Objective:

2

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:

2

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:

2

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:

2

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.