Electroacupuncture Alleviates Visceral Hypersensitivity in IBS-D Rats by Inhibiting EGCs Activity through Regulating BDNF/TrkB Signaling Pathway.
Electroacupuncture Alleviates Visceral Hypersensitivity in IBS-D Rats by Inhibiting EGCs Activity through Regulating BDNF/TrkB Signaling Pathway.
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电针通过调节 BDNF/TrkB 信号通路抑制 EGC 活性减轻 IBS-D 大鼠内脏过敏
DOI：
10.1155/2022/2497430
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发表时间：
2022
期刊：
影响因子：
--
通讯作者：
Zheng QH
中科院分区：
文献类型：
--
作者：
Zhao Y;Jiang HL;Shi Y;Zhang W;Zhang LX;Hou YJ;Yang ZQ;He BY;Liang FR;Zheng QH
目的：探讨电针治疗腹泻型肠易激综合征(IBS-D)大鼠是否通过BDNF/TrkB信号通路抑制EGCs活性，从而减轻内脏超敏反应。将SD大鼠随机分为对照组(n = 8)和模型制备组(n = 32)，连续14 d灌胃给予番泻叶水溶液和慢性不可预见性轻度应激(CUMS)，并进一步分为模型组、电针组(单纯电针)、电针 + 受体B激动剂组(电针+TrkB)和电针+二甲基亚砜(n + ，n = 8)。电针组大鼠每天针刺足月25、36、3号穴20 m in，连续14天。用腹部戒断反射(AWR)定量测定内脏敏感性，逆转录-聚合酶链式反应(RT-PCR)和免疫荧光双重染色检测GFAP/BDNF和GFAP/TrkB的共存表达。免疫印迹法(WB)检测结肠组织中PLC和SP的表达。用流式细胞仪检测细胞内钙离子的表达。电针能有效缓解IBS-D大鼠内脏超敏反应(P<；0.05)。与对照组相比，模型组BDNF、TrkB、PLC、P物质、钙离子的表达增加(P<；0.05)，GFAP/BDNF、GFAP/TrkB的共存表达增加(P<；0.05)，而电针干预后上述指标均降低(P<；0.05)。此外，电针 + 受体激动剂组与对照组之间无显著差异(P>；005)。电针可减轻IBS-D大鼠的内脏高敏感性，其机制可能是通过抑制结肠BDNF/TrkB-PLC-Ca~(2+)信号通路抑制EGCs的活性。
To determine whether electroacupuncture (EA) could alleviate visceral hypersensitivity in diarrhea-predominant irritable bowel syndrome (IBS-D) rats by inhibiting EGCs activity via the BDNF/TrkB signaling pathway. Sprague Dawley rats were randomly divided to a control group (n = 8) and a model preparation group (n = 32), which received Senna solution by gavage and CUMS (chronic unpredictable mild stress) for 14 consecutive days and was further divided to a Model group, an EA group (only electroacupuncture), an EA + TrkB agonist group (electroacupuncture and TrkB), and an EA + DMSO group (electroacupuncture and DMSO, n = 8 for each). Rats in the three EA groups were acupunctured at ST25, ST36, and LR3 for 20 min every day for 14 days. Abdominal withdrawal reflex (AWR) was used to quantify visceral sensitivity; reverse transcription polymerase chain reaction (RT-PCR) and double immunofluorescent staining were used to detect the colocalized expression of GFAP/BDNF and GFAP/TrkB. Western Blot (WB) was used to detect the expression of PLC and SP in the colon. Flow cytometry was used to detect the expression of Ca2+. EA effectively alleviated visceral hypersensitivity in IBS-D rats (P < 0.05). Compared to the control group, the expression of BDNF, TrkB, PLC, SP, and Ca2+ and the colocalized expression of GFAP/BDNF and GFAP/TrkB increased in the Model group (P < 0.05), while all these parameters decreased in the EA group following EA intervention (P < 0.05). In addition, no significant difference was found between the EA + TrkB agonist group and the control group (P > 0.05). EA alleviates visceral hypersensitivity of IBS-D rats possibly by inhibiting the activity of EGCs through the BDNF/TrkB-PLC-Ca2+ signaling pathway in the colon.
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