Study on the protective effect of menatetrenone against the oxidative stress of osteoblasts
10.12206/j.issn.1006-0111.202005047
- VernacularTitle:四烯甲萘醌保护成骨细胞氧化损伤的作用研究
- Author:
Yizhong JIANG
1
;
Lijuan LIN
2
;
Hailiang XIN
2
;
Yu’e JIN
3
;
Yiping JIANG
2
;
Liming XUE
3
Author Information
1. Dongyang Traditional Chinese Medicine Hospital of Zhejiang, Dongyang 322105, China.
2. Department of Pharmacognosy, School of Pharmacy, Naval Medical University, Shanghai 200433, China.
3. Institute of Chemical Toxicity, Shanghai Municipal Center for Disease Control and Prevention, Shanghai 200336, Chian.
- Keywords:
menatetrenone;
osteoporosis;
osteoblasts;
oxidative stress;
FoxO pathway
- From:
Journal of Pharmaceutical Practice
2020;38(6):523-527
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the protective effect of menatetrenone (MK4) on the osteoblasts in oxidative stress, and to clarify the anti-osteoporosis mechanism of MK4. Methods Mouse osteoblasts (MC3T3-E1) induced by hydrogen peroxide (H2O2) was used. Cell viability, ALP activity and the area of bone nodule were observed. The level of ROS was detected by DCFH-DA, mitochondrial membrane potential by JC-1, apoptosis rate by annexin V-FITC/PI, and the expression of FoxO1, FoxO3, SOD, bcl-2 and bax by RT-PCR. Results Menatetrenone at 10 μmol/L significantly increased the proliferation of osteoblasts stimulated by H2O2, ALP activity, bone nodule formation area, cell membrane potential, the antioxidant SOD and transcription factors FoxO1 and FoxO3 mRNA expression. In the meantime, the elevated malondialdehyde and reactive oxygen species level in cells induced by H2O2, the apoptosis rate and the mRNA expression level of bax/Bcl-2 were significantly reduced. Conclusion menatetrenone can protect osteoblasts from oxidative damage by regulating FoxO pathway and reduce osteoblasts apoptosis by up regulating the proportion of Bcl-2/bax.
