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Inflammation. 2019 Nov 14. doi: 10.1007/s10753-019-01125-8. [Epub ahead of print]

Piceatannol Inhibits P. acnes-Induced Keratinocyte Proliferation and Migration by Downregulating Oxidative Stress and the Inflammatory Response.

Author information

1
Department of Dermatology, The First Affiliated Hospital of Soochow University, No.188, Shizi Street, Suzhou, 215006, China.
2
Department of Dermatology, First Affiliated Hospital of Kunming Medical University, Kunming, 650032, China.
3
Department of Dermatology, The People's Hospital of Baoshan, Baoshan City, 678000, China.
4
Department of Dermatology, The First Affiliated Hospital of Soochow University, No.188, Shizi Street, Suzhou, 215006, China. syuxiuqin2010@163.com.
5
Department of Dermatology, Henan Provincial People's Hospital, The People's Hospital of Zhengzhou University, Zhengzhou, 450000, China. yangli180409@163.com.

Abstract

The Cutibacterium acnes (also called Propionibacterium acnes, P. acnes)-induced proliferation and migration of keratinocytes contribute to acne vulgaris (AV), which is a common inflammatory skin disease that causes physical and psychological impairments. Piceatannol (3, 5, 3', 4'-tetrahydroxy-trans-stilbene, PCT) is naturally present in many human diets and plays antioxidant and anti-inflammatory roles that inhibit cell proliferation and migration. We aimed to analyse the functions and underlying mechanisms of PCT in P. acnes-stimulated keratinocytes. First, PCT showed no toxicity against the normal human keratinocyte cell line HaCaT but inhibited P. acnes-induced HaCaT cell proliferation. Next, PCT promoted the nuclear translocation and target gene transcription of the antioxidant transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), thereafter decreasing intracellular reactive oxygen species (ROS) levels. In addition, PCT inhibited the nuclear translocation of p65 [a subunit of nuclear factor kappa B (NF-κB)] and the secretion of pro-inflammatory cytokines, including interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α) and interleukin-8 (IL-8). Finally, a transfection assay showed that PCT inhibited P. acnes-induced HaCaT cell proliferation and migration by activating the antioxidant Nrf2 pathway and inhibiting the inflammatory NF-κB pathway. Our data suggested that PCT alleviated P. acnes-induced HaCaT cell proliferation and migration through its antioxidant and anti-inflammatory roles, suggesting the potential of PCT to treat AV.

KEYWORDS:

Piceatannol; Propionibacterium acnes; acne vulgaris; anti-inflammation; nuclear factor erythroid 2-related factor 2

PMID:
31728743
DOI:
10.1007/s10753-019-01125-8

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