Department of Biochemistry, Periyar University, Salem, 636016 Tamil Nadu, India.
Mol Cell Biochem. 2011 Aug;354(1-2):1-10. doi: 10.1007/s11010-011-0785-6. Epub 2011 Jun 3.
Cigarette smoking is a major risk factor for cardiovascular diseases and exerts negative effects on the lipid profile. This study was aimed to evaluate the preventive role of (-)-epigallocatechin-gallate (EGCG) on lipid metabolism and cardiac inflammatory changes in cigarette smoke (CS) induced myocardial dysfunction. Adult male albino rats were exposed to side stream CS for a period of 12 weeks and simultaneously administered with EGCG (20 mg/kg b.w./day, p.o.). Exposure to CS showed significant increased (P < 0.05) activities of cardiac injury markers such as, creatine kinase-MB (CKMB) and lactate dehydrogenase (LDH) in serum and subsequent decrease in these enzyme activities in heart. A significant increase (P < 0.05) in serum total cholesterol, fatty acids, phospholipids, and triglycerides were observed in CS exposed rats, along with elevated low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) cholesterol and decreased high density lipoprotein (HDL) cholesterol. In myocardium, total cholesterol, fatty acids and triglycerides were increased, whereas the phospholipids were found to be decreased. Cardiac lecithin: cholesterol acyl trasferase (LCAT), lipoprotein lipase (LPL), and plasma LCAT activities were significantly decreased (P < 0.05) on CS exposure. Supplementation of EGCG reverted the cardiac injury markers, abnormalities of lipid profile, and lipid-metabolizing enzymes in serum and myocardium. Western blot analysis showed a significant increase in protein expression levels of nuclear factor kappa-B (NF-κB), cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNF-α), and inducible nitric oxide synthase (iNOS) in heart of CS exposed rats. EGCG-treated rats showed a significant decrease in the expression of inflammatory markers. Our data suggest that chronic CS causes lipidemic anomalies and cardiac inflammatory aberrations which may promote cardiac dysfunction and that the antioxidant EGCG exerts a cardio protective effect via reduction of oxidative stress.
吸烟是心血管疾病的主要危险因素，对脂质谱有负面影响。本研究旨在评估（-）-表没食子儿茶素没食子酸酯（EGCG）对香烟烟雾（CS）诱导心肌功能障碍中脂质代谢和心脏炎症变化的预防作用。成年雄性白化大鼠连续 12 周暴露于侧流 CS，并同时给予 EGCG（20mg/kgbw/d，po）。CS 暴露导致血清中心脏损伤标志物肌酸激酶-MB（CKMB）和乳酸脱氢酶（LDH）的活性显著增加（P<0.05），随后心脏中这些酶的活性降低。CS 暴露大鼠血清总胆固醇、脂肪酸、磷脂和甘油三酯显著增加，同时低密度脂蛋白（LDL）和极低密度脂蛋白（VLDL）胆固醇升高，高密度脂蛋白（HDL）胆固醇降低。心肌中总胆固醇、脂肪酸和甘油三酯增加，而磷脂减少。心脏卵磷脂：胆固醇酰基转移酶（LCAT）、脂蛋白脂肪酶（LPL）和血浆 LCAT 活性在 CS 暴露后显著降低（P<0.05）。EGCG 的补充使血清和心肌中心脏损伤标志物、脂质谱异常和脂质代谢酶得到恢复。Western blot 分析显示，CS 暴露大鼠心脏中核因子 kappa-B（NF-κB）、环氧化酶-2（COX-2）、肿瘤坏死因子-α（TNF-α）和诱导型一氧化氮合酶（iNOS）的蛋白表达水平显著增加。EGCG 处理大鼠炎症标志物的表达显著降低。我们的数据表明，慢性 CS 导致脂质代谢异常和心脏炎症异常，这可能促进心脏功能障碍，而抗氧化剂 EGCG 通过减少氧化应激发挥心脏保护作用。
