Therapeutic adaptation of cardiac expression of adiponectin

脂联素心脏表达的治疗适应

• 批准号: 17590767
• 负责人: KANDA Tsugiyasu
• 金额: $ 2.3万
• 依托单位: Kanazawa Medical University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2005
• 资助国家: 日本
• 起止时间: 2005 至 2006
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-17590767/
• 关键词: angiotensin II receptor; myocarditis; adiponectin; obesity; heart failure; in situ hybridization; 心筋肥大; 心筋; 再生; 心筋炎

Purpose.We examined the effects of the angiotensin II receptor type1 blocker, candesartan, on myocarditis injury in a murine model of acute myocarditis. We hypothesized that candesartan improves cardiac damage by inducing cardiac expression of adiponectin.Methods and Results.We examined changes in heart failure caused by myocarditis in mice by candesartan based on induction of cardiac adiponectin expression. We intraperitoneally injected encephalomyocarditis virus in C3H mice then treated them with oral administration of candesartan (10 mg/kg/day candesartan) or vehicle (Control). The 7 day survival rate was 18% in the Control group, but 60% in the Candesartan group. The heart weight/body weight ratio in the Candesartan group was significantly lower than in the Control group. Circulating adiponectin concentrations on day 7 were significantly higher in the Candesartan group compared with Control group (7.91± 0.61 vs. 6.04±2.26.μ g/ml, P<0.05). Comparative expression of cardiac adiponectin mRNA in the Candesartan group was significantly higher than in the Control group on day 7 (55.4 ± 41.3 vs. 5.3 ± 7.7, P<0.05). Immunohistochemical staining and in situ hybridization showed that cardiac expression of adiponectin protein and mRNA was present in the Candesartan group on day 7.Conclusion.Oral administration of canndesartan improves survival and decreases myocardial damage in mice with viral myocarditits and induces expression of cardiac adiponectin. The induction of adiponectin might provide cardioprotective effects against acute heart failure due to viral myocarditis.

目的：我们检测了血管紧张素II受体1型阻断剂坎地沙坦对急性心肌炎小鼠模型心肌炎损伤的影响。我们假设坎地沙坦通过诱导心脏脂联素表达来改善心脏损伤。方法和结果：我们研究了坎地沙坦诱导心脏脂联素表达的基础上，在小鼠心肌炎引起的心力衰竭的变化。我们在C3 H小鼠中腹膜内注射脑心肌炎病毒，然后经口给予坎地沙坦（10 mg/kg/天坎地沙坦）或溶剂（对照）对其进行治疗。对照组7天生存率为18%，坎地沙坦组为60%。坎地沙坦组的心脏重量/体重比显著低于对照组。坎地沙坦组第7天循环脂联素浓度显著高于对照组（7.91± 0.61 vs.6.04 ±2.26 μ g/ml，P<0.05）。心肌脂联素mRNA的相对表达量在第7天坎地沙坦组显著高于对照组（55.4 ± 41.3vs.5.3 ± 7.7，P<0.05）。免疫组织化学染色和原位杂交显示，坎地沙坦组心肌脂联素蛋白和mRNA在第7天开始表达。结论：坎地沙坦可提高病毒性心肌炎小鼠的存活率，减轻心肌损伤，并诱导心肌脂联素的表达。脂联素的诱导可能对病毒性心肌炎引起的急性心力衰竭提供心脏保护作用。

项目成果

Impaired expression of cardiac adiponectin in leptin-deficient mice with viral myocarditis.

• DOI: 10.1536/ihj.47.107
• 发表时间: 2006
• 期刊: International heart journal
• 影响因子: 1.5
• 作者: Takashi Takahashi;F. Yu;S. Saegusa;H. Sumino;T. Nakahashi;K. Iwai;S. Morimoto;M. Kurabayashi;T. Kanda

Beneficial effect of brewers7 yeast extract on daily activity in a murine model of chronic fatigue syndrome

Brewers7 酵母提取物对慢性疲劳综合症小鼠模型日常活动的有益影响

• 发表时间: 2006
• 期刊: eCAM 3・1
• 作者: Takahashi T;et al.
• 通讯作者: et al.

Adiponectin, T-cadherin and tumour necrosis factor-alpha in damaged cardiomyocytes from autopsy specimens.

尸检标本中受损心肌细胞中的脂联素、T-钙粘蛋白和肿瘤坏死因子-α。

• 发表时间: 2005
• 期刊: J. Int. Med. Res 33(2)
• 作者: Zheng M;Uchino T;Takebayashi S;Kaku T;Wang Y;Ono K;Sakai M;T.Takahashi
• 通讯作者: T.Takahashi

Reduced-Energy Diet Improves Survival of Obese KKAy Mice with Viral Myocarditis: Induction of Cardiac Adiponectin Expression

低能量饮食可改善患有病毒性心肌炎的肥胖 KKAy 小鼠的存活率：诱导心脏脂联素表达

• 发表时间: 2007
• 期刊: Int J Cardiol 119(3)
• 作者: Chen R;Moriya J;Yamakawa JI;Takahashi T;Kanda T.;竹原 有史;T Kanda.
• 通讯作者: T Kanda.

Adiponectin Replacement Therapy Attenuates Myocardial Damage in Leptin-deficient Mice with Viral Myocarditis

• DOI: 10.1177/147323000503300208
• 发表时间: 2005-03
• 期刊: Journal of International Medical Research
• 影响因子: 1.6
• 作者: T. Takahashi;S. Saegusa;H. Sumino;T. Nakahashi;K. Iwai;S. Morimoto;T. Kanda