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<p>Psoriasis is a chronic inflammatory skin disease characterized by keratinocyte hyperproliferation and aberrant immune responses. Puerarin (PUE), a natural isoflavone from <i>Pueraria lobata</i>, exhibits multiple pharmacological activities, but its role in psoriasis remains unclear. The M5-induced HaCaT cell model was used to evaluate the effects of PUE on proliferation, apoptosis, and inflammation. Cell viability, proliferation, and apoptosis were assessed by CCK-8, EdU, and flow cytometry, while cytokine levels were measured by ELISA. TIMP2 and endoplasmic reticulum (ER) stress-related proteins were detected by RT-qPCR and Western blot. A TIMP2 overexpression assay was performed to verify the mechanism. PUE showed no cytotoxicity in HaCaT cells, but significantly inhibited M5-induced proliferation and inflammatory cytokine release while promoting apoptosis. Mechanistically, PUE reduced the expression of TIMP2 and ERS-related proteins, and TIMP2 overexpression partially reversed these effects. PUE alleviates proliferation and inflammation of keratinocytes in association with downregulation of TIMP2 and inhibition of ER stress-related markers, suggesting that the TIMP2-ERS axis may be implicated as a potential therapeutic target in psoriasis.</p>

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Puerarin attenuates keratinocyte proliferation and inflammatory responses in psoriasis via downregulating TIMP2 and alleviating endoplasmic reticulum stress

  • 期刊论文

  • 发表日期：

    2026年5月9日

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  • Qing Wang,
  • Jie Xia

摘要

Psoriasis is a chronic inflammatory skin disease characterized by keratinocyte hyperproliferation and aberrant immune responses. Puerarin (PUE), a natural isoflavone from Pueraria lobata, exhibits multiple pharmacological activities, but its role in psoriasis remains unclear. The M5-induced HaCaT cell model was used to evaluate the effects of PUE on proliferation, apoptosis, and inflammation. Cell viability, proliferation, and apoptosis were assessed by CCK-8, EdU, and flow cytometry, while cytokine levels were measured by ELISA. TIMP2 and endoplasmic reticulum (ER) stress-related proteins were detected by RT-qPCR and Western blot. A TIMP2 overexpression assay was performed to verify the mechanism. PUE showed no cytotoxicity in HaCaT cells, but significantly inhibited M5-induced proliferation and inflammatory cytokine release while promoting apoptosis. Mechanistically, PUE reduced the expression of TIMP2 and ERS-related proteins, and TIMP2 overexpression partially reversed these effects. PUE alleviates proliferation and inflammation of keratinocytes in association with downregulation of TIMP2 and inhibition of ER stress-related markers, suggesting that the TIMP2-ERS axis may be implicated as a potential therapeutic target in psoriasis.