Inhibitory Effects of NO-Fluvastatin on Proliferation of Human Lens Epithelial Cells in vitro by Modulating Cell Cycle Regulatory Proteins
10.1007/s11596-008-0522-x
- Author:
WANG ZHI
1
;
GAO RUIYING
;
SHI QIANQIAN
;
HUANG YUKAN
;
CHEN WEN
;
SHI KAIYING
Author Information
1. Department of Ophthalmology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China
- Keywords:
posterior capsular opacification;
NO-Fluvastatin;
human lens epithelial cell;
cell cycle;
regulatory protein
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2008;28(5):588-591
- CountryChina
- Language:Chinese
-
Abstract:
Summary: The effects of NO-Fluvastatin on proliferation of human lens epithelial cells (HLECs) and the action mechanism were investigated. Cell proliferation was assessed by MTT assay. Cell cycle was analyzed by flow cytometry. The expression of cell cycle regulatory proteins CyclinE mRNA and P21wafl mRNA was detected by reverse transcription polymerase chain reaction (RT-PCR). MTT staining colorimetry showed that HLECs proliferation was markedly inhibited by NO-Fluvastatin and the effect was dependently related to time (24, 48 and 72 h) and dosage (1, 5 and 20 μmol/L). Flow cytometry revealed that NO-Fluvastatin could significantly block HLECs in the G0/G1 phase, resulting in the increased cells in the G0G1 phase and decreased in the S phase (P<0.05). RT-PCR showed that NO-Fluvastatin could obviously inhibit the CyclinE mRNA expression and induce the P21wafl mRNA expression as compared with the negative control groups (P<0.05). This experiment suggested that NO-Fluvastatin could suppress the proliferation of HLECs by regulating cell cycle regulatory proteins (inhibiting the expression of CyclinE mRNA and inducing the expression of P21wafl mRNA), resulting in the arrest of HLECs in the G0/G1 phase, which can offer theory basis for NO-Fluvastatin in treating posterior capsular opacification in clinic practice.
