BACKGROUND:Cadmium is one of the potent cardiotoxic heavy metals in the environment, which induces oxidative stress, dyslipidemia and membrane disturbances in heart. Quercetin is an effective antioxidant and free radical scavenger against oxidative stress. This study was designed to evaluate the protective effect of quercetin (QE) on cardiac marker enzymes, lipid peroxidation products, lipid profile, membrane bound ATPases and antioxidant status in cadmium (Cd)-intoxicated rats. MATERIALS AND METHODS:Twenty four male albino rats were used. Cadmium induced oxidative cardiotoxicity was induced by the oral administration of Cd for four weeks. Quercetin  was pretreated along with Cd for four weeks to assess its cardioprotective effect against Cd intoxication. Rats treated with vehicles alone were used as controls. RESULTS:Rats intoxicated with cadmium (5 mg/kg/day) for 4 weeks in combination with quercetin (50 mg/kg/day) respectively. Cd-induced cardiotoxicity and dyslipidemia was indicated by increased activities of marker enzymes such as creatine kinase-MB, aspartate transaminase, alanine transaminase, alkaline phosphatase and lactate dehydrogenase in serum. In addition, the levels of lipid peroxidation products and protein carbonyl contents in heart were significantly (p < 0.05) increased and the activities of enzymic antioxidants such as superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase in the heart and non-enzymic antioxidants such as glutathione, vitamin C and E in the heart were significantly (p < 0.05) decreased in Cd intoxicated rats. The levels total cholesterol (TC), triglycerides (TG), phospholipidis (PL), free fatty acids (FFA), LDL and VLDL were significantly (p < 0.05) increased and the level of HDL was significantly decreased in the serum of Cd-treated rats. Cd intoxication also increased the levels of TC, TG and FFA and decreased the level of PL in the heart tissue. Further Cd treatment significantly (p < 0.05) decreased the levels of membrane bound ATP ases in heart. QE treatment along with Cd showed significant protective effect on all the biochemical parameters studied. Histopathological findings of QE and Cd treated heart confirmed the biochemical findings of this study. Thus, QE protects the myocardium against Cd-induced oxidative stress and dyslipidemia in rats. CONCLUSIONS:Quercetin may be beneficial in combating the cadmium induced oxidative cardiotoxicity and dyslipidemia in rats.  

译文

背景:镉是环境中有效的心脏毒性重金属之一,可引起心脏氧化应激,血脂异常和膜紊乱。槲皮素是一种有效的抗氧化剂和自由基清除剂,可抵抗氧化应激。这项研究旨在评估槲皮素(QE)对镉(Cd)中毒大鼠心脏标志物酶,脂质过氧化产物,脂质分布,膜结合ATP酶和抗氧化剂状态的保护作用。
材料与方法:使用24只雄性白化病大鼠。口服镉持续四周可诱发镉引起的氧化性心脏毒性。槲皮素与Cd一起进行了为期四周的预处理,以评估其对Cd中毒的心脏保护作用。仅用媒介物治疗的大鼠用作对照。
结果:分别用镉(5 mg / kg /天)和槲皮素(50 mg / kg /天)中毒的大鼠连续4周。血清中肌酸激酶-MB,天冬氨酸转氨酶,丙氨酸转氨酶,碱性磷酸酶和乳酸脱氢酶等标记酶活性的增加表明了镉诱导的心脏毒性和血脂异常。此外,心脏中脂质过氧化产物和蛋白质羰基含量的水平显着增加(p <0.05),并且酶抗氧化剂的活性,例如超氧化物歧化酶,过氧化氢酶,谷胱甘肽过氧化物酶,谷胱甘肽还原酶和谷胱甘肽S-转移酶镉中毒大鼠心脏中的非酶类抗氧化剂如谷胱甘肽,维生素C和E显着降低(p <0.05)。 Cd-血清中的总胆固醇(TC),甘油三酸酯(TG),磷脂(PL),游离脂肪酸(FFA),LDL和VLDL的水平显着升高(p <0.05),HDL的水平显着降低治疗的大鼠。镉中毒还会增加心脏组织中TC,TG和FFA的水平,并降低PL的水平。进一步的Cd处理显着(p <0.05)降低了心脏中与膜结合的ATP酶的水平。 QE处理和Cd处理对所研究的所有生化参数均显示出显着的保护作用。 QE和Cd治疗的心脏的组织病理学发现证实了这项研究的生化发现。因此,QE保护心肌免受Cd诱导的大鼠氧化应激和血脂异常的影响。
结论:槲皮素可能有助于对抗镉诱导的大鼠氧化性心脏毒性和血脂异常。

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