BACKGROUND: The mechanism of electroacupuncture on multi-acupoints in the treatment of
peripheral facial paralysis is still unknown. Glial cell-derived neurotrophic
factor (GDNF) is currently the most effective factor in promoting the survival
of motoneurons in vitro, and the
PI3K/AKT pathway plays an important role in protecting damaged motoneurons.
There is yet no research on GDNF/PI3K/AKT pathway involved in
electroacupuncture promoting facial nerve regeneration in rabbits.
OBJECTIVE: To observe the effect of
electroacupuncture on regeneration after peripheral facial nerve crush injury,
and to explore the protective mechanism of electroacupuncture on facial
motoneurons through the GDNF/PI3K/AKT signaling pathway.
METHODS: Sixty-six adult healthy New Zealand
white rabbits provided by the Animal Experimental Center of Southwest Medical
University were randomly divided into a normal group and a model group. The
facial nerves on the right side in the model group were subjected to a crush
injury. Then the animal models were randomly divided into a model control group
and an electroacupuncture group. Animals in the model control group recovered
naturally, while those in the electroacupuncture group underwent
electroacupuncture at Yifeng, Jiache, Sibai, Dicang, Yangbai, and Quanliao acupoints daily for 30 minutes. The improvement of facial
paralysis symptoms in experimental animals were observed and scored. Tissue
samples were directly taken form the normal group, and pons tissues with facial
neurons were taken in the model group at 1, 4, 7, 14, and 28 days
postoperatively. The morphologies of facial motoneurons and Nissl bodies were
observed by hematoxylin-eosin staining and Nissl staining, respectively.
Immunohistochemical techniques and western blot assay were used to detect the
protein expression of GDNF, PI3K, AKT, and p-AKT in the facial motoneurons. The
study protocol was approved by the Animal Ethics Committee of Southwest Medical
University with approval No. 20170120001.
RESULTS AND CONCLUSION: The symptoms of facial
paralysis were that the animal’s mouth was drooped at the affected side, with
lodging tentacles and the movement being weakened, and the eyelids that could
not be lifted, which recovered faster and more completely in the
electroacupuncture group than the model control group. The morphological
changes of facial neurons and changes of Nissl bodies in the electroacupuncture
group were lighter than those in the model control group. At each time point
postoperatively, the stronger GDNF immune response could be seen in the
electroacupuncture group, and the number of GDNF-positive cells was higher than
that of the model control group except 1 day postoperatively (P < 0.001). The expressions of GDNF,
PI3K, p-AKT proteins in the facial motoneurons were significantly increased in
the electroacupuncture group compared with the model control group (P < 0.05; P < 0.01; P < 0.001).
To conclude, electroacupuncture can effectively treat the peripheral facial
paralysis caused by the crushed injury of facial nerve and promote the recovery
of facial neurons. The up-regulation of GDNF expression in the facial
motoneurons and the activation of PI3K/AKT signaling pathway may be the
underlying protective mechanism of electroacupuncture.