Connexin 43(Cx43) is the major structural protein of gap junctions in the ventricular myocardium and a major determinant of myocardial electrical properties.Cx43 expression is decreased in the wild type mice after myocardial infarction and this effect is attenuated in MMP-7-/mice.Matrix metalloproteinase expression is regulated at the transcription level by the modulation of the activation of transcription factors such as activator protein(AP)-1 and nuclear factor kappa-light-chain enhancer of activated B cells(NF-κB).Methods Rat myocardial cells(H9c2) were cultured and maintained at 37 ℃ and 5% CO 2.H9c2 cells in 6-well plates were treated with lipopolysaccharides(LPS),NF-kB inhibitor(JSH 23,30 μ,Santa Cruz) + LPS and c-Jun N-terminal kinase(JNK) inhibitor(SP600125,10 μM,Sigma) + LPS for 6,12 and 24 h.Apoptosis rate of cells was determined by flow cytometry.Cx43 expression was assessed by Western blotting.Results LPS induced a time-dependent apoptosis in all cell line.We have found that the treatment with LPS induced increase of apoptosis in H9c2 cells at 6 h,12 h and 24 h,but the effect was decreased by the addition of JSH-23 and SP600125 to LPS respectively(P < 0.05).LPS resulted in decreased expression of Cx43 expression at 6 h,12 h and 24 h.However,JSH-23 and SP600125 attenuated the loss of Cx43 respectively(P < 0.05).Conclusion Transcription factors NF-kB and JNK /AP-1 signaling pathway participates in the regulation of LPS-induced Cx43 expression in the H9c2 cells,and maybe play an important role in regulation of Cx43 expression.
