纳米SiO_2对大鼠肺氧化损伤的研究

Nano SiO2 oxidative damage to the lungs in rats

目的探讨纳米SiO2对大鼠肺氧化损伤作用机制。方法将24只体质量200 g左右的雄性大鼠随机分成3组(对照组、微米SiO2组和纳米SiO2组),每组8只。用一次性气管注入法,分别给予1 mL的50 mg/mL石英粉尘(微米SiO2)混悬液、1 mL的50 mg/mL纳米SiO2混悬液、1 mL生理盐水。30 d后进行肺泡灌洗,测定2种粉尘染尘后大鼠肺泡灌洗液(BALF)中的巨噬细胞凋亡率、总蛋白含量、总抗氧化能力(T-AOC)、丙二醛(MDA)含量、羟脯氨酸(HYP)含量;观察肺脏病理形态学改变;采用免疫组织化学法检测肺组织中转化生长因子β-1(TGF-β1)和白介素-4(IL-4)蛋白的表达。结果微米SiO2组和纳米SiO2组巨噬细胞凋亡率高于对照组;纳米SiO2组凋亡率高于微米SiO2组,差异有统计学意义。微米SiO2组及纳米SiO2组较对照组MDA、HYP和总蛋白含量均增加,T-AOC下降。免疫组化结果显示:微米SiO2组TGF-β1及IL-4表达明显高于纳米SiO2组和对照组。结论纳米SiO2能够对肺组织造成一定的氧化损伤,但其氧化损伤并不是肺纤维化的主要因素。

Objective To explore the nano SiO2 on the mechanism of oxidative damage in rats＇ lungs. Methods Twenty - four male rats with the body weight of about 200 g were randomly divided into three groups （control group, micro- SiO2 and nano- SiO2 group）, 8 in each group. With disposable tracheal injection, the rats were given 1 mL of 50 mg/mL of quartz dust （micron SiO2） suspension, 1 mL of 50 mg/mL suspension of nano- SiO2 and 1 mL saline respectively. Thirty days later, the pulmonary alveolus was lavaged, and the rate of macrophage apoptosis, total protein content, total antioxidant capacity （T - AOC）, malondialdehyde （MDA） content and hy- droxyproline （HYP） content of alveolar lavage fluid （BALF） were detected. The lung pathological changes were observed. The TGF -β1 and IL - 4 protein expression in lung tissue were detected with immunohistochemistry. Results The rates of macrophage apoptosis of dye dust groups were higher than those of the control group. The rates of macrophage apoptosis of the nano - SiO2 group were higher than those of the micro- SiO2 group. The MY）A, HYP and protein content of the nano - SiO2 group and the micro - SiO2 group were higher than those of the control group, and the T - AOC decreased. Immunohistochemistry results showed that the TGF- β1 and IL- 4 expressions of the micro- SiO2 group were significantly higher than those of the nano - SiO2 group and the control group. Conclusion Nano - SiO2 can cause some lung tissue oxidative damage, but is not the major factor in pulmonary fibrosis.