Effect of midazolam on mantle cell lymphoma JeKo-1 cell line and its relevant mechanisms.
10.7534/j.issn.1009-2137.2013.06.017
- Author:
Jin-Quan HONG
1
;
Shan-Hu WU
1
;
Zhi-Yuan CHEN
1
;
Wei-Huang ZHUANG
2
;
Hong-Zhi GAO
3
Author Information
1. Department of Anesthesia, The Second Affiliated Hospital of Fujian Medical University, Quanzhou 362000, Fujian Province, China.
2. Department of Hematology, The Second Affiliated Hospital of Fujian Medical University, Quanzhou 362000, Fujian Province, China.
3. Scientific Research Center, The Second Affiliated Hospital of Fujian Medical University, Quanzhou 362000, Fujian Province, China. E-mail: hongjinquan1114@163.com.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
drug effects;
Caspase 3;
metabolism;
Caspase 8;
metabolism;
Caspase 9;
metabolism;
Cell Line, Tumor;
Cytochromes c;
metabolism;
Humans;
Lymphoma, Mantle-Cell;
metabolism;
Midazolam;
pharmacology;
Proto-Oncogene Proteins c-bcl-2;
metabolism
- From:
Journal of Experimental Hematology
2013;21(6):1460-1463
- CountryChina
- Language:Chinese
-
Abstract:
This study was aimed to explore the effect of midazolam on mantle cell lymphoma cell line JeKo-1 and the relevant mechanisms. Effects of midazolam on the proliferation and apoptosis of JeKo-1 cells were observed by CCK8 assay and flow cytometry, respectively. Effect of midazolam on the expression of BCL-2, cytochrome C (Cyto-C), pro-caspase-9, pro-caspase-8 and pro-caspase-3 protein were detected by Western blot. The results showed that midazolam could inhibit the growth of JeKo-1 cells significantly and the concentration of 50% growth inhibition (IC50) at 48 hours was approximately 40 µmol/L. After treatment with 20, 40, 80 µmol/L midazolam for 48 hours, a dose-dependent apoptosis of JeKo-1 cells could be observed. Meanwhile, a dose-dependent reduction of BCL-2, pro-caspase-9 and pro-caspase-3 protein expression and increase of Cyto-C protein expression in JeKo-1 cells were found, but the expression of pro-caspase-8 protein did not change. It is concluded that midazolam possibly initiates the mitochondrial pathway, not the death receptor pathway, by reducing the expression of BCL-2, leading in turn to the releasing of Cyto-C in mitochondria, then activating caspase-9 and caspase-3 protein, triggers the caspase cascade, and induces the apoptosis of JeKo-1 cells ultimately.
