Abstract

Objective To explore the effects of mechanical stimuli on the expression of signal transduction molecule Caspase-3,B-cell lymphoma-2 ( bcl-2),bax mRNA.Methods Rabbit knee articular cartilage cells obtained by enzymatic digestion were cultured and passaged for 3 generations.The chondrocytes were cultivated in a culture plate added with different doses of inhibitor of Caspase-3,bcl-2,bax by a closed container with 90 kPa pressure for 24 h.Chondrocytes apoptosis was detected by flow cytometry (FCM),and the expression of Caspase-3,bcl-2,bax mRNA by semiquantitative analysis of polymerase chain reaction (PCR).Results Mechanical pressure could induce chondrocytes apoptosis.There was significant difference in apoptosis rate between inhibitors-treated groups and contral group ( all P < 0.05 ).There was significant difference in the expression of signal transduction molecule Caspase-3,bcl-2 and bax between inhibitors-treated groups and control group ( all P < 0.05).There were correlations between apoptosis rate and expression of Caspase-3,bcl-2 and bax in Caspase-3,bcl-2 and bax inhibitors-treated groups respectively ( for Caspase-3,r =0.69,t =3.41,P < 0.01 ; for bcl-2,r =0.73,t =3.97,P < 0.O1 ; for bax,r =0.89,t =6.69,P<0.01).Conclusion The inhibitors of Caspase-3,bcl-2 and bax can influence the apoptosis of chondrocytes,and make the expression of Caspase-3,bcl-2 and bax mRNA change. Key words: Chondrocyte; Mechanical pressure; Apoptosis

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.