Mechanism of electroacupuncture involve in lens-induced myopia guinea pigs by inhibiting wnt/β-catenin signaling pathway.

Zhao Ping, H E Xingbo, Han Xudong, Chen Xinyue, L I Zhanglong, Song Jike, Xing Wenjia, W U Jiangfeng, Guo Bin, B I Hongsheng
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Abstract

Objective: To determine the mechanism of electro-acupuncture (EA) effect by the wingless-related integration site (Wnt)/β-catenin pathway in the guinea pig myopia model.

Methods: Following myopia induction and EA, guinea pigs were treated with biometry to evaluate refraction and axial length. Hematoxylin and eosin (HE) staining was used to observe that the retina, choroid, and sclera had abnormal morphology. At 4, 6, and 8 weeks, quantitative polymerase chain reaction (qPCR) was used to identify the expression of matrix metallopeptidase-2 (MMP-2)/MMP-3/tissue inhibitor of metalloprotease-2 (TIMP-2)/TIMP-3/Wnt family member 2B (WNT2B)/WNT3A/ WNT7B/beta-catenin 1 (CTNNB1), and dickkopf wnt signaling pathway inhibitor 1 (DKK-1) mRNAs in the retina, choroid, and sclera. Western blot was used to detect the protein expression of WNT7B/2B/3A, CTNNB1 and DKK-1 in retina, choroid and sclera at 4 weeks. Enzyme-linked immunosorbent assay was used to detect the protein expression of MMP-2/TIMP-2 and MMP-3/TIMP-3 in serum at 4 weeks. Moreover, a DKK-1 inhibitor was injected into the vitreous cavity, and the expression of the above molecules was detected.

Results: EA could reduce the optic axial length and diopter and ameliorate ocular pathology, inhibited the expression of MMP-2/MMP-3 and WNT2B/WNT3A/ WNT7B/CTNNB1, while increased the expression levels of TIMP-2/TIMP-3 and DKK-1. However, the expression levels of WNT2B/WNT3A/WNT7B/CTNNB1 and MMP-2/MMP-3 were significantly increased, and the TIMP-2/TIMP-3 and DKK-1 expression levels were decreased after injected DKK-1 inhibitor.

Conclusion: The mechanism of EA's effects on myopia may involve the downregulation of the Wnt/β-catenin pathway and correct MMP-2/MMP-3/TIMP-2/TIMP-3 balance.

电针通过抑制wnt/β-catenin信号通路参与晶状体性近视豚鼠的机制研究。
目的:探讨电针无翼相关整合位点(Wnt)/β-catenin通路在豚鼠近视模型中的作用机制。方法:对豚鼠进行近视诱导和EA治疗后,采用生物测量法评估屈光和眼轴长度。苏木精伊红(HE)染色观察视网膜、脉络膜、巩膜形态异常。在4、6和8周时,采用定量聚合酶链反应(qPCR)检测基质金属肽酶-2 (MMP-2)/MMP-3/金属蛋白酶-2组织抑制剂(TIMP-2)/TIMP-3/Wnt家族成员2B (WNT2B)/WNT3A/ WNT7B/ β -连环蛋白1 (CTNNB1)和dickkopf Wnt信号通路抑制剂1 (DKK-1) mrna在视网膜、脉络膜和巩膜中的表达。Western blot检测4周大鼠视网膜、脉络膜、巩膜组织中WNT7B/2B/3A、CTNNB1、DKK-1蛋白表达。采用酶联免疫吸附法检测血清中MMP-2/TIMP-2和MMP-3/TIMP-3蛋白的表达。在玻璃体腔内注射DKK-1抑制剂,检测上述分子的表达。结果:EA可减少眼轴长度和屈光度,改善眼病理,抑制MMP-2/MMP-3和WNT2B/WNT3A/ WNT7B/CTNNB1表达,提高TIMP-2/TIMP-3和DKK-1表达水平。然而,注射DKK-1抑制剂后,WNT2B/WNT3A/WNT7B/CTNNB1和MMP-2/MMP-3的表达水平显著升高,TIMP-2/TIMP-3和DKK-1的表达水平降低。结论:EA对近视的作用机制可能与下调Wnt/β-catenin通路,纠正MMP-2/MMP-3/TIMP-2/TIMP-3平衡有关。
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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