[TGF-β1/ERK/CTGF pathway involved in effect of acupuncture on exercise-induced skeletal muscle fibrosis]

To observe the changes of the skeletal muscle fibrosis and changes of transforming growth factor-β1(TGF-β1)/ extracellular signal-regulated kinase (ERK) / connective tissue growth factor (CTGF)pathway in rats after long-term eccentric exercise and acupuncture intervention, so as to explore the mechanism of acupuncture in regulating exercise-induced skeletal muscle fibrosis.

A total of 30 male SD rats were randomly divided into normal control, exercise and acupuncture group, with 10 rats in each group. The rat model of skeletal muscle fibrosis was established by eccentric exercise for 3 weeks. After exercise trained every time, the rats of the acupuncture group received acupuncture stimulation by holding the acupuncture needle to obliquely and longitudinally penetrate the ventral part of triceps of the lower leg along its lateral side, followed by retaining the needle for 2 min. Changes of the collagen fibers in each group was observed by scanning electron microscope. The expressions of Collagen Ⅰ, TGF-β1, phosphated (p)-ERK/ERK and CTGF proteins were detected by Western blot.

After 3 weeks of eccentric exercise and acupuncture, the fibrosis and deposition of collagen fibers in the exercise group were significantly higher than that in the normal control group,the degree of fibrosis in the acupuncture group was significantly lower than that in the exercise group. Compared with the normal control group, the expression levels of Collagen Ⅰ, TGF-β1, CTGF and p-ERK/ERK in the exercise group was significantly higher (P<0.01，P<0.05). After EA interventions, the increased levels of the above indicators were significantly reversed (P<0.05，P<0.01) apart from p-ERK/ERK which had a downward trend, but the difference was not statistically significant.

The accumulation of chronic sports injury can lead to the deposition of collagen fibers in skeletal muscle, which leads to the fibrosis of skeletal muscle. Acupuncture can inhibit skeletal muscle fibrosis via down-regulating TGF-β1/ERK/CTGF signaling pathway.