Shengji solution accelerates the wound angiogenesis of full-thickness skin defect in rats via activation of TGF-β1/Smad3-VEGF signaling pathway.

Autor: Li, Yuntao, Duan, Wenxu, Shen, Lin, Ma, Xinlong, Ma, Jianxiong, Zhang, Yang, Guo, Yue
Zdroj: Biotechnology & Genetic Engineering Reviews; Nov2024, Vol. 40 Issue 3, p1855-1872, 18p
Abstrakt: Shengji solution is made according to the classic prescription – Shengji prescription. Shengji solution is a external prescription of traditional Chinese medicine with the functions of nourishing blood, relieving pain, producing muscle and shrinking the wound. In the present study, we investigated the therapeutic effects of Shengji solution on dorsal full-thickness skin defects in rats. We also detected the activation of transforming growth factor beta1 (TGF-β1)/SMAD3/vascular endothelial growth factor (VEGF) signaling pathways in the wound-healing process. The results showed that the wound was cleaned with normal saline followed by bandaging with cotton gauze according to the groups, respectively: (a) control group; (b) Kangfuxin group, the wound was moistened with Kangfuxin solution; (c) Shengji solution group, the wounds were moistened with Shengji solution; (d) Shengji solution+SB431542 inhibitor group, the wound was moistened with Shengji solution, and then SB431542 inhibitor (10 mg/kg) was injected intraperitoneally for 5 days. On the 14th day after operation, the wound-healing rate of Shengji solution group was more than 95% and also greater than that in the control group and Shengji solution+SB431542 inhibitor group. Besides, Shengji solution could inhibit the inflammation and capillary production by enhancing the epithelial regeneration, dermal repair and angiogenesis. Moreover, Shengji solution could also increase CD34 content, the expressions of TGF-β1, VEGF proteins and the phosphorylation of SMAD3 in wound granulation tissue. In conclusion, Shengji solution can accelerate the dermal cutaneous wound healing in rats, stimulate angiogenesis and collagen synthesis by activating TGF-β1/SMAD3/VEGF pathway. [ABSTRACT FROM AUTHOR]
Databáze: Supplemental Index