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目的探讨急性百草枯中毒大鼠肺组织氧化应激及脂质过氧化损伤机制及姜黄素的干预作用。方法将120只成年雄性SD大鼠按不同造模方法用随机数字表法分成对照组、百草枯中毒组、姜黄素干预组,每组大鼠40只。百草枯中毒组腹腔注射百草枯15 mg/kg,姜黄素干预组腹腔注射姜黄素200 mg/kg,15 min后腹腔注射百草枯15 mg/kg,对照组腹腔注射等容量的生理盐水。百草枯中毒组及姜黄素干预组于染毒后(对照组于腹腔注射后)3 h、6 h、24 h、3 d、7 d分别随机抽取8只大鼠取材。荧光实时定量PCR法测定各组大鼠肺组织中的转化生长因子(TGF)-β1mRNA的表达量,硫代巴比妥酸比色法、分光光度计比色法、黄嘌呤氧化酶法分别测定肺组织匀浆中丙二醛、髓过氧化物酶(MPO)、超氧化物歧化酶(SOD)活性,光镜下观察各组肺组织病理变化。结果染毒后6 h、24 h、3 d、7 d,与对照组相比,百草枯中毒组和姜黄素干预组肺组织TGF-β1mRNA的表达量明显升高(F=136.928、32.282、52.008、30.940,P均<0.05),丙二醛(F=132.896、64.988、30.622、30.192)、MPO(F=34.738、202.578、122.019、119.626)含量升高(P均<0.05),而SOD活力降低(F=34.738、202.578、122.019、119.626,P均<0.05);与百草枯中毒组相比,姜黄素干预组各时间点肺组织TGF-β1mRNA表达量、丙二醛及MPO含量均降低(P均<0.05),肺组织SOD活力均升高(P均<0.05)。结论氧化应激及细胞膜脂质过氧化过程的启动可能是百草枯中毒急性肺损伤的机制之一,姜黄素可能通过阻止该过程减轻肺损伤的程度。
Objective To investigate the mechanism of oxidative stress and lipid peroxidation in lungs of acute paraquat poisoning rats and the intervention of curcumin. Methods 120 adult male SD rats were randomly divided into control group, paraquat poisoning group and curcumin intervention group, with 40 rats in each group. Paraquat poisoning group was given intraperitoneal injection of paraquat 15 mg / kg, curcumin intervention group was intraperitoneally injected with curcumin 200 mg / kg, and paraquat 15 mg / kg was intraperitoneal injected 15 minutes later. The control group was injected intraperitoneally with equal volume of normal saline. In the paraquat poisoning group and the curcumin intervention group, 8 rats were randomly drawn at 3 h, 6 h, 24 h, 3 d, and 7 d after exposure (control group was injected intraperitoneally). Real-time quantitative PCR was used to detect the expression of transforming growth factor (TGF) -β1mRNA in the lung tissue of each group, thiobarbituric acid colorimetric method, spectrophotometer colorimetric method and xanthine oxidase method respectively Pulmonary tissue homogenate malondialdehyde, myeloperoxidase (MPO), superoxide dismutase (SOD) activity, the pathological changes of lung tissue were observed under light microscope. Results Compared with the control group, the expression of TGF-β1 mRNA in the lung tissue of paraquat poisoning group and curcumin intervention group was significantly increased at 6 h, 24 h, 3 d, and 7 d after exposure (F = 136.928, 32.282, 52.008 , 30.940 (all P <0.05). The contents of malondialdehyde (F = 132.896,64.988,30.622,30.192) and MPO (F = 34.738,202.578,122.019,119.626) (F = 34.738, 202.578, 122.019, 119.626, P <0.05). Compared with paraquat poisoning group, the expression of TGF-β1mRNA, All <0.05), the activity of SOD in lung tissue was increased (all P <0.05). Conclusions The initiation of oxidative stress and cell membrane lipid peroxidation may be one of the mechanisms of paraquat poisoning in acute lung injury. Curcumin may reduce the extent of lung injury by preventing this process.