Department of Public Health and Infectious Diseases, Sapienza University, Rome, Italy.
J Biol Regul Homeost Agents. 2013 Apr-Jun;27(2):509-18.
The involvement of Chlamydia pneumoniae in the pathogenesis of atherosclerosis has been suggested by numerous seroepidemiological, in vivo and in vitro studies. In particular, it has been shown that C. pneumoniae is able to promote the accumulation of low-density lipoproteins into macrophages, thus facilitating foam cell formation. The aim of our study was to investigate the effects of resveratrol on macrophage derived foam cell formation induced by C. pneumoniae, examining its underlying biochemical mechanisms. Our results showed a relevant decrease in the number of foam cells, in the production of thiobarbituric acid reactive substances, superoxide anion and IL 17A while treating C. pneumoniae infected macrophages with resveratrol. Furthermore, the inhibition of Peroxisome Proliferator-Activated Receptors gamma by a specific antagonist (GW 9662), in presence of resveratrol and C. pneumoniae, enhanced intracellular lipid and cholesterol accumulation and the subsequent foam cell formation. In conclusion, the main result of our study is the evidence of an antiatherogenic effect of resveratrol on macrophage-derived foam cell formation and IL-17A production induced by C. pneumoniae.
已有的大量血清流行病学、体内和体外研究表明，肺炎衣原体参与了动脉粥样硬化的发病机制。特别是，已经表明肺炎衣原体能够促进低密度脂蛋白在巨噬细胞中的积累，从而促进泡沫细胞的形成。我们的研究目的是研究白藜芦醇对肺炎衣原体诱导的巨噬细胞源性泡沫细胞形成的影响，探讨其潜在的生化机制。我们的结果表明，在用白藜芦醇处理肺炎衣原体感染的巨噬细胞时，泡沫细胞的数量、硫代巴比妥酸反应物质、超氧阴离子和白细胞介素 17A 的产生显著减少。此外，在白藜芦醇和肺炎衣原体存在的情况下，过氧化物酶体增殖物激活受体 γ 的特异性拮抗剂（GW9662）抑制，增强了细胞内脂质和胆固醇的积累，随后泡沫细胞形成。总之，我们研究的主要结果是证明白藜芦醇对肺炎衣原体诱导的巨噬细胞源性泡沫细胞形成和白细胞介素 17A 产生具有抗动脉粥样硬化作用。
