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）-I and nuclear factor kappa-light-chain enhancer of activated B cells （NF-KB）. Methods Rat myocardial cells （H9c2） were cultured and maintained at 37 ~C and 5% CO2. 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, 10μM, 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.
