QingReDu capsule ameliorates psoriasis vulgaris by regulating EZH2/NF-κB signaling pathway

QingReDu Capsule is commonly used clinically to treat psoriasis vulgaris, the mechanism of treating psoriasis vulgaris is still unclear. Using the ultra-performance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS/MS), we analyzed the components in rat plasma after QingReDu Capsule administration. We then predicted the mechanistic pathways of QingReDu Capsule in ameliorating psoriasis vulgaris by screening the intersecting targets of the QingReDu Capsule plasma entry components and psoriasis vulgaris using network pharmacology and molecular docking. Combined with pharmacodynamic evaluation and HE staining, we investigated the efficacy and mechanism of QingReDu Capsule in treating psoriasis vulgaris. Forty-one compounds were identified in the rat plasma after QingReDu Capsule administration, thirty-seven QingReDu Capsule components with the InChI SMILES structure were screened, and two hundred and thirty-five targets intersected with psoriasis vulgaris. network pharmacology revealed that QingReDu Capsule is not only involved in the regulation of the inflammatory response, reactive oxygen species metabolism, and intracellular oxidative stress, but also related to the nuclear factor kappa-B (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways. The molecular docking results showed that 10 components, including Myristicin, had good affinity with the screened core targets. The pharmacodynamic results showed that QingReDu Capsule reduced the serum levels of tumor necrosis factor α (TNF-α), interleukin 17 (IL-17), and interleukin 23 (IL-23) by down-regulating the protein levels of enhancer of Zeste Homolog 2 (EZH2) and NF-κB, reduced erythema and the scaling of skin lesions, and treated histopathological damage to the skin, such as hyperkeratosis with keratosis imperfecta and the thickening of the sphenoid layer. These findings illustrated that QingReDu Capsule treat psoriasis vulgaris by affecting the EZH2/NF-κB signaling pathway and influencing the level of inflammatory factors.