Chen Luzhu, Li Rong, Huang Xiansheng
Department of Cardiovascular Medicine, Second Xiangya Hospital, Central South University, Changsha 410011, China.
Department of Stomatology, Second Xiangya Hospital, Central South University, Changsha 410011, China.
Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2017 Jul 28;42(7):790-795. doi: 10.11817/j.issn.1672-7347.2017.07.008.
To investigate the effect of acute myocardial infarction (AMI)-activated inflammation on adipokine imbalance and the therapeutic effects of statin. Methods: A total of 32 C57BL/6 mice were divided into 4 groups: a sham group, an AMI group, a low-dose atorvastatin [2 mg/(kg.d)] group and a high-dose atorvastatin [20 mg/(kg.d)] group. AMI models were established by surgical coronary artery ligation. Plasma levels of high sensitive C reaction protein (hs-CRP), adiponectin and resistin were measured. Adiponectin and resistin expressions were determined. In addition, mouse 3T3-L1 preadipocytes in vitro were differentiated and they were stimulated by oxidized low density lipoprotein (ox-LDL). The protein expressions of adiponectin and resistin in adipocytes were detected. The effects of atorvastatin on ox-LDL-induced adipokine imbalance in adipocytes were identified. Results: The plasma levels of hs-CRP and resistin in AMI mice were significantly increased, whereas the plasma levels of adiponectin were remarkably decreased. However, atorvastatin treatment blocked the changes in the plasma levels of hs-CRP, resistin and adiponectin in AMI mice in a dose-dependent manner. Consistent findings regarding the adipose expressions of the two adipokines were obtained. The plasma levels of hs-CRP were positively correlated with resistin but negatively with adiponectin. In vitro study, ox-LDL increased resistin protein and adiponectin expressions in adipocytes, which were dose-dependently reversed by atorvastatin. Conclusion: Inflammation activation in AMI mice leads to adipokine imbalance. Atorvastatin ameliorates the AMI-induced adipokine imbalance via anti-inflammation.
探讨急性心肌梗死（AMI）激活的炎症对脂肪因子失衡的影响及他汀类药物的治疗作用。方法：将32只C57BL/6小鼠分为4组：假手术组、AMI组、低剂量阿托伐他汀[2mg/（kg·d）]组和高剂量阿托伐他汀[20mg/（kg·d）]组。通过外科冠状动脉结扎建立AMI模型。检测血浆高敏C反应蛋白（hs-CRP）、脂联素和抵抗素水平。测定脂联素和抵抗素表达。此外，体外分化小鼠3T3-L1前脂肪细胞，并用氧化低密度脂蛋白（ox-LDL）刺激。检测脂肪细胞中脂联素和抵抗素的蛋白表达。确定阿托伐他汀对ox-LDL诱导的脂肪细胞脂肪因子失衡的影响。结果：AMI小鼠血浆hs-CRP和抵抗素水平显著升高，而血浆脂联素水平显著降低。然而，阿托伐他汀治疗以剂量依赖方式阻断了AMI小鼠血浆hs-CRP、抵抗素和脂联素水平的变化。在两种脂肪因子的脂肪表达方面也得到了一致的结果。血浆hs-CRP水平与抵抗素呈正相关，与脂联素呈负相关。体外研究中，ox-LDL增加了脂肪细胞中抵抗素蛋白和脂联素表达，阿托伐他汀可剂量依赖性逆转这些变化。结论：AMI小鼠炎症激活导致脂肪因子失衡。阿托伐他汀通过抗炎改善AMI诱导的脂肪因子失衡。
