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奥克美兰醉茄甲醇提取物通过减少自由基生成、脂质和蛋白质损伤,保护鼠腹腔巨噬细胞免受尼古丁毒性,并增强抗氧化保护。

Methanol extract of Ocimum gratissimum protects murine peritoneal macrophages from nicotine toxicity by decreasing free radical generation, lipid and protein damage and enhances antioxidant protection.

机构信息

Immunology and Microbiology Laboratory, Department of Human Physiology, Community Health, Vidyasagar University, Midnapore, West Bengal, India.

出版信息

Oxid Med Cell Longev. 2009 Sep-Oct;2(4):222-30. doi: 10.4161/oxim.2.4.9000.

Abstract

In the present study, methanol extract of Ocimum gratissimum Linn (ME-Og) was tested against nicotine-induced murine peritoneal macrophage in vitro. Phytochemical analysis of ME-Og shown high amount of flavonoid and phenolic compound present in it. The cytotoxic effect of ME-Og was studied in murine peritoneal macrophages at different concentrations (0.1 to 100 microg/ml) using the 3-(4, 5-dimethylthiazol-2-yl)-2, 5 diphenyltetrazolium bromide (MTT) method. To establish the protective role of ME-Og against nicotine toxicity, peritoneal macrophages from mice were treated with nicotine (10 mM), nicotine+ME-Og (1 to 25 microg/ml) for 12h in culture media. The significantly (P< 0.05) increased super oxide anion generation, reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity, myeloperoxidase (MPO) activity, lipid peroxidation, protein carbonyls, oxidized glutathione levels were observed in nicotine-treated group as compared to control group; those were significantly (p < 0.05) reduced in ME-Og supplemented groups in concentration dependent manner. More over, significantly (p < 0.05) reduced antioxidant status due to nicotine exposure was effectively ameliorated by ME-Og supplementation in murine peritoneal macrophages. Among the different concentration of ME-Og, maximum protective effect was observed by 25 microg/ml, which does not produce significant cell cytotoxicity in murine peritoneal macrophages. These findings suggest the potential use and beneficial role of O. gratissimum as a modulator of nicotine-induced free radical generation, lipid-protein damage and antioxidant status in important immune cell, peritoneal macrophages.

摘要

在本研究中,我们测试了罗勒甲醇提取物(ME-Og)对尼古丁诱导的小鼠腹腔巨噬细胞的体外作用。ME-Og 的植物化学成分分析表明,其中含有大量的类黄酮和酚类化合物。我们采用 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐(MTT)法,在不同浓度(0.1 至 100μg/ml)下研究 ME-Og 对小鼠腹腔巨噬细胞的细胞毒性作用。为了确定 ME-Og 对尼古丁毒性的保护作用,我们用尼古丁(10mM)处理小鼠腹腔巨噬细胞,在培养物中与 ME-Og(1 至 25μg/ml)共同孵育 12 小时。与对照组相比,在尼古丁处理组中观察到超氧阴离子生成显著增加(P<0.05)、烟酰胺腺嘌呤二核苷酸磷酸(NADPH)氧化酶活性、髓过氧化物酶(MPO)活性、脂质过氧化、蛋白羰基、氧化型谷胱甘肽水平降低;这些变化在 ME-Og 补充组中呈浓度依赖性降低。此外,由于尼古丁暴露导致的抗氧化状态显著降低,通过 ME-Og 补充得到了有效改善。在不同浓度的 ME-Og 中,25μg/ml 的效果最佳,在小鼠腹腔巨噬细胞中没有产生显著的细胞毒性。这些发现表明,罗勒具有作为尼古丁诱导的自由基生成、脂质-蛋白质损伤和重要免疫细胞——腹腔巨噬细胞中抗氧化状态调节剂的潜在用途和有益作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b241/2763260/f1264dcbd18d/omcl0204_0222_fig001.jpg

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