The protein kinase A signaling pathway mediates the effect of electroacupuncture on excessive contraction of the bladder detrusor in a rat model of neurogenic bladder.

IF 2.4 3区医学 Q2 INTEGRATIVE & COMPLEMENTARY MEDICINE

Acupuncture in Medicine Pub Date : 2024-02-01 Epub Date: 2023-10-29 DOI:10.1177/09645284231206154

Qiong Liu, Qi-Rui Qu, Ming Xu, Ji-Sheng Liu, Fang Qi, Xi-Qin Yi, Hong Zhang, Lu Zhou, Kun Ai

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引用次数: 0

Abstract

Background: Neurogenic bladder (NB) is a form of neurological bladder dysfunction characterized by excessive contraction of the bladder detrusor. Protein kinase A (PKA) signaling is involved in the contraction of the detrusor muscle.

Aims: To investigate whether PKA signaling mediates the effect of electroacupuncture (EA) on the excessive contraction of the bladder detrusor in NB.

Methods: Sixty rats were randomly divided into control, sham, NB, NB + EA, and NB + EA + H89 (a PKA receptor antagonist) groups. The modified Hassan Shaker spinal cord transection method was used to generate a NB model. After EA intervention for one week, urodynamic tests were used to evaluate bladder function, hematoxylin and eosin staining was conducted to assess morphological changes, enzyme-linked immunosorbent assay (ELISA) was performed to measure the concentration of PKA, and Western blotting was conducted to measure the protein levels of phosphorylated myosin light chain kinase (p-MLCK)/p-MLC.

Results: The results showed that NB resulted in morphological disruption, impairment of urodynamics, and decreases in the concentration of PKA and the protein levels of p-MLCK/p-MLC. EA reversed the changes induced by NB dysfunction. However, the improvement in urodynamics and the increases in the concentration of PKA and the protein levels of p-MLCK/p-MLC were inhibited by H89.

Conclusion: Our findings indicate that the PKA signaling pathway mediates the beneficial effect of EA on excessive contraction of the bladder detrusor in a rat model of NB.

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蛋白激酶A信号通路介导电针对神经源性膀胱大鼠模型中膀胱逼尿肌过度收缩的影响。

背景：神经源性膀胱（NB）是一种以膀胱逼尿肌过度收缩为特征的神经性膀胱功能障碍。蛋白激酶A（PKA）信号传导参与逼尿肌的收缩。目的：探讨PKA信号传导是否介导电针对NB膀胱逼尿肌过度收缩的影响 + EA和NB + EA + H89（PKA受体拮抗剂）组。采用改良的Hassan Shaker脊髓横断法建立NB模型。电针干预一周后，用尿动力学测试评估膀胱功能，苏木精和伊红染色评估形态学变化，酶联免疫吸附试验（ELISA）测量PKA浓度，并用蛋白质印迹法测定磷酸化肌球蛋白轻链激酶（p-MLCK）/p-MLC的蛋白水平。结果：NB可导致形态学破坏、尿动力学受损，PKA浓度和p-MLCK/p-MLC蛋白水平降低。电针逆转NB功能障碍引起的变化。然而，H89抑制了尿动力学的改善、PKA浓度和p-MLCK/p-MLC蛋白水平的增加。结论：我们的研究结果表明，PKA信号通路介导了电针对NB大鼠膀胱逼尿肌过度收缩的有益作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Acupuncture in Medicine INTEGRATIVE & COMPLEMENTARY MEDICINE-

CiteScore

4.70

自引率

4.00%

发文量

审稿时长

6-12 weeks

期刊介绍： Acupuncture in Medicine aims to promote the scientific understanding of acupuncture and related treatments by publishing scientific investigations of their effectiveness and modes of action as well as articles on their use in health services and clinical practice. Acupuncture in Medicine uses the Western understanding of neurophysiology and anatomy to interpret the effects of acupuncture.