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The Effect of Simastatin on Serum Interleukin-18, Interleukin-10 in Rats with Chronic Heart Failure

Author: YangShuHan
Tutor: ZhaoYuLan
School: Zhengzhou University
Course: Department of Cardiology
Keywords: Heart Failure Congestive Simvastatin IL-18 IL-10 Cytokines
CLC: R541.6
Type: Master's thesis
Year: 2007
Downloads: 178
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Abstract

The background and purpose of congestive heart failure (Congestive Heart Failure, CHF) is a clinical syndrome, the final stage of various heart diseases. Heart failure, the molecular basis of the development of ventricular remodeling, regulation and control of the network in which various cytokines play an important role in the development of heart failure in recent years. Include two categories: cytokines induced by inflammatory cytokines and anti-inflammatory cytokines. Caused by inflammatory cytokines have tumor necrosis factor-a (of TNF-a), White mediated hormone (interleukin, IL) 1, interleukin Su-6 (IL-6), interleukin 18 (of IL-18) and other anti-inflammatory cytokines to White mediated Su-10 ( IL-10) by interleukin-4 (IL-4), interleukin -12 (IL-12), transforming growth factor (TGF-β) and other representatives. IL-18 is a new cytokine recently discovered, with a variety of cardiovascular diseases. It has been reported that, IL-18 has the role of promoting cell growth, so changes in heart failure IL-18 helps to clarify the relationship between cytokines and heart failure. Disease development depends not only on the proinflammatory cytokine levels of pro-inflammatory cytokines and anti-inflammatory cytokine interactions affect each other, jointly developed heart failure, prognostic impact. Therefore, to study the relationship of anti-inflammatory cytokines and proinflammatory cytokines have special significance. In addition to lowering cholesterol, the statins also has the role of multi-effect, has been widely used lipid-lowering treatment of coronary heart disease, clinical and animal experiments show that: Statins also have a beneficial effect in heart failure, but its role the mechanism is still unknown. Observed in patients with chronic heart failure, IL-18, IL-10 levels and their ratio of the change in the role of inflammatory cytokines in the pathogenesis of heart failure, and the simvastatin drug intervention, to understand their role in heart failure and its mechanism. Materials and methods. Male Wistar rats adaptive feeding one week after renal the epigastric aortic coarctation produced chronic heart failure model, random sample of 10 rats detect hemodynamic parameters after 8 weeks, that reached the heart failure (LVEDP = 15mmHg as a sham operation), the remaining rats were randomly divided into two groups, the control group with heart failure (CHF-C group) and heart failure statin intervention group (CHF-S group); Another eight separate abdominal aortic suture ligation group (SH group). CHF-S Press 5mg/kg.d ig the control group of heart failure, SH daily irrigation equal amount of saline, a total of about 4 weeks. 2. Hemodynamics and cytokine detection before the animals were killed from the carotid artery was cannulated connection polygraph recorder to record hemodynamic parameters: systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (Mean artery pressure, MAP), left ventricular end-diastolic pressure (Left ventricular end-diastolic pressure, LVEDP), left ventricular pressure rise in the maximum rate (dp / dt _max), the largest decline in the rate of left ventricular pressure (- dp / dt _max), 10 ml of blood was taken from the chambers of the heart, centrifugal 4000r / m × 10 minutes, the supernatant was the 2ml placed in -40 ° C refrigerator, specific enzyme-linked immunosorbent assay ( ELISA) determination of IL-18, IL-10, steps in accordance with the kit instructions. The animals were killed after take heart free left ventricular weighing, calculation of left ventricular mass index (LV / rat weight). 3. Statistical analysis All data were presented as mean ± standard deviation ((?) ± s) application SPSS10.0 software package for the analysis of homogeneity of variance and normality test, in line with the conditions of application of the single-factor analysis of variance between groups compare application Student-Newman-Keuls method, correlation analysis using Pearson method (Pearson), P ≤ 0.05 as the difference was significant standard. Results 1. CHF-C and CHF-S in 8 weeks showed varying degrees of decreased appetite, decreased activity, cyanosis, edema, dyspnea, heart failure performance, SH no such changes. 2. Animals in each group hemodynamic parameters: MAP, dp / dt max , _{the -dp/dt _max, LVEDP in each group were significantly different (P <0.05) ; compared with the SH group CHF-C rats MAP dp / dt _max max} -dp/dt _{decreased significantly (P <0.05), while LVEDP significantly higher (P <0.05); CHF-S group and CHF-C group, MAP, and dp / dt _max} -dp/dt _{max, LVEDP a significant improvement (P <0.05). 3. IL-18, IL-10, IL-18/IL-10 in all groups were significantly different (P <0.05); compared with the SH group, CHF-group C rat IL-18, IL-10, IL -18/IL-10 significantly higher (P <0.05); CHF-S group and CHF-C group compared with IL-18, IL-10, IL-18/IL-10 showed significant improvement (P < 0.05). 4. There are significant differences in left ventricular mass index in each group, CHF-C and SH than the increase in cardiac index, CHF-S and CHF-C, cardiac index decreased. 5. IL-18, and left ventricular mass index was significantly positively correlated (r = 0.772, P = 0.001); IL-18 and IL-10 was a significant positive correlation (r = 0.777, P <0.001). Conclusion 1. IL-18 may have caused the role of cardiomyocyte hypertrophy. 2. Heart failure exist TH1/TH2 cytokine imbalance participate in the development of heart failure. 3. Simvastatin can improve the symptoms of heart failure, may play its role by correcting the imbalance of the cytokine network.}

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