2025, Vol. 29 ›› Issue (8): 1600-1608

Mechanism of Lijin manipulation regulating scar formation in skeletal muscle injury repair in rabbits

Li Kaiying1, 2, 3, Wei Xiaoge1, 2, 3, Song Fei1, 2, 3, Yang Nan1, 2, 3, Zhao Zhenning1, 2, 3, Wang Yan1, Mu Jing1, Ma Huisheng1, 2, 3   

Abstract: BACKGROUND: Lijin manipulation can promote skeletal muscle repair and treat skeletal muscle injury. However, the formation of fibrosis and scar tissue hyperplasia are closely related to the quality of skeletal muscle repair. To study the regulatory effect of Lijin manipulation on the formation of fibrosis and scar tissue hyperplasia is helpful to explain the related mechanism of Lijin manipulation to improve the repair quality of skeletal muscle injury.
OBJECTIVE: To explore the mechanism of Lijin manipulation to improve the repair quality of skeletal muscle injury in rabbits, thereby providing a scientific basis for clinical treatment.
METHODS: Forty-five healthy adult Japanese large-ear white rabbits were randomly divided into blank group, model group and Lijin group, with 15 rats in each group. Gastrocnemius strike modeling was performed in both model group and Lijin group. The Lijin group began to intervene with tendon manipulation on the 3rd day after modeling, once a day, and 15 minutes at a time. Five animals in each group were killed on the 7th, 14th and 21st days after modeling. The morphology and inflammatory cell count of gastrocnemius were observed by hematoxylin-eosin staining, the collagen fiber amount was observed by Masson staining, the expression of interleukin-6 and interleukin-10 in gastrocnemius was detected by ELISA. The protein and mRNA expressions of paired cassette gene 7, myogenic differentiation factor, myoblastogenin, alpha-actin, transforming growth factor beta 1, and type I collagen were detected by western blot and RT-PCR, respectively, and the expression of type I collagen protein was detected by immunohistochemistry.
RESULTS AND CONCLUSION: Hematoxylin-eosin staining and Masson staining showed that compared with the model group, inflammatory cell infiltration and collagen fiber content decreased in the Lijin group (P < 0.01), and the muscle fibers gradually healed. ELISA results showed that compared with the model group, the expression of interleukin-6 in the Lijin group continued to decrease (P < 0.05), and the expression of interleukin-10 increased on the 7th day after modeling (P < 0.05) and then showed a decreasing trend (P < 0.05). Western blot and RT-PCR results showed that compared with the model group, the protein and mRNA expressions of paired cassette gene 7, myogenic differentiation factor, myoblastogenin in the Lijin group were significantly increased on the 14th day after modeling (P < 0.05), but decreased on the 21st day (P < 0.05); the protein and mRNA expressions of alpha-actin, transforming growth factor beta 1, and type I collagen in the Lijin group were significantly decreased compared with those in the model group (P < 0.05). Immunohistochemical results showed that the expression of type I collagen in the Lijin group was significantly lower than that in the model group (P < 0.05). To conclude, Lijin manipulation could improve the repair quality of skeletal muscle injury by inhibiting inflammation, promoting the proliferation and differentiation of muscle satellite cells, and reducing fibrosis.
Key words: Lijin manipulation, injury of tendons, skeletal muscle injury, inflammation, muscle satellite cell, fibrosis, scar tissue, repair quality