[Effect of electroacupuncture on denervated skeletal muscle atrophy and expression of IGF-1/PI3K/AKT in rats]

Objective: To observe the effects of electroacupuncture (EA) on denervated skeletal muscle atrophy and expression of IGF-1/PI3K/AKT signaling pathway in rats, and to explore the possible mechanisms of it.

Methods: Thirty-six male SD rats were randomly divided into a control group, a model group and an EA group. Denervated muscle atrophy model was made by cutting off the left hindlimb sciatic nerve in the model group and the EA group. In the EA group, EA, dense-disperse wave, 2 Hz/33 Hz and 1.5-2 mA, was connected at "Zusanli" (ST 36) and "Shangjuxu" (ST 37). The treatment was given for 30 min every time, once a day and a total of 20 times were needed, there was 2 days interval every 5 times. The rats in the control group and model group were fixed in the same cage every day but not applied EA. Sciatic nerve function index (SFI) and ratio of muscle wet weight (RWW) were measured after treatment. HE staining was used to determine the ratio of cross-sectional area (RCA) and the ratio of fiber diameter (RFD). TUNEL and double immunofluorescence staining were used to evaluate the myocyte apoptosis, proliferation and differentiation. The mRNA expressions of IGF-1 and AKT were detected by real-time PCR. The total protein of AKT, p-AKT (Ser473) and p-AKT (Thr308) were detected by western blot.

Results: Compared with the control group, SFI, RWW, RCA and RFD of the model group were significantly decreased and apoptotic index of myocytes were significantly increased (all P<0.01). Compared with the model group, the above indexes of the EA group were improved (all P<0.05), and the expressions of PAX3 and PAX7 related to proliferation and differentiation of muscle satellite cells were significantly increased (both P<0.01), p-AKT (Ser473) protein level was increased (P<0.05).

Conclusion: EA can improve the atrophy of denervated muscles, reduce myocyte apoptosis, and promote the proliferation and differentiation of muscle satellite cells. The mechanism may be related to the increase of p-AKT (Ser473) level and activation of AKT signaling pathway.