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目的探讨丙烯酸甲酯(MA)对小鼠肺组织的损伤作用机制。方法昆明种小鼠40只,体质量18～22g,雌雄各半,随机分为对照组和MA吸入染毒280、560、1120mg/m3组,置于静式染毒柜中,每天吸入染毒2h,连续染毒30d,末次染毒后禁食24h处死,称量各组小鼠的脏器系数,观察病理形态学改变,采用酶标仪检测肺组织中的肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)水平的变化。结果与对照组比较,除染毒280mg/m3组TNF-α水平略有降低外,其余各染毒组TNF-α和IL-6水平都有不同程度的升高(P<0.05);肺心指数和肺脏湿干比与对照组比较差异无统计学意义(P>0.05);光镜观察显示:MA染毒各组小鼠肺组织均有炎性细胞浸润、充血,1120mg/m3组肺组织有水肿出现。结论 MA可导致小鼠肺组织中TNF-α、IL-6水平的升高,引起小鼠肺组织的炎性损伤。
Objective To investigate the mechanism of methyl methacrylate (MA) on lung injury in mice. Methods Forty Kunming mice, weighing 18-22 g and male and female, were randomly divided into control group and MA inhalation exposure groups of 280, 560, and 1120 mg / m3. The mice were placed in a static exposure cabinet and inhaled for 2 hours daily , Continuously exposed for 30 days. After the last exposure, fasted for 24 hours. The organ coefficients of mice in each group were weighed and the pathological changes were observed. The levels of tumor necrosis factor-α (TNF-α ), Interleukin-6 (IL-6) levels. Results Compared with the control group, the levels of TNF-α and IL-6 in the other groups were all increased to some extent (P <0.05) except for the TNF-α level of 280 mg / There was no significant difference in index and lung wet-dry ratio between the two groups (P> 0.05). The results of light microscope showed that the inflammatory cells infiltration, hyperemia and lung tissue of 1120mg / m3 group Edema appears. Conclusion MA can induce the increase of TNF-α and IL-6 levels in the lungs of mice, leading to the inflammatory injury in the lungs of mice.