Warm acupuncture therapy alleviates neuronal apoptosis after spinal cord injury via inhibition of the ERK signaling pathway

Ding, Li-Li-Qiang; Hu, Songfeng; He, Xing-wei; Zhang, Peng; Zhao, Fenfen; Cheng, Lihong; Huang, Bing-Lin; Liu, Ting-Ping; Zhang, Qin; He, Fuchu; Hu, Shasha; Yu, Ying; Xiong, Peng; Wang, Changkang

doi:10.1080/10790268.2022.2088498

Cited by 2 publications

(1 citation statement)

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“…Previous studies have documented that the Jiaji (EX-B2) acupoint has a synergistic effect on reducing neuronal damage post-SCI by regulating autophagy and apoptosis [ 12 , 13 ]. In addition, there is mounting evidence that EA at the Zusanli (ST36) acupoint promotes recovery from SCIs via the protection of nerve cells and the prevention of apoptosis in SCI rats [ 30 ]. Consistent with these results, our data also demonstrate that EA treatment at the Jiaji (EX-B2) and Zusanli (ST36) acupoints can increase BBB scores, improve the survival of motor neurons, and alleviate pathological tissue damage.…”

Section: Discussionmentioning

confidence: 99%

Electroacupuncture-Modulated MiR-106b-5p Expression Enhances Autophagy by Targeting Beclin-1 to Promote Motor Function Recovery After Spinal Cord Injury in Rats

Guo¹,

Chen²,

Yang³

et al. 2023

Neurospine

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Objective: Electroacupuncture (EA) has a definite effect on the treatment of spinal cord injuries (SCIs), but its underlying molecular mechanism remains unclear. Meanwhile, MiR106b-5p is an autophagy- and apoptosis-related microribonucleic acid, but whether it regulates the progression of autophagy and apoptosis in SCIs is yet undetermined. As such, this study aimed to elucidate the involvement of miR-106b-5p in the EA treatment of an SCI.Methods: The miR-106b-5p level was detected by quantitative real-time polymerase chain reaction. In vitro, SH-SY5Y cells were transfected with miR-106b-5p mimics or inhibitors to regulate the miR-106b-5p expression, while <i>in vivo</i>, SCI rats were treated with EA for 7 days at the bilateral Zusanli (ST36) and Jiaji (EX-B2) acupoints. The motor function was evaluated using the Basso-Beattie-Bresnahan (BBB) criteria. Further, autophagic vacuoles, pathological damage, and neuronal cell morphology were observed by transmission electron microscopy, as well as by hematoxylin and eosin and Nissl staining, respectively.Results: The miR-106b-5p level, which can interact directly with Beclin-1 by influencing its expression, as well as the expressions of P62, Caspase-3, and Bax, was upregulated after an SCI, but it decreased after EA. Moreover, the ratio of LC3-II to LC3-I was upregulated after EA. EA can enhance autophagy, reduce neuronal apoptosis, and minimize motor dysfunction and histopathological deficits after an SCI. More importantly, however, all the above effects induced by EA can be reversed after an injection of miR-106-5p agomir to produce an overexpression of miR-106b-5p.Conclusion: EA treatment could downregulate miR-106b-5p to alleviate SCI-mediated injuries by promoting autophagy and inhibiting apoptosis.

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Section: Discussionmentioning

confidence: 99%