz，强度0.5 mA，每次20分钟，每天1次，共14天。观察各组大鼠胃排空率和小肠推进率；采用HE染色观察十二指肠黏膜形态；采用甲苯胺蓝染色观察十二指肠黏膜肥大细胞数量及脱颗粒情况；采用蛋白质免疫印迹法和实时荧光定量PCR检测十二指肠中NGF、NTRK1的蛋白和mRNA表达；采用酶联免疫吸附测定法检测十二指肠白细胞介素-1β（IL-1β）水平。
与正常组比较，模型组大鼠胃排空率和小肠推进率降低（P<0.01）；与模型组比较，酮替芬组和电针组大鼠胃排空率和小肠推进率升高（P<0.01）；电针组小肠推进率高于酮替芬组（P<0.01）。模型组十二指肠黏膜局部有缺损，少量炎性细胞浸润，其他组十二指肠黏膜未见明显异常。与正常组比较，模型组十二指肠黏膜肥大细胞数量明显增多，脱颗粒明显；与模型组比较，酮替芬组和电针组十二指肠黏膜肥大细胞数量明显减少，脱颗粒不明显。与正常组比较，模型组十二指肠中NGF、NTRK1的蛋白和mRNA表达及IL-1β水平升高（P<0.01）；与模型组比较，酮替芬组和电针组十二指肠中NGF、NTRK1的蛋白和mRNA表达及IL-1β水平降低（P<0.01，P<0.05）；与酮替芬组比较，电针组十二指肠中NGF的mRNA表达及NTRK1的蛋白和mRNA表达降低（P<0.05，P<0.01）。
电针“足三里”（ST 36）可抑制十二指肠肥大细胞激活，调节NGF及其受体表达，改善十二指肠低度炎症反应，从而对FD发挥治疗作用。
