Anti-Angiogenic Efficacy of PSORI-CM02 and the Associated Mechanism in Psoriasis In Vitro and In Vivo

• Published in: Frontiers in immunology Vol. 12; p. 649591
• Main Authors: Lu, Yue, Yang, Yuqi, Zhang, Junhong, Zhang, Hongyu, Ma, Changju, Tang, Xiaojuan, Wu, Jingjing, Li, Li, Wei, Jianan, Chen, Haiming, Lu, Chuanjian, Han, Ling
• Format: Journal Article
• Language: English
• Published: Switzerland Frontiers Media S.A 30.04.2021
• Subjects: angiogenesis; Immunology; inflammation; MAPK signalling pathway; oxidative stress; PSORI-CM02; psoriasis; PSORI-CM02; inflammation; angiogenesis; psoriasis; oxidative stress; MAPK signalling pathway
• ISSN: 1664-3224; 1664-3224
• DOI: 10.3389/fimmu.2021.649591

Psoriasis is a chronic proliferative autoimmune dermatologic disease characterised by abnormal angiogenesis. Thus, regulating angiogenesis in the skin is an important treatment strategy for psoriasis. PSORI-CM02, an empirical Chinese medicine formula optimised from Yin Xie Ling, was created by the Chinese medicine specialist, Guo-Wei Xuan. Clinical studies have shown that PSORI-CM02 is safe and effective for the treatment of psoriasis. However, its anti-psoriatic mechanisms remain to be further explored. In this study, we investigated the effects of PSORI-CM02 on angiogenesis in the skin and the underlying mechanisms in IL-17A-stimulated human umbilical vein endothelial cells (HUVECs) and a murine model of imiquimod (IMQ)-induced psoriasis. , PSORI-CM02 significantly inhibited the proliferation and migration of IL-17A-stimulated HUVECs in a dose-dependent manner. Further, it markedly regulated the antioxidative/oxidative status and inflammation; suppressed the expression of VEGF, VEGFR1, VEGFR2, ANG1, and HIF-1α; and reduced the phosphorylation of MAPK signalling pathway components in IL-17A-stimulated HUVECs. studies showed that PSORI-CM02 markedly reduced angiogenesis in the skin of mice with IMQ-induced psoriasis, while significantly rebalancing antioxidant/oxidant levels; inhibiting the production of IL-6, TNF-α, IL-17A, and IL-17F; and repressing the synthesis of angiogenic mediators. In addition, PSORI-CM02 markedly reduced the activation of the MAPK signalling pathway in psoriatic skin tissue. Taken together, our results demonstrated that PSORI-CM02 inhibited psoriatic angiogenesis by reducing the oxidative status and inflammation, suppressing the expression of angiogenesis-related molecules, and inhibiting the activation of the MAPK signalling pathway and .