Wang Hongcai, Zhao Kaile, Shi Ning, Niu Qiong, Liu Chengxia, Chen Yan
Department of Neurology, Binzhou Medical University Hospital, Binzhou, China.
Department of Gastroenterology, Binzhou Medical University Hospital, Binzhou, China.
Front Physiol. 2021 Apr 1;12:560738. doi: 10.3389/fphys.2021.560738. eCollection 2021.
BACKGROUND/AIMS: Gastric dysmotility is a frequent complication among patients with diabetes mellitus. Electroacupuncture (EA) has been empirically used to relieve gastrointestinal symptoms. The aims of this study were to investigate the effects of EA on gastric contraction and the mechanisms of interstitial cells of Cajal (ICC) involved.
Male Sprague-Dawley rats were randomized into the normal control, diabetes (DM), diabetic and sham EA (DM + SEA), diabetic and low-frequency EA (DM + LEA), and diabetic and high-frequency EA (DM + HEA) groups. Diabetic models were established and then treated with EA for 8 weeks. Body weight and blood glucose were recorded every 2 weeks. The spontaneous contractions of distal gastric strips were analyzed. Immunostaining and RT-PCR were used to test the apoptotic ICC, IGF-1/IGF-1R, and Nrf2/HO-1 pathways.
The body weight in the DM + LEA and DM + HEA groups were increased compared with that of the DM group, though there was no effect on the blood glucose. The gastric contractions were obviously disordered in the DM group, but EA could regularize the contractions. The number of apoptotic ICC was dramatically increased in the DM group, but reduced with EA treatment. Meanwhile, the IGF-1/IGF-1R pathway was verified to be significantly altered in diabetic rats. The Nrf2/HO-1 pathway was not significantly increased in the DM group. EA with different frequencies efficiently improved the expression of IGF-1/IGF-1R signaling and activated the Nrf2/HO-1 pathway.
EA could improve gastric motility dysfunction and attenuate ICC apoptosis possibly through the regulation of IGF-1/IGF-1R and Nrf2/HO-1 pathways. EA may be a potential therapeutic method for diabetic gastric motility dysfunction.
背景/目的:胃动力障碍是糖尿病患者常见的并发症。电针已被经验性地用于缓解胃肠道症状。本研究旨在探讨电针治疗对胃收缩的影响以及所涉及的 Cajal 间质细胞(ICC)机制。
将雄性 Sprague-Dawley 大鼠随机分为正常对照组、糖尿病组(DM)、糖尿病假电针组(DM + SEA)、糖尿病低频电针组(DM + LEA)和糖尿病高频电针组(DM + HEA)。建立糖尿病模型后,用电针治疗 8 周。每 2 周记录体重和血糖。分析胃远端条带的自发收缩。采用免疫染色和 RT-PCR 检测凋亡的 ICC、IGF-1/IGF-1R 和 Nrf2/HO-1 通路。
与糖尿病组相比,DM + LEA 组和 DM + HEA 组的体重增加,尽管对血糖无影响。糖尿病组胃收缩明显紊乱,但电针可使其收缩规律化。糖尿病组凋亡的 ICC 数量显著增加,但电针治疗后减少。同时,证实糖尿病大鼠的 IGF-1/IGF-1R 通路有显著改变。糖尿病组 Nrf2/HO-1 通路未显著增加。不同频率的电针有效改善了 IGF-1/IGF-1R 信号的表达并激活了 Nrf2/HO-1 通路。
电针可能通过调节 IGF-1/IGF-1R 和 Nrf2/HO-1 通路改善胃动力障碍并减轻 ICC 凋亡。电针可能是治疗糖尿病胃动力障碍的一种潜在治疗方法。