Ramesh Thiyagarajan, Sureka Chandrabose, Bhuvana Shanmugham, Begum Vavamohaideen Hazeena
Department of Biochemistry, College of Medicine, Salman Bin Abdulaziz University, Al-Kharj, 11942, Kingdom of Saudi Arabia,
Metab Brain Dis. 2015 Apr;30(2):573-82. doi: 10.1007/s11011-014-9614-4. Epub 2014 Sep 9.
Cigarette smoking is concerned as a major risk factor in the development of various neurological disorders. Oxidative stress is suggested as a possible contributing factor in the pathogenesis of cigarette smoking-induced toxicity. Therefore, the present study was intended to evaluate the neuroprotective role of Sesbania grandiflora (S. grandiflora) against chronic cigarette smoke induced oxidative damage in rat brain. Adult male Wistar-Kyoto rats were exposed to cigarette smoke for a period of 90 days and consecutively treated with S. grandiflora aqueous suspension (SGAS, 1,000 mg/kg body weight per day by oral gavage) for a period of 3 weeks. Lipid peroxidation and antioxidants status were analyzed in the brain. Rats exposed to cigarette smoke showed significant increase in conjugated diens (CD), hydroperoxides (HP) and malendialdehyde (MDA) levels with concomitant decrease in superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione-S-transferase (GST) and glucose-6-phosphate dehydrogenase (G6PDH) activities and the levels of reduced glutathione (GSH), vitamin C and vitamin E. Also cigarette smoke-exposure resulted in a marked increase in copper and decrease in zinc, manganese and selenium levels in brain. Administration of SGAS attenuates lipid peroxidation, enhanced the antioxidant status, restored the levels of micronutrients and retained the brain histology. The results of our study indicate that chronic cigarette smoke-exposure accelerates oxidative stress, thereby disquieting the brain defensive mechanism and S. grandiflora protects the brain from the oxidative damage through its biopotency.
吸烟被认为是各种神经疾病发生的主要风险因素。氧化应激被认为是吸烟诱导毒性发病机制中一个可能的促成因素。因此，本研究旨在评估大花田菁对慢性香烟烟雾诱导的大鼠脑氧化损伤的神经保护作用。成年雄性Wistar-Kyoto大鼠暴露于香烟烟雾中90天，并连续3周用大花田菁水悬浮液（SGAS，每天1000毫克/千克体重，经口灌胃）治疗。分析了脑中的脂质过氧化和抗氧化剂状态。暴露于香烟烟雾的大鼠共轭二烯（CD）、氢过氧化物（HP）和丙二醛（MDA）水平显著增加，同时超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GPx）、谷胱甘肽还原酶（GR）、谷胱甘肽-S-转移酶（GST）和葡萄糖-6-磷酸脱氢酶（G6PDH）活性以及还原型谷胱甘肽（GSH）、维生素C和维生素E水平降低。此外，香烟烟雾暴露导致脑中铜含量显著增加，锌、锰和硒含量降低。给予SGAS可减轻脂质过氧化，增强抗氧化状态，恢复微量营养素水平并保持脑组织学。我们的研究结果表明，慢性香烟烟雾暴露会加速氧化应激，从而扰乱脑防御机制，而大花田菁通过其生物活性保护脑免受氧化损伤。
