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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Puerarin protects endothelial cells from oxidized low density lipoprotein induced injuries via the suppression of LOX-1 and induction of eNOS
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Puerarin protects endothelial cells from oxidized low density lipoprotein induced injuries via the suppression of LOX-1 and induction of eNOS

机译：葛根素通过抑制LOX-1和诱导eNOS保护内皮细胞免受氧化的低密度脂蛋白诱导的损伤

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Oxidized low density lipoprotein (oxLDL) induced injury of endothelial cells is considered to be the first step in the pathogenesis of atherosclerosis. This study aimed to investigate some of the effects and mechanisms of puerarin on oxLDL-induced endothelial injuries. We measured cell viability, and the release of lactate dehydrogenase (LDH), nitric oxide (NO), and interleukin-8 (IL-8) to evaluate the protective effects of puerarin. Intracellular reactive oxygen species (ROS) were detected using 2′,7′-dichlorofluorescein diacetate (DCFH-DA). The expression of lectin-like low-density lipoprotein receptor-1 (LOX-1), endothelial nitric oxide synthase (eNOS), cyclooxygenase 2 (COX-2), p38MAPK, and protein kinase B (PKB) phosphorylation, nuclear factor-κB (NF-κB) nuclear translocation, and inhibitor of κB (IκB) degradation were detected using quantitative real-time PCR or Western blot. The results showed that oxLDL significantly decreased cell viability, increased LDH and IL-8 release, inhibited NO production, and induced COX-2 expression. Pretreatment with puerarin led to a strong inhibition of these effects. OxLDL stimulated the expression of LOX-1, the overproduction of ROS, the phosphorylation of p38MAPK, the dephosphorylation of PKB, activation of NF-κB, and the degradation of IκB. These oxLDL-induced effects were suppressed after puerarin pretreatment. These results suggest that puerarin inhibits oxLDL-induced endothelial cell injuries, at least in part, via inhibition of the LOX-1-mediated p38MAPK-NF-κB inflammatory and the PKB-eNOS signaling pathways.
机译：氧化的低密度脂蛋白（oxLDL）诱导的内皮细胞损伤被认为是动脉粥样硬化发病机理的第一步。这项研究旨在调查葛根素对oxLDL诱导的内皮损伤的某些作用和机制。我们测量了细胞活力，以及乳酸脱氢酶（LDH），一氧化氮（NO）和白介素8（IL-8）的释放，以评估葛根素的保护作用。使用2'，7'-二氯荧光素二乙酸酯（DCFH-DA）检测细胞内活性氧（ROS）。凝集素样低密度脂蛋白受体-1（LOX-1），内皮型一氧化氮合酶（eNOS），环氧合酶2（COX-2），p38MAPK和蛋白激酶B（PKB）磷酸化，核因子-κB的表达（NF-κB）核易位和κB（IκB）降解抑制剂使用实时定量PCR或Western blot检测。结果表明，oxLDL显着降低了细胞活力，增加了LDH和IL-8的释放，抑制了NO的产生，并诱导了COX-2的表达。葛根素的预处理导致对这些作用的强烈抑制。 OxLDL刺激了LOX-1的表达，ROS的过度产生，p38MAPK的磷酸化，PKB的去磷酸化，NF-κB的活化以及IκB的降解。葛根素预处理后，这些oxLDL诱导的作用被抑制。这些结果表明，葛根素至少部分地通过抑制LOX-1介导的p38MAPK-NF-κB炎性反应和PKB-eNOS信号通路来抑制oxLDL诱导的内皮细胞损伤。

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