1. Academic Validation
  2. 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

  • Evid Based Complement Alternat Med. 2022 Feb 14;2022:2497430. doi: 10.1155/2022/2497430.
Ying Zhao 1 Hui-Ling Jiang 1 Yu Shi 2 Wei Zhang 3 Lei-Xiao Zhang 4 Yu-Jun Hou 1 Zuo-Qin Yang 5 Bao-Yu He 2 Fan-Rong Liang 1 Qian-Hua Zheng 1
Affiliations

Affiliations

  • 1 Acupuncture and Tuina School of Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan 610075, China.
  • 2 Department of Chongqing Beibei Traditional Chinese Medical Hospital, Chongqing, China.
  • 3 Department of Traditional Chinese Medicine, The People's Hospital of Shifang, Shifang, China.
  • 4 Department of Integrated Traditional and Western Medicine, West China Hospital, Sichuan University, Chengdu 610041, China.
  • 5 Department of Acupuncture and Moxibustion, Chengdu Pidu District Hospital of Traditional Chinese Medicine, Chengdu, China.
Abstract

Objective: 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.

Methods: 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+.

Results: 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).

Conclusions: 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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