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Shikonin induces apoptosis and suppresses growth in keratinocytes via CEBP-δ upregulation. | LitMetric

Shikonin induces apoptosis and suppresses growth in keratinocytes via CEBP-δ upregulation.

Int Immunopharmacol

China Medical University, No.77 Puhe Road, Shenyang North New Area, Shenyang, Liaoning Province, China; Department of Dermatology, No.1 Hospital of China Medical University, 155N, Nanjing Street, Heping District, Shenyang, Liaoning Province, China. Electronic address:

Published: July 2019

AI Article Synopsis

  • - Shikonin, a compound from the medicinal plant Leptospermum erythrorhizon, has been shown to inhibit inflammation related to psoriasis by affecting keratinocyte behavior, specifically by promoting apoptosis and inhibiting cell proliferation. - The study found that shikonin works by targeting CEBPD and suppressing the JAK/STAT3 signaling pathway, which is linked to reduced cell survival and proliferation in both in vitro and in vivo models. - In animal models, shikonin treatment significantly improved psoriasis-like symptoms, suggesting that targeting CEBPD and the JAK/STAT3 pathway could be a promising approach for treating psoriasis.

Article Abstract

Shikonin is an active compound of the oriental medicinal plant, Leptospermum erythrorhizon, which has been previously shown to inhibit psoriasis-like inflammation. However, the underlying mechanism is unclear. In the present study, the mechanisms of keratinocyte proliferation and apoptosis in psoriasis in response to shikonin were explored both in vitro and in vivo. Our results showed that shikonin significantly inhibits cell proliferation and induces apoptosis in both HaCaT and LV-STAT3 HaCaT cells by targeting CEBPD, while a decrease in cell survival, proliferation and viability were found through flow-cytometry and MTS assay. Furthermore, gavage with shikonin markedly alleviated psoriasis-like manifestations in IMQ-induced BALB/c mice clinically (PASI Score) and histopathologically. Immunohistochemistry revealed that shikonin potently suppresses the JAK/STAT3 signaling pathway in local skin lesions and increases CEBPD expression. These results imply that shikonin inhibits keratinocyte proliferation and induces apoptosis, which results in psoriasis treatment through the JAK/STAT3 dependent pathway. In addition, the activation of JAK/STAT3 downregulates CEBPD in HaCaT cells and IMQ-induced BALB/c mice. However, shikonin can reverse these effects, suggesting that CEBPD may be a potential therapeutic target for psoriasis.

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Source
http://dx.doi.org/10.1016/j.intimp.2019.04.047DOI Listing

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