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天然硫磺通过NF-κB信号通路抑制CCD-986Sk皮肤成纤维细胞中脂多糖诱导的炎症反应。

Natural Sulfurs Inhibit LPS-Induced Inflammatory Responses through NF-κB Signaling in CCD-986Sk Skin Fibroblasts.

作者信息

Sp Nipin, Kang Dong Young, Kim Hyoung Do, Rugamba Alexis, Jo Eun Seong, Park Jong-Chan, Bae Se Won, Lee Jin-Moo, Jang Kyoung-Jin

机构信息

Department of Pathology, School of Medicine, Institute of Biomedical Science and Technology, Konkuk University, Chungju 27478, Korea.

Pharmacological Research Division, National Institute of Food and Drug Safety Evaluation, Osong Health Technology Administration Complex, Cheongju 28159, Korea.

出版信息

Life (Basel). 2021 May 10;11(5):427. doi: 10.3390/life11050427.

DOI:10.3390/life11050427
PMID:34068523
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8151259/
Abstract

Lipopolysaccharide (LPS)-induced inflammatory response leads to serious damage, up to and including tumorigenesis. Natural mineral sulfur, non-toxic sulfur (NTS), and methylsulfonylmethane (MSM) have anti-inflammatory activity that may inhibit LPS-induced inflammation. We hypothesized that sulfur compounds could inhibit LPS-induced inflammatory responses in CCD-986Sk skin fibroblasts. We used Western blotting and real-time PCR to analyze molecular signaling in treated and untreated cultures. We also used flow cytometry for cell surface receptor analysis, comet assays to evaluate DNA damage, and ELISA-based cytokine detection. LPS induced TLR4 activation and NF-κB signaling via canonical and protein kinase C (PKC)-dependent pathways, while NTS and MSM downregulated that response. NTS and MSM also inhibited LPS-induced nuclear accumulation and binding of NF-κB to proinflammatory cytokines COX-2, IL-1β, and IL-6. Finally, the sulfur compounds suppressed LPS-induced ROS accumulation and DNA damage in CCD-986Sk cells. These results suggest that natural sulfur compounds could be used to treat inflammation and may be useful in the development of cosmetics.

摘要

脂多糖(LPS)诱导的炎症反应会导致严重损伤,直至包括肿瘤发生。天然矿物硫、无毒硫(NTS)和甲基磺酰甲烷(MSM)具有抗炎活性,可能抑制LPS诱导的炎症。我们假设硫化合物可以抑制CCD - 986Sk皮肤成纤维细胞中LPS诱导的炎症反应。我们使用蛋白质印迹法和实时PCR分析处理和未处理培养物中的分子信号传导。我们还使用流式细胞术进行细胞表面受体分析、彗星试验评估DNA损伤以及基于ELISA的细胞因子检测。LPS通过经典途径和蛋白激酶C(PKC)依赖性途径诱导TLR4激活和NF - κB信号传导,而NTS和MSM下调该反应。NTS和MSM还抑制LPS诱导的NF - κB核积累以及NF - κB与促炎细胞因子COX - 2、IL - 1β和IL - 6的结合。最后,硫化合物抑制了CCD - 986Sk细胞中LPS诱导的ROS积累和DNA损伤。这些结果表明天然硫化合物可用于治疗炎症,并且可能在化妆品开发中有用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7041/8151259/103ef65c2681/life-11-00427-g007.jpg
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