摘要
【目的】探讨罗红霉素对白介素-22（IL-22）诱导的HaCaT角质形成细胞增殖的影响。【方法】①0、12．5、25、50、100、200μg／mL的11．-22处理HaCaT细胞48h后。MTT法检测细胞活力。②0、10、20、40、80、160、320ug／mL的罗红霉素处理HaCaT细胞48h后，MTT法检测细胞活力。③细胞分为5组：正常对照纽，模型对照组（100ug／mL IL-22），罗红霉素低、中、高剂量组（40、80、160ug／mL＋100μg／mL IL-22）。MTT法检测各组细胞活力。Western blot检测各组细胞中角蛋白16（K16）、K17表达量。[结果]12．5、25、50、100μg／mL的IL-22提高HaCaT细胞活力（P〈0．05）；10、20μg／mL的罗红霉素显著的提高HaCaT细胞活力（P〈0．01），40、80、160、320μg／mL的罗红霉素降低HaCaT细胞活力（P〈0．01）；与正常对照组比较，模型对照组中K16、K17、Bcl-2表达上调（P〈0．01）；与模型对照组比较，罗红霉素低、中、高剂量组中K17表达依次下调（P〈0．01）；与正常对照组比较，模型对照组中Bax表达下调；与模型对照组比较，罗红霉素低、中、高剂量组中Bax表达依次上调（P〈0．01）。【结论】罗红霉素能通过下调角蛋白表达及调控细胞凋亡相关蛋白表达进而抑制IL-22诱导的HaCaT细胞增殖。
[Objective]To explore the inhibition of roxithromycin on the proliferation of HaCaT keratinocyte cells induced by interleukin-22 （IL-22）. [Methods]Firstly, HaCaT cell viability was detected by MTT after cells were cultured with IL-22 at concentrations of 0, 12.5, 25, 50, 100 and 200 ptg/mL for 48 h. Secondly, HaCaT cell viability was also detected by MTT after cells were cultured with roxithromycin at concentrations of 0, 10, 20, 40, 80, 160 and 320 /μg/mL for 48 h. Lastly, experiments were divided into the control group （vehicle treat- ment）, the model group （100 μg/mL IL-22） and roxithromycin groups at low, medium and high-dose groups （100, 300, 1000 μg/mL-7100μg/mL IL-22, respectively）. The cell viability was measured by MTT methodand expressions of eytokeratin16 （K16）, K17, Bax and Bcl-2 were detected by Western blot. [Results]Cell viability of HaCaT was increased by IL-22 at concentrations of 12.5, 25, 50 and 100μg/mL. However, the cell viability was decreased by IL22 at a concentration of 200μg/mL. Similarly, cell viability was increased by roxithromycin at concentrations of 10.20 μg/mL, but the cell viability was decreased by roxithromycin at concentrations of 40.80. 160.320μg/mL. Compared to the vehicle control group, while the cell viability of IL-22 treated model group was increased, the expression of K16, K17 and Bel 2 was up-regulated（ P 〈0.01）, the expression of Bax was down regulated. Compared to the model group, the cell viability in low, medium and high-dose of roxithromycin groups was decreased, and the expression of K17 was down-regulated. The expression of Bax was up-regulated （ P 0.01 ）. The expression of K16 and Bcl-2 was down-regulated in roxithromycin medium and high-dose groups. [Conclusion] Roxithromycin can inhibit IL 22-induced proliferation of HaCaT keratinocyte cells by down-regulating the expression of cytokeratin and regulating the expression of cell apoptotic related proteins.
出处
《医学临床研究》
CAS
2017年第11期2098-2100,2103,共4页
Journal of Clinical Research
