Polyphyllin I Inhibits -Induced IL-8 Secretion in HaCaT Cells by Downregulating the CD36/NOX1/ROS/NLRP3/IL-1 Pathway.

Acne vulgaris (AV) is a chronic skin disease involving inflammation of the pilosebaceous units. () hypercolonization is one pathogenic factor for AV. that triggers interleukin-1 (IL-1) by activating the pyrin domain-containing 3 protein (NLRP3) inflammasome of the NOD-like receptor family in human monocytes. Reactive oxygen species (ROS) acts as a trigger for the production of IL-8 and activates theNLRP3 inflammasome. IL-8 promotes the metastasis and multiplication of different cancerous cells, whereas keratinocyte proliferation and migration contribute to the progression of AV. A steroidal saponin called polyphyllin I (PPI) that is extracted from 's rhizomes has anti-inflammatory properties. This study investigates the regulatory role of in the secretion of IL-8 mediated by the CD36/NADPH oxidase 1 (NOX1)/ROS/NLRP3/IL-1 pathway and the effects of PPI on the CD36/NOX1/ROS/NLRP3/IL-1/IL-8 pathway and human keratinocyte proliferation and migration. HaCaT cells were cultured and stimulated with 10 CFU/ml of for 0, 6, 12, 18, 24, 30, and 36 hours. induced IL-8 secretion from HaCaT cells via the CD36/NOX1/ROS/NLRP3/IL-1 pathway. PPI inhibited the CD36/NLRP3/NOX1/ROS/IL-8/IL-1 pathway and HaCaT cell proliferation and migration. PPI alleviates -induced inflammatory responses and human keratinocyte proliferation and migration, implying a novel potential therapy for AV.