Effect of chitosan/pCDNA3.1 (+) CrmA on matrix metalloproteinase-1 and tissue inhibitor of metalloproteinase-1 expressions of chondrocytes induced by interleukin-1β
10.3760/cma.j.issn.1007-7480.2014.12.009
- VernacularTitle:壳聚糖/pCDNA3.1(+)CrmA对软骨细胞基质金属蛋白酶1及其抑制因子表达的影响
- Author:
Shizhen ZHU
;
Bo QIU
;
Hailong MEN
;
Panghu ZHOU
- Publication Type:Journal Article
- Keywords:
Osteoarthritis;
Chitosan;
Matrix metalloproteinases;
Cytokine response modifier A
- From:
Chinese Journal of Rheumatology
2014;18(12):828-831
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of chitosan/pCDNA3.1 (+) CrmA on matrix metalloproteinase (MMP)-1 and tissue inhibitor of metalloproteinase (TIMP)-1 expression of chondrocytes induced by interleukin-1β (IL-1β) in mRNA and protein levels.Methods Rabbit chondrocytes were isolated and cultured.Chondrocytes were treated with PBS,10 μg/ml chitosan (CS) and chitosan/ pCDNA3.1 (+)CrmA respectively for 6 hours.Then 10 ng/ml IL-1β was added into the culture medium.After 48 hours,real time polymerase chain reaction (real time PCR) and Western blot assay were used to examine the changes of MMP1 and TIMP-1 in mRNA and protein levels.Results In CS/pCDNA3.1 (+)CrmA treated group (0.44±0.04),the messenger RNA expression of MMP-1 in chondrocytes was significantly suppressed compared with corresponding samples of PBS treated group (1.00±0.05) and CS treated group (0.76±0.07),There was significant difference between three groups (F=106.93,P＜0.01).The MMP-1 protein expression of chondrocytes in CS/pCDNA3.1 (+)CrmA treated group (0.28±0.03) was lower than that of PBS treated group (0.73±0.06) and CS treated group (0.46±0.05)(F=59.66,P＜0.01).No significant difference of TIMP-1 expression among the three groups was observed in mRNA and protein levels.Conclusion CS/pCDNA3.1(+) CrmA can significantly inhibit the mRNA and protein expressions of MMP-1 of chondrocytes induced by IL-1β,which leads to up-regulation the ratio of TIMPs to MMPs of IL-1β induced chondrocytes.It may be a part of the mechanisms of the therapeutic effects of CS/pCDNA3.1 (+)CrmA on osteoarthritis.
