脂多糖
牙周纤维
化学
炎症
活力测定
免疫印迹
细胞毒性
NF-κB
细胞生物学
肿瘤坏死因子α
MTT法
基质金属蛋白酶
前列腺素E2
分子生物学
细胞
免疫学
体外
生物
生物化学
医学
牙科
内分泌学
基因
作者
Seul Ah Lee,Bo-Ram Park,Sungmin Moon,Sang Hun Shin,Jae-Sung Kim,Do Kyung Kim,Chun Sung Kim
标识
DOI:10.1016/j.archoralbio.2020.104944
摘要
To investigate whether cynaroside protects human periodontal ligament (hPDL) cells from lipopolysaccharide (LPS)-induced damage and inflammation and to analyze the underlying mechanism. LPS was used to stimulate hPDL and RAW264.7 cells. MTT assay was used to detect cell viability, and protein expression levels were measured via western blot analysis. Nitrite oxide and prostaglandin E2 were used to quantify the inflammatory response. Alizarin Red S staining was used to detect mineralized nodules. Cynaroside inhibited the expression of iNOS, COX-2, TNF-α, and IL-6 in LPS-stimulated hPDL and RAW264.7 cells without cytotoxicity. Furthermore, cynaroside significantly suppressed LPS-induced protein expression of matrix metalloproteinase 3. Additionally, cynaroside prevented LPS-induced NF-κB p65 subunit translocation to the nucleus by inhibiting the phosphorylation and degradation of IκB-α. Moreover, cynaroside could restore the mineralization ability of hPDL cells reduced by LPS. Cynaroside protected hPDL cells from LPS-induced damage and inflammation via inhibition of NF-κB activation. These results suggest that cynaroside may be a potential therapeutic agent for the alleviation of periodontitis.
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