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首页> 外文期刊>Medical Gas Research >Molecular hydrogen attenuates fatty acid uptake and lipid accumulation through downregulating CD36 expression in HepG2 cells
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Molecular hydrogen attenuates fatty acid uptake and lipid accumulation through downregulating CD36 expression in HepG2 cells

机译：分子氢通过下调HepG2细胞中CD36的表达来减少脂肪酸的摄取和脂质的积累

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Background There is accumulating evidence that obesity is closely associated with an impaired free fatty acid metabolism as well as with insulin resistance and inflammation. Excessive fatty acid uptake mediated by fatty acid translocase CD36 plays an important role in hepatic steatosis. Molecular hydrogen has been shown to attenuate oxidative stress and improve lipid, glucose and energy metabolism in patients and animal models of hepatic steatosis and atherosclerosis, but the underlying molecular mechanisms remain largely unknown. Methods Human hepatoma HepG2 cells were exposed to palmitate-BSA complex after treatment with or without hydrogen for 24?h. The fatty acid uptake was measured by using spectrofluorometry and the lipid content was detected by Oil Red O staining. JNK phosphorylation and CD36 expression were analyzed by Western blot and real-time PCR analyses. Results Pretreatment with hydrogen reduced fatty acid uptake and lipid accumulation after palmitate overload in HepG2 cells, which was associated with inhibition of JNK activation. Hydrogen treatment did not alter CD36 mRNA expression but reduced CD36 protein expression. Conclusion Hydrogen inhibits fatty acid uptake and lipid accumulation through the downregulation of CD36 at the protein level in hepatic cultured cells, providing insights into the molecular mechanism underlying the hydrogen effects in vivo on lipid metabolism disorders.
机译：背景技术越来越多的证据表明，肥胖症与游离脂肪酸代谢受损以及胰岛素抵抗和炎症密​​切相关。脂肪酸转座酶CD36介导的过量脂肪酸摄取在肝脂肪变性中起重要作用。在肝脂肪变性和动脉粥样硬化的患者和动物模型中，分子氢已被证明可减轻氧化应激并改善脂质，葡萄糖和能量代谢，但基本的分子机制仍然未知。方法人肝癌HepG2细胞在有或无氢处理24？h后暴露于棕榈酸酯-BSA复合物。使用荧光分光光度法测量脂肪酸摄取，并通过油红O染色检测脂质含量。通过Western印迹和实时PCR分析分析JNK磷酸化和CD36表达。结果氢预处理减少了HepG2细胞棕榈酸酯超负荷后脂肪酸的摄取和脂质的积累，这与抑制JNK活化有关。氢处理不会改变CD36 mRNA的表达，但会降低CD36蛋白的表达。结论氢通过在肝细胞中蛋白质水平上CD36的下调来抑制脂肪酸的摄取和脂质的积累，从而为体内氢对脂质代谢紊乱的潜在分子机制提供了见识。

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