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Taurocholic acid lowers the inflammatory response of gingival fibroblasts, epithelial cells, and macrophages.
Journal of Oral Science ( IF 1.9 ) Pub Date : 2020-06-23 , DOI: 10.2334/josnusd.19-0342
Reza Talebian 1, 2 , Othman Hashem 1 , Reinhard Gruber 1, 3
Affiliation  

Taurocholic acid (TCA), a conjugation of cholic acid with taurine, is one of the main bile acids that is elevated in liver disease. Considering the epidemiologic linkage of periodontal disease to liver disease, the question arises about the possible effect of elevated TCA levels on periodontal cells. To answer this question, gingival fibroblasts and human oral squamous cell carcinoma cell line (HSC-2) were pretreated with interleukine1β (IL1β) and tumor necrosis factorα (TNFα) in the presence and absence of TCA. Also, mouse macrophages (RAW 264.7) were incubated with sterile-filtered human saliva with and without TCA. Inflammatory cytokines were measured by real time polynucleotide chain reaction (RT-PCR) and an immunoassay. The nuclear translocation of the p65 subunit was visualized by immunostaining. In pretreated gingival fibroblasts and HSC-2 cells, TCA considerably reduced the expression of IL1β, IL6, and IL8. In support of these observations, TCA lowered the saliva-induced expression of IL1α, IL1β and IL6 in RAW 264.7 cells. An immunoassay confirmed the capacity of TCA to diminish inflammation-induced expression of IL6 in gingival fibroblasts, HSC-2 and RAW 264.7 cells. Consistently, TCA blocked the nuclear translocation of p65 in fibroblasts. These findings suggest that TCA has anti-inflammatory activity in gingival fibroblasts, human oral squamous cell carcinoma cells and macrophages in vitro.



中文翻译:

牛磺胆酸可降低牙龈成纤维细胞,上皮细胞和巨噬细胞的炎症反应。

牛磺胆酸(TCA)是胆酸与牛磺酸的结合物,是肝脏疾病中升高的主要胆汁酸之一。考虑到牙周疾病与肝病的流行病学联系,关于TCA水平升高对牙周细胞可能产生的影响的问题出现了。为了回答这个问题,在存在和不存在TCA的情况下,使用白细胞介素1β(IL1β)和肿瘤坏死因子α(TNFα)预处理牙龈成纤维细胞和人口腔鳞状细胞癌细胞系(HSC-2)。同样,将小鼠巨噬细胞(RAW 264.7)与经过无菌过滤的人唾液(有或没有TCA)一起孵育。通过实时多核苷酸链反应(RT-PCR)和免疫测定法测量炎性细胞因子。通过免疫染色观察到p65亚基的核易位。在经过预处理的牙龈成纤维细胞和HSC-2细胞中,TCA大大降低了IL1β,IL6和IL8的表达。为了支持这些观察,TCA降低了唾液诱导的RAW 264.7细胞中IL1α,IL1β和IL6的表达。免疫测定证实了TCA能够减少牙龈成纤维细胞,HSC-2和RAW 264.7细胞中炎症诱导的IL6表达。始终如一,TCA阻止了成纤维细胞中p65的核易位。这些发现表明,TCA在牙龈成纤维细胞,人口腔鳞状细胞癌细胞和巨噬细胞中具有抗炎活性。免疫测定证实了TCA能够减少牙龈成纤维细胞,HSC-2和RAW 264.7细胞中炎症诱导的IL6表达。始终如一,TCA阻止了成纤维细胞中p65的核易位。这些发现表明,TCA在牙龈成纤维细胞,人口腔鳞状细胞癌细胞和巨噬细胞中具有抗炎活性。免疫测定证实了TCA能够减少牙龈成纤维细胞,HSC-2和RAW 264.7细胞中炎症诱导的IL6表达。始终如一,TCA阻止了成纤维细胞中p65的核易位。这些发现表明,TCA在牙龈成纤维细胞,人口腔鳞状细胞癌细胞和巨噬细胞中具有抗炎活性。体外

更新日期:2020-08-23
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