Effect Of Berberine Of Serum Cytokine And Myocyte Inducible Nitric Oxide Synthase Gene Expression In A Rat Models Of Chronic Heart Failure

Object This study was designed to investigate the mechanism of Berberine ameliorate the pathological physiology of heart failure in a model of chronic heart failure through the observe of serum tumor necrosis factor-a(TNF-a), interleukin-1(IL-1), interleukin-6(IL-6), interleukin-10(IL-10) and myocyte inducible nitric oxide synthase(iNOS) gene expression.Method The Sprague-Dawley(SD) rat of experimental heart failure (HF) model were established by intraperitoneal injection of adriamycin2.8mg/kg/week for10weeks. Then HF model rats (n=32) divided into berberine treated group(n=16) and HF control group (n=16). And12randomly selected rats as normal control group. Normal control group was intraperitoneal injection of saline. Two weeks later, echocardiogram was introduced to measure left ventricular end diastolic internal diameter (LViDd), left ventricular end systolic internal diameter (LViSd) and left ventricular ejection fraction (LVEF). Serum BNP, TNF-a, IL-1, IL-6and IL-10was assessed by Elisa. The berberine therapy group was administered with berberine21mg/kg/d for4weeks, HF control group and normal control group was administered with saline. Serum BNP, TNF-a, IL-1, IL-6and IL-10was assessed by Elisa. Inducible nitric oxide synthase gene expression was measured by Real-time PCRResult LViDd and LViDs of HF model rats was larger than normal group. LVEF of HF model rats was lower than normal control group. Compared with HF control group and before treatment, Berberine therapy significantly attenuated serum BNP, IL-1, IL-6and TNF-α (p<0.05); Berberine down-regulated iNOS gene expression in HF rats myocyte (p<0.01). Between groups, serum IL-10has no difference.Conclusion Berberine attenuate serum TNF-a, IL-1, IL-6and down-regulate iNOS gene expression ameliorate the pathological physiology of heart failure and then it may be beneficial to the recovery of heart failure.