[ROLE OF MITOCHONDRIAL REACTIVE OXYGEN SPECIES IN LIPOPOLYSACCHARIDE-PROMOTED ACCUMULATION OF INTRACELLULAR LIPID DROPLETS].

E M Fock, E V Fedorova, V T Bachteeva, E A Lavrova, R G Parnova
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Abstract

It is known that in various cell types bacterial lipopolysaccharide (LPS) causes mitochondrial disfunction and promotes accumulation of triglycerides in intracellular lipid droplets. The precise mechanisms which mediate LPS-induced neutral lipid deposition remain poorly understood. In the present work performed on primary cultured epithelial cells isolated from the frog urinary bladder we studied the possible role of mitochondrial reactive oxygen species (mROS) in LPS-in-duced alteration of lipid metabolism. It was shown that LPS stimulated ROS production, decrea- 705 sed fatty acids oxidation, enhanced intracellular triglyceride deposition and promoted the formation of lipid droplets visualized by Nile red staining. Pretreatment of cells with mitochondrial-tar-geted antioxidant MitoQ at dose 25 nM for 2 h almost completely eliminated all the above effects of LPS. In contrast to MitoQ, a-tocopherol was ineffective. The data obtained indicate that increase of mROS level is a critical factor that mediates LPS-induced intracellular deposition of neutral lipids in epithelial cells.

[线粒体活性氧在脂多糖促进细胞内脂滴积累中的作用]。
众所周知,在各种细胞类型中,细菌脂多糖(LPS)引起线粒体功能障碍并促进细胞内脂滴中甘油三酯的积累。介导脂多糖诱导的中性脂质沉积的确切机制仍然知之甚少。在目前的工作中,我们对从青蛙膀胱分离的原代培养上皮细胞进行了研究,研究了线粒体活性氧(mROS)在lps诱导的脂质代谢改变中的可能作用。结果表明,LPS刺激ROS生成,减少a- 705 sed脂肪酸氧化,增强细胞内甘油三酯沉积,促进脂滴形成(尼罗红染色)。线粒体靶向抗氧化剂MitoQ预处理细胞,剂量为25 nM,作用2 h,几乎完全消除LPS的上述影响。与MitoQ相比,a-生育酚是无效的。结果表明,mROS水平的升高是介导lps诱导上皮细胞内中性脂质沉积的关键因素。
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