The efficacy of
electroacupuncture in the treatment of
peripheral facial paralysis is known, but the specific mechanism has not been clarified.
Glial cell-derived neurotrophic factor (
GDNF) has been shown to protect neurons by binding to
N-cadherin. Our previous results have shown that
electroacupuncture could increase the expression of
N-cadherin mRNA in facial neurons and promote facial nerve regeneration. In this study, the potential mechanisms by which
electroacupuncture promotes nerve regeneration were elucidated through assessing the effects of
electroacupuncture on
GDNF and
N-cadherin expression in facial motoneurons of rabbits with peripheral facial nerve
crush injury. New Zealand rabbits were randomly divided into a normal group (normal control, n = 21), injury group (n = 45) and
electroacupuncture group (n = 45). Model rabbits underwent facial nerve
crush injury only. Rabbits in the
electroacupuncture group received
facial nerve injury, and then underwent
electroacupuncture at Yifeng (TE17), Jiache (ST6), Sibai (ST2), Dicang (ST4), Yangbai (GB14), Quanliao (SI18), and Hegu (LI4; only acupuncture, no electrical stimulation). The results showed that in behavioral assessments, the total scores of blink reflex, vibrissae movement, and position of apex nasi, were markedly lower in the EA group than those in the injury group.
Hematoxylin-
eosin staining of the right buccinator muscle of each group showed that the cross-sectional area of buccinator was larger in the
electroacupuncture group than in the injury group on days 1, 14 and 21 post-surgery.
Toluidine blue staining of the right facial nerve tissue of each group revealed that on day 14 post-surgery, there was less axonal
demyelination and fewer inflammatory cells in the
electroacupuncture group compared with the injury group. Quantitative real time-polymerase chain reaction showed that compared with the injury group,
N-cadherin mRNA levels on days 4, 7, 14 and 21 and
GDNF mRNA levels on days 4, 7 and 14 were significantly higher in the
electroacupuncture group. Western blot assay displayed that compared with the injury group, the expression of
GDNF protein levels on days 7, 14 and 21 were significantly upregulated in the
electroacupuncture group. The histology with
hematoxylin-
eosin staining and Nissl staining of brainstem tissues containing facial neurons in the middle and lower part of the pons exhibited that on day 7 post-surgery, there were significantly fewer apoptotic neurons in the
electroacupuncture group than in the injury group. By day 21, there was no significantly difference in the number of neurons between the
electroacupuncture and normal groups. Taken together, these results have confirmed that
electroacupuncture promotes regeneration of peripheral
facial nerve injury in rabbits, inhibits neuronal apoptosis, and reduces peripheral inflammatory response, resulting in the recovery of facial muscle function. This is achieved by up-regulating the expression of
GDNF and
N-cadherin in central facial neurons.