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研究采集PM_(2.5)样本,制备PM_(2.5)生理盐水混悬液,对雄性SD大鼠进行染毒实验,检测大鼠肺组织病理学改变,测定肺中炎症因子和CK-18mRNA和蛋白表达。结果显示,随着PM_(2.5)染毒剂量增加,肺组织出现肺充血和炎性细胞浸润等炎症反应,冬季PM_(2.5)所致肺病理学损伤比夏季严重。冬季PM_(2.5)中、高剂量组和夏季高剂量组大鼠肺中TNF-α、IL-6、TGF-β、CK-18mRNA和蛋白表达比对照组显著增加。这说明PM_(2.5)亚慢性染毒可增加炎症因子表达水平,促进肺炎症反应。CK-18表达上调提示PM_(2.5)致肺组织处于氧化应激状态。太原市冬季PM_(2.5)引起大鼠肺炎症损伤效应比夏季严重。
The samples of PM 2.5 were collected and the suspension of PM 2.5 was prepared. The male SD rats were exposed to the virus and the pathological changes of the lung were detected. The expressions of inflammatory cytokines and CK-18 mRNA and protein . The results showed that with the increase of the dose of PM 2.5, the inflammatory reaction such as lung congestion and inflammatory cell infiltration occurred in lung tissue. The lung pathological damage caused by PM 2.5 in winter was more serious than in summer. Compared with the control group, the mRNA and protein expressions of TNF-α, IL-6, TGF-β and CK-18 in the PM_ (2.5) mid-winter and high-dose summer groups were significantly increased. This shows PM_ (2.5) sub-chronic exposure can increase the expression of inflammatory cytokines and promote lung inflammation. The up-regulation of CK-18 suggests that PM_ (2.5) induced oxidative stress in lungs. Taiyuan winter PM_ (2.5) induced lung injury in rats than in summer.