甲醛对大鼠肺细胞醛糖还原酶的影响及醛糖还原酶功能研究

Effects of Formaldehyde on Activity of Aldose Reductase in Rat Lung Cells and AR Function Study

为了研究甲醛作用后大鼠肺细胞醛糖还原酶(AR)的活性变化以及AR在肺细胞损伤中的功能,首先通过大鼠肺细胞分离培养,观察甲醛对大鼠肺细胞AR活性的影响及AR抑制剂——盐酸小檗碱对AR活性的抑制作用;其次通过流式细胞仪检测甲醛及盐酸小檗碱对大鼠肺细胞周期和凋亡的影响.结果表明:1.0mmol·L-1甲醛作用24h使大鼠肺细胞AR活性显著增加,盐酸小檗碱对AR活性具有抑制作用;甲醛能够引起大鼠肺细胞凋亡,使G0/G1和S期的细胞比例下降,G2/M期的细胞比例增加;甲醛和盐酸小檗碱共同作用使大鼠肺细胞凋亡率较单纯甲醛组更高,同时G0/G1期的细胞比例增加,S和G2/M期的细胞比例下降.结果提示甲醛能够使大鼠肺细胞AR活性增加;AR活性增加可减少细胞凋亡,对甲醛引起的大鼠肺细胞损伤具有保护作用.

In order to study effects of formaldehyde（FA）on activity of aldose reductase（AR）in rat lung cells and function of AR in lung cell injury, Firstly, effects of FA on activity of AR in rat lung cells and inhibition of berberine hydrochloride on AR activity were observed by rat lung cell detachment and culture. Secondly effects of FA and berberine hydrochloride on cell cycle and apoptosis of rat lung were detected by flow cytometry. The results showed that AR activity was increased significantly in rat lung cells that were exposed to 1.0mmol·L^-1 FA for 24h; Berberine hydrochloride displayed inhibition on AR activity; FA could induce apoptosis of rat lung cells, decrease of cell percent of G0/G1 and S phase and increase of cell percent of G2/M phase; The percent of apoptosis in rat lung cells that were exposed to FA and berberine hydrochloride were higher than that in rat lung cells exposed to FA only. Meanwhile, cell percent of G0/G1 phase was increased, and cell percents of S and G2/M phase were decreased. It can be concluded that FA could cause increase of AR activity in rat lung cells; and the increase of AR activity could reduce apoptosis, thus it had protection on rat lung cell damage induced by FA.