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机构地区:[1]四川省南充市川北医学院附属医院呼吸内科,637000
出 处:《国际呼吸杂志》2012年第16期1252-1255,共4页International Journal of Respiration
基 金:四川省卫生厅科研项目(070293)
摘 要:目的探讨巨噬细胞刺激蛋白(MSP)对烟熏大鼠肺泡巨噬细胞氧化应激和细胞因子产生的影响。方法培养正常和烟熏不同时间(1个月、2个月、3个月)的大鼠肺泡巨噬细胞,给予不同浓度MSP处理24h,采用酶联免疫法检测细胞上清液中细胞因子肿瘤坏死因子α(TNF-α)、白介素8(IL-8)和IL-1β的浓度,比色法榆测细胞上清液中丙二醛(MDA)和超氧化物歧化酶(SOD)的水平。结果①MSP旱浓度依赖性促进正常组和各烟熏组大鼠肺泡巨噬细胞分泌TNF—α、IL-8和IL-1β;经MSP处理后,各烟熏组大鼠肺泡巨噬细胞上清液中TNF-α、IL-8和IL-1浓度均高于正常组(P〈0.05);大鼠肺泡巨噬细胞上清液中TNF-α、IL -8和IL-1β浓度随烟熏时间延长呈时间依赖性增加。②MSP呈浓度依赖性促进正常组和各烟熏组大鼠肺泡巨噬细胞分泌MDA,抑制其产生SOD;烟熏2个月组和烟熏3个月组大鼠肺泡巨噬细胞上清液中MDA水平均高于正常组(P〈0.05),SOD水平均低于正常组(P〈O.05);随着烟熏时间延长,大鼠肺泡巨噬细胞上清液中MDA水平呈时间依赖性增加。SOD水平呈时间依赖性降低。结论MSP呈浓度依赖性促进正常和烟熏大鼠肺泡巨噬细胞分泌TNF—α、IL-8、IL-1β和MDA,抑制其产生SOD。MSP促烟熏大鼠肺泡巨噬细胞分泌TNF-α、IL-8、IL-18、MDA及抑制其产生SOD的作用较正常大鼠更显著,日烟熏时间越长此作用越明显。Objective To investigate the effect of mcrophage stimulating protein (MSP)on the release of cytokine and oxidative stress of alveolar macrophages (AM) in cigarette exposure rats. Methods Cultured normal and cigarette exposure (1 month, 2 months, 3 months) rats AM were treated with different concentrations of MSP for 24 h. The levels of TNF-α,IL-8 and IL-lβ in the supernatant of AM were determined with ELISA. The levels of malondialdehyde (MDA) and superoxide dismutase (SOD) in the supernatant of AM were assayed by chromatometry method. Results ①MSP increased TNF-α,Il-8 and Il-1β levels in the supernatant of AM from normal and cigarette exposure rats in a concentrationdependent manner. After treated with MSP,the levels of TNF-α,IL-8 and IL-lβ in the supernatant of AM from each cigarette exposure group were significantly higher than that in normal group ( P 〈0.05). With the cigarette exposure time extension, the levels of TNF-α,IL-8 and IL-1β in the supernatant of AM were increased in a time dependent manner. ②MSP increased the level of MDA and inhibited the level of SOD in the supernatant of AM from normal and cigarette exposure rats in a concentration-dependent manner. Compared with control group, the levels of MDA in the supernatant of AM from the cigarette exposure 2 months and 3 months groups rats were increased, but the levels of SOD were decreased. The level of MDA was increased and the level of SOD was decreased in a time dependent manner with the cigarette exposure time extension. Conclusions MSP increases significantly the release of TNF-α,IL-8,IL-lβ,MDA and inhibits the production of SOD in cultured normal and cigarette exposure rats AM in a concentration-dependent manner. These effects of MSP in cigarette exposure rats are more pronounced than in normal rats, and cigarette exposure the longer these effects are more obvious.
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