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目的研究叶黄素对脂多糖(LPS)所致小鼠急性肺损伤(ALI)的保护作用。方法雄性昆明种小鼠60只,随机分为正常对照组、急性肺损伤模型组、地塞米松阳性对照组(5mg/kg)以及叶黄素低、中、高剂量组(10,15,20mg/kg)共6组。不同剂量叶黄素给大鼠连续灌胃30d后,腹腔注射脂多糖6.0mg/kg建立ALI模型。在注射后6h,收集腹主动脉血并进行左侧支气管肺泡原位灌洗以收集灌洗液,测定血中淋巴细胞亚群CD3+、CD4+、CD8+、肿瘤坏死因子α(TNF-α)、白细胞介素8(IL-8)及丙二醛(MDA)及超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性;测定各组的肺湿重/干重比、肺组织中性粒细胞髓过氧化物酶(MPO)含量及肺组织匀浆TNF-α、白细胞介素10(IL-10)含量。结果叶黄素各剂量组的血TNF-α含量由低到高依次为(390.10±81.50),(374.20±80.09),(340.18±84.39)ng/L,低于模型组(475.29±93.12)ng/L;IL-8含量由低到高依次为(111.13±16.30),(107.33±15.39),(103.39±14.36)ng/L,低于模型组(124.56±20.21)ng/L;MPO含量由低到高依次为(5.12±1.02),(5.03±0.80),(4.48±0.73)U/g低于模型组(6.02±1.06)U/g;MDA含量由低到高依次为:(9.20±0.62),(8.29±1.30),(7.10±1.21)nmol/(mgpro),低于模型组(11.28±2.14)nmol/(mgpro);肺组织湿重/干重比亦低于对照组,差异均有统计学意义(P<0.001),表明叶黄素各剂量组均可降低LPS诱发的过氧化反应。同时叶黄素各剂量组的IL-10含量由低到高依次为(71.23±22.39),(78.28±21.27),(85.18±28.15)ng/L,高于模型组(60.13±20.28)ng/L;血SOD含量由低到高依次为(114.30±41.50),(130.53±40.23),(149.19±41.77)U/(mgpro),高于模型组(74.52±24.40)U/(mgpro);GSH-Px活性由低到高依次为(77.70±12.15),(85.20±12.03),(90.47±13.12)U/(mgpro),高于模型组(62.24±10.13)U/(mgpro);并改善血中淋巴细胞亚群分布;差异均有统计学意义(P<0.001),表明叶黄素各剂量组均可拮抗LPS引起的抗氧化机制的损伤。结论叶黄素对LPS所致急性肺损伤具有预防性保护作用。
Objective To study the protective effect of lutein on acute lung injury (ALI) induced by lipopolysaccharide (LPS) in mice. Methods Sixty male Kunming mice were randomly divided into normal control group, acute lung injury model group, dexamethasone positive control group (5mg / kg) and lutein low, middle and high dose group (10,15,20mg / kg) a total of 6 groups. Different doses of lutein to rats after continuous gavage 30d, intraperitoneal injection of lipopolysaccharide 6.0mg / kg to establish ALI model. Six hours after injection, abdominal aorta blood was collected and left bronchial alveolar lavage was performed to collect lavage fluid. The level of CD3 +, CD4 +, CD8 +, TNF- α, leukocyte (IL-8), malondialdehyde (MDA) and superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) (P> 0.05). The levels of myeloperoxidase (MPO) in lung tissue and contents of TNF-α and IL-10 in lung homogenates were also compared. Results The levels of TNF-αin the lutein groups were (390.10 ± 81.50), (374.20 ± 80.09) and (340.18 ± 84.39) ng / L, respectively, lower than those in the model group (475.29 ± 93.12) ng / L, the levels of IL-8 from low to high were (111.13 ± 16.30), (107.33 ± 15.39) and (103.39 ± 14.36) ng / L, respectively, lower than those in the model group (124.56 ± 20.21) ng / (5.12 ± 1.02), (5.03 ± 0.80) and (4.48 ± 0.73) U / g were lower than those of the model group (6.02 ± 1.06) U / g respectively. The MDA content from low to high was (9.20 ± 0.62), (8.29 ± 1.30) and (7.10 ± 1.21) nmol / (mgpro) respectively, which was lower than that of model group (11.28 ± 2.14) nmol / (mgpro) (P <0.001), indicating that lutein in each dose group can reduce the LPS-induced peroxidation. At the same time, the levels of IL-10 in the lutein groups were (71.23 ± 22.39), (78.28 ± 21.27) and (85.18 ± 28.15) ng / L, L; the blood SOD levels were (114.30 ± 41.50), (130.53 ± 40.23) and (149.19 ± 41.77) U / (mgpro), respectively, which were higher than those in the model group (74.52 ± 24.40 U / mgpro) The activity of -Px from low to high was (77.70 ± 12.15), (85.20 ± 12.03) and (90.47 ± 13.12) mg / L, higher than that of model group (62.24 ± 10.13) U / (mgpro) (P <0.001), indicating that lutein in each dose group can antagonize the anti-oxidative mechanism of LPS-induced injury. Conclusion Lutein has a preventive effect on LPS-induced acute lung injury.