Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Captopril reduces cardiac inflammatory markers in spontaneously hypertensive rats by inactivation of NF-kB. | Miguel-Carrasco et al. Journal of Inflammation 2010 7 21 http content 7 1 21 JOURNAL OF INFLAMMATION RESEARCH Open Access Captopril reduces cardiac inflammatory markers in spontaneously hypertensive rats by inactivation of NF-kB José L Miguel-Carrasco Sonia Zambrano Antonio J Blanca Alfonso Mate and Carmen M Vazquez Abstract Background Captopril is an angiotensin-converting enzyme ACE inhibitor widely used in the treatment of arterial hypertension and cardiovascular diseases. Our objective was to study whether captopril is able to attenuate the cardiac inflammatory process associated with arterial hypertension. Methods Left ventricle mRNA expression and plasma levels of pro-inflammatory interleukin-1 p IL-1 P and IL-6 and anti-inflammatory IL-10 cytokines were measured in spontaneously hypertensive rats SHR and their control normotensive Wistar-Kyoto WKY rats with or without a 12-week treatment with captopril 80 mg Kg day n six animals per group . To understand the mechanisms involved in the effect of captopril mRNA expression of ACE angiotensin II type I receptor AT1R and p22phox a subunit of NADPH oxidase as well as NF-kB activation and expression were measured in the left ventricle of these animals. Results In SHR the observed increases in blood pressures heart rate left ventricle relative weight plasma levels and cardiac mRNA expression of IL-1P and IL-6 as well as the reductions in the plasma levels and in the cardiac mRNA expression of IL-10 were reversed after the treatment with captopril. Moreover the mRNA expressions of ACE AT1R and p22phox which were enhanced in the left ventricle of SHR were reduced to normal values after captopril treatment. Finally SHR presented an elevated cardiac mRNA expression and activation of the transcription nuclear factor NF-kB accompanied by a reduced expression of its inhibitor IkB captopril administration corrected the observed changes in all these parameters. Conclusion These findings show that