Electroacupuncture Promotes Functional Recovery after Facial Nerve Injury in Rats by Regulating Autophagy via GDNF and PI3K/mTOR Signaling Pathway.
10.1007/s11655-023-3610-7
- Author:
Jun-Peng YAO
1
;
Xiu-Mei FENG
2
;
Lu WANG
1
;
Yan-Qiu LI
1
;
Zi-Yue ZHU
1
;
Xiang-Yun YAN
1
;
Yu-Qing YANG
1
;
Ying LI
1
;
Wei ZHANG
3
Author Information
1. Acupuncture and Tuina School, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China.
2. Department of Rehabilitation Medicine, Guanghan People's Hospital, Guanghan, Sichuan Province, 618399, China.
3. Academic Affairs Office, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China. zhangwei@cdutcm.edu.cn.
- Publication Type:Journal Article
- Keywords:
Chinese medicine;
autophagy;
electroacupuncture;
facial nerve injury;
glial cell line-derived neurotrophic factor;
phosphatidylinositol-3-kinase/mammalian target of rapamycin
- MeSH:
Rats;
Male;
Animals;
Rats, Sprague-Dawley;
Electroacupuncture;
Phosphatidylinositol 3-Kinase/metabolism*;
Facial Nerve Injuries/therapy*;
Phosphatidylinositol 3-Kinases/metabolism*;
Beclin-1;
Glial Cell Line-Derived Neurotrophic Factor;
Signal Transduction;
TOR Serine-Threonine Kinases/metabolism*;
Autophagy;
Mammals/metabolism*
- From:
Chinese journal of integrative medicine
2024;30(3):251-259
- CountryChina
- Language:English
-
Abstract:
OBJECTIVE:To explore the mechanism of electroacupuncture (EA) in promoting recovery of the facial function with the involvement of autophagy, glial cell line-derived neurotrophic factor (GDNF), and phosphatidylinositol-3-kinase (PI3K)/mammalian target of rapamycin (mTOR) signaling pathway.
METHODS:Seventy-two male Sprague-Dawley rats were randomly allocated into the control, sham-operated, facial nerve injury (FNI), EA, EA+3-methyladenine (3-MA), and EA+GDNF antagonist groups using a random number table, with 12 rats in each group. An FNI rat model was established with facial nerve crushing method. EA intervention was conducted at Dicang (ST 4), Jiache (ST 6), Yifeng (SJ 17), and Hegu (LI 4) acupoints for 2 weeks. The Simone's 10-Point Scale was utilized to monitor the recovery of facial function. The histopathological evaluation of facial nerves was performed using hematoxylin-eosin (HE) staining. The levels of Beclin-1, light chain 3 (LC3), and P62 were detected by immunohistochemistry (IHC), immunofluorescence, and reverse transcription-polymerase chain reaction, respectively. Additionally, IHC was also used to detect the levels of GDNF, Rai, PI3K, and mTOR.
RESULTS:The facial functional scores were significantly increased in the EA group than the FNI group (P<0.05 or P<0.01). HE staining showed nerve axons and myelin sheaths, which were destroyed immediately after the injury, were recovered with EA treatment. The expressions of Beclin-1 and LC3 were significantly elevated and the expression of P62 was markedly reduced in FNI rats (P<0.01); however, EA treatment reversed these abnormal changes (P<0.01). Meanwhile, EA stimulation significantly increased the levels of GDNF, Rai, PI3K, and mTOR (P<0.01). After exogenous administration with autophagy inhibitor 3-MA or GDNF antagonist, the repair effect of EA on facial function was attenuated (P<0.05 or P<0.01).
CONCLUSIONS:EA could promote the recovery of facial function and repair the facial nerve damages in a rat model of FNI. EA may exert this neuroreparative effect through mediating the release of GDNF, activating the PI3K/mTOR signaling pathway, and further regulating the autophagy of facial nerves.
