摘要
目的:探究高良姜素(galangin)对压力负荷诱导的心脏纤维化的影响。方法:32只C57小鼠随机分成4组:假手术组、高良姜素组、主动脉缩窄组、主动脉缩窄+高良姜素组。主动脉缩窄术(AB)后4周,分别记录心重、体质量和血流动力学变化;天狼猩红染色(PSR)评价心脏纤维化程度;实时荧光定量PCR(qPCR)检测纤维化标志物的mRNA水平;Western Blot检测相关信号通路的变化;试剂盒检测心脏组织中超氧化物歧化酶(SOD)活性和过氧化氢酶(CAT)活性。结果:AB后4周,高良姜素明显减轻压力负荷诱导的心肌肥厚(P<0.05)、血流动力学紊乱(P<0.05)和纤维化程度(P<0.05)。主动脉缩窄+高良姜素组的胶原Ⅰ、胶原Ⅲ、结缔组织生长因子(CTGF)和转化生长因子β(TGFβ1)mRNA明显低于主动脉缩窄组(P<0.05)。主动脉缩窄+高良姜素组核因子E2相关因子2(Nrf2)、血红素氧合酶1(HO-1)、Kelch样环氧氯丙胺相关蛋白1(Keap1)、SOD和CAT活性明显高于主动脉缩窄组(P<0.05)。结论:高良姜素能明显减轻压力负荷诱导的心脏纤维化,其机制可能与氧化应激有关。
Objectives:To study the effect of galangin on pressure overload induced cardiac fibrosis in mice.Methods:Thirty-two C57 mice were randomly divided into four groups,including the sham operation group,the galangin group,the aortic banding(AB)group,and the AB+galangin group.Four weeks after surgery,the heart weight,body weight and hemodynamic changes were measured respectively.Picrosirius red(PSR)staining was performed to assess the degree of cardiac fibrosis.Real-time quantitative PCR(qPCR)was carried out to determinate the mRNA levels of fibrosis markers.The changes of relative pathways were detected by Western Blot.The activities of superoxide dismutase(SOD)and catalase(CAT)in heart were measured by relative kits respectively.Results:Four weeks after AB,galangin obviously mitigated the pressure overload induced cardiac hypertrophy(P<0.05),hemodynamic disorder(P<0.05),and fibrosis in AB+galangin group(P<0.05).The results of qPCR showed that the mRNA levels of collagenⅠ,collagenⅢ,connective tissue growth factor(CTGF)and transforming growth factorβ1(TGFβ1)were significantly lower in AB+galangin group as compared with AB group(all P<0.05).The results of Western Blot suggested that galangin could alleviate AB induced oxidative stress,characterized by a higher levels of nuclear factor-E2-related factor 2(Nrf2),heme oxygenase-1(HO-1),and Kelch-like ECH-associated protein 1(Keap1)in AB+galangin group as compared with AB group(P<0.05).Conclusion:Galangin apparently alleviates the pressure overload induced cardiac fibrosis,and the mechanism might be relate to oxidative stress.
作者
杨晶晶
王辉波
廖海含
吴海明
唐其柱
YANG Jingjing;WANG Huibo;LIAO Haihan;WU Haiming;TANG Qizhu(Dept.of Cardiology,Renmin Hospital of Wuhan University,Wuhan 430060,Hubei,China;Hubei Key Laboratory of Metabolic and Chronic Diseases,Wuhan 430060,Hubei,China)
出处
《武汉大学学报（医学版）》
CAS
2020年第6期889-893,共5页
Medical Journal of Wuhan University
基金
国家自然科学基金重点项目(编号:81530012)
国家重点研发计划资助(编号:2018YFC1311300)
作者简介
杨晶晶,男,1993-,医学硕士生,主要从事心血管疾病的研究,E⁃mail:yangjingjing@whu.edu.cn;通讯作者:唐其柱,男,1963-,医学博士,主任医师,教授,主要从事心血管及慢性疾病的研究,E⁃mail:qztang@whu.edu.cn
