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作 者:顾勇 许草 俞文超 储紫嫣 高洁 GU Yong;XU Cao;YU Wenchao;CHU Ziyan;GAO Jie(Department of Pediatrics,The First Affiliated Hospital of Wannan Medical College,Wuhu 241001,Anhui,China)
机构地区:[1]皖南医学院第一附属医院弋矶山医院儿科,安徽芜湖241001 [2]皖南医学院研究生学院,安徽芜湖241002
出 处:《皖南医学院学报》2025年第1期7-11,共5页Journal of Wannan Medical College
基 金:安徽高校自然科学研究项目(KJ2020A0600)。
摘 要:目的:探讨酪氨酸激酶受体B/脑源性神经营养因子(TrkB/BDNF)信号通路参与食道扩张内脏痛动物模型大脑前扣带回皮层(ACC)神经元高敏机制。方法:40只新生雄性SD大鼠随机分成两组,实验组20只,对照组20只。实验组大鼠常规腹腔注射麻醉,利用末端带有小乳胶球的超细PE-240管,插入胸段食道,给予1 h重复的食道扩张(ED)刺激,对照组只给予腹腔注射麻醉,不给予ED刺激。收集的ED组及对照组大脑ACC神经元培养14 d后,免疫荧光检测ED组和对照组大脑ACC神经元BDNF、TrkB的表达,同时检测ACC神经元突起数目。结果:免疫荧光结果显示,ED组与对照组相比,BDNF蛋白表达增高(t=3.809,P<0.001),TrkB的蛋白表达也增高(t=5.327,P<0.001)。ED组大鼠ACC神经元突起数目和分支增多(t=3.063,P<0.01)。结论:TrkB/BDNF信号通路可能参与食道扩张内脏痛动物模型内脏高敏机制的发生。Objective:To investigate the involvement of the TrkB/BDNF signaling pathway in the hypersensitivity mechanism of neurons in the anterior cingulate cortex of the brain in rat models with esophageal dilation visceral pain.Methods:Forty newborn male SD rats were randomly divided into experimental group(n=20)and control group(n=20).Rats in the experimental group were anesthetized by conventional intraperitoneal injection.After that,ultra-fine PE-240 tube with a small latex ball at the end was inserted into the thoracic esophagus to stimulate esophageal dilation(ED)that was repeated in 1-hour.Rats in the control group were only anesthetized by intraperitoneal injection without ED stimulation.The neurons collected in the anterior cingulate cortex of rats from both groups were cultured for 14 days.Immunofluorescence was used to detect the expression of BDNF and TrkB in the neurons of the ED and control groups,and the number of cortical neuronal protrusions was also measured.Results:Semi-quantitative analysis of BDNF/TrkB protein expression in neurons of the anterior cingulate cortex in the ED group and control group using average fluorescence intensity detection showed that compared with the control group,the expression of BDNF protein was significantly increased in the ED group(t=3.809,P<0.001),and the protein expression of TrkB was also increased notably(t=5.327,P<0.001).The number and branches of neuronal processes in the anterior cingulate cortex of rats in the ED group were significantly increased(t=3.063,P<0.01).Conclusion:TrkB/BDNF signaling pathway may be involved in the development of visceral hypersensitivity mechanisms in the animal models with esophageal dilation visceral pain.
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