Heat shock protein 70 gene transfection protects rat myocardium cell against anoxia-reoxygeneration injury.

摘要: BACKGROUND A number of studies suggest that the expression heat shock protein 70 (HSP(70)) induced by stress are associated with protection against ischemia-reperfusion injury. But protective effects may be contaminated other factors in same stress. This study was conducted to explore role HSP(70) acute myocardial anoxia/reoxygeneration (A/R) injury a liposome-mediated gene transfer technique for introduction pCDNA into neonatal rat cells. In addition, cytoprotection also investigated comparison. METHODS The cultured primary myocardiocytes an A/R model and HS-treated myocardiocyte were used. Three-day randomly divided four groups (n = 8): control group, HS + group group. liposome-coated plasmid transfected myocardiocytes; mRNA its confirmed reverse transcriptase polymerase chain reaction (RT-PCR) Western blotting. cell viability assayed monotetrazolium (MTT) lactate dehydrogenase (LDH) creatine phosphokinase (CPK) activity cells during incubation changes ultrastructure examined. NF-kappaB measured flow cytometry. RESULTS Compared ((35.4 +/- 6.9)%) ((72.8 11.6)%) ((76.3 12.2)%) improved significantly (P < 0.05). LDH CPK elevated However, significant decreases observed. abnormal, whereas nearly normal observed slightly expressed obvious overexpression 0.01). And there difference between high (5.76 0.64) detected statistically decrease compared (3.11 0.52 vs 5.76 0.64, P (2.83 0.49 CONCLUSIONS Overexpression alone transfection leads cardiac myocyte anoxia-reoxygeneration. These cardioprotective related reduction activation NF-kappaB.