CAJ | 학술논문

目的：观察阿托伐他汀对小鼠主动脉弓缩窄（TAC）术后心室重构的保护作用并探讨其可能机制。 　　方法：采用主动脉弓缩窄法建立小鼠心肌肥厚模型。选取48只C57BL/6小鼠，随机分为4组（每组12只）：假手术组、TAC组、TAC＋缬沙坦组，TAC＋阿托伐他汀组，术后4周成功造模并分别给予生理盐水、缬沙坦（5 mg/kg）、阿托伐他汀（10 mg/kg）处理。8周后进行超声心动图检查，测量左心室舒张期前壁厚度（LVAWd），左心室舒张期后壁厚度（LVPWd），左心室射血分数（LVEF）及短轴缩短率（FS），计算心肌肥厚指数。应用免疫蛋白印迹（Western blot）法检测核转录因子-κB （NF-κB）的蛋白表达水平。碱水解法检测心肌组织羟脯氨酸（Hyp）的含量、采用酶联免疫吸附（ELISA）法检测血清肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）的浓度。苏木素-伊红（HE）染色及马松（Masson）染色方法测定心肌胶原沉积。 　　结果：与假手术组相比，TAC组LVAWd、LVPWd、心肌肥厚指数、心肌纤维化面积明显增加（P<0.01），NF-κB的蛋白水平，Hyp含量、TNF-α、IL-1β浓度明显升高（P<0.01）。与TAC组相比，TAC＋阿托伐他汀组和TAC＋缬沙坦组心肌肥厚指数明显改善， LVAWd和LVPWd减小，纤维化面积减小（P均<0.01），NF-κB的蛋白水平，Hyp含量、TNF-α、IL-1β浓度明显下降（P均<0.01）。 　　结论：阿托伐他汀对压力超负荷诱导的心肌肥厚有保护作用，其作用机制可能与抗炎作用有关。
목적：관찰아탁벌타정대소서주동맥궁축착（TAC）술후심실중구적보호작용병탐토기가능궤제。 　　방법：채용주동맥궁축착법건립소서심기비후모형。선취48지C57BL/6소서，수궤분위4조（매조12지）：가수술조、TAC조、TAC＋힐사탄조，TAC＋아탁벌타정조，술후4주성공조모병분별급여생리염수、힐사탄（5 mg/kg）、아탁벌타정（10 mg/kg）처리。8주후진행초성심동도검사，측량좌심실서장기전벽후도（LVAWd），좌심실서장기후벽후도（LVPWd），좌심실사혈분수（LVEF）급단축축단솔（FS），계산심기비후지수。응용면역단백인적（Western blot）법검측핵전록인자-κB （NF-κB）적단백표체수평。감수해법검측심기조직간포안산（Hyp）적함량、채용매련면역흡부（ELISA）법검측혈청종류배사인자-α（TNF-α）、백세포개소-1β（IL-1β）적농도。소목소-이홍（HE）염색급마송（Masson）염색방법측정심기효원침적。 　　결과：여가수술조상비，TAC조LVAWd、LVPWd、심기비후지수、심기섬유화면적명현증가（P<0.01），NF-κB적단백수평，Hyp함량、TNF-α、IL-1β농도명현승고（P<0.01）。여TAC조상비，TAC＋아탁벌타정조화TAC＋힐사탄조심기비후지수명현개선， LVAWd화LVPWd감소，섬유화면적감소（P균<0.01），NF-κB적단백수평，Hyp함량、TNF-α、IL-1β농도명현하강（P균<0.01）。 　　결론：아탁벌타정대압력초부하유도적심기비후유보호작용，기작용궤제가능여항염작용유관。
Objective: To observe the protective roll of atorvastatin on post-operative cardiac remodeling induced by transverse aortic constriction (TAC) in experimental mice with its possible mechanism. Methods: A total of 48 C57BL/6 mice were randomly divided into 4 groups: Sham group, TAC group, TAC + valsartan group and TAC + atorvastatin group,n=12 in each group. Myocardial hypertrophy model was successfully established at 4 weeks after the operation, and then the animals were further treated by normal saline, valsartan 5mg/kg and atorvastatin 10mg/kg respectively for 8 weeks. Left ventricular anterior wall thickness at diastole (LVAWd), left ventricular posterior wall thickness at diastole (LVPWd), LVEF and left ventricular fractional shortening (FS) were examined by echocardiography, cardiac hypertrophy indexes were calculated. Protein expression of NF-κB was detected by Western blot analysis, cardiac tissue hydroxyproline (Hyp) level was measured by alkaline hydrolysis, serum levels of TNF-α, IL-1β were determined by ELISA, cardiac collagen deposition was identiifed by HE and Masson staining. Results: Compared with Sham group, TAC group had increased LVAWd, LVPWd, cardiac hypertrophy indexes and increased area of cardiac fibrosis, allP<0.01; elevated protein expressions of NF-κB, Hyp, TNF-α, IL-1β, all P<0.01. Compared with TAC group, TAC + valsartan group and TAC + atorvastatin group presented improved cardiac hypertrophy indexes, decreased LVAWd, LVPWd and decreased area of cardiac ifbrosis, allP<0.01; reduced protein expressions of NF-κB, Hyp, TNF-α, IL-1β, allP<0.01. Conclusion: Atorvastatin had protective roll on myocardial hypertrophy induced by pressure overload in experimental mice, which might be related to its anti-inlfammatory effect.