中国药理学与毒理学杂志
中國藥理學與毒理學雜誌
중국약이학여독이학잡지
CHINESE JOURNAL OF PHARMACOLOGY AND TOXICOLOGY
2010年
1期
69-72
,共4页
钱为国%严文华%吕海涛%孙凌
錢為國%嚴文華%呂海濤%孫凌
전위국%엄문화%려해도%손릉
褪黑素%多柔比星%心肌疾病%NF-κB%一氧化氮%一氧化氮合酶%细胞凋亡
褪黑素%多柔比星%心肌疾病%NF-κB%一氧化氮%一氧化氮閤酶%細胞凋亡
퇴흑소%다유비성%심기질병%NF-κB%일양화담%일양화담합매%세포조망
melatonin%doxorubicin%cardiomyopathies%NF-κB%nitric oxide%nitric oxide synthase%apoptosis
目的 探讨NF-κB在多柔比星(Dox)心肌病中的作用及褪黑素(MT)的干预作用.方法 30只雄性SD大鼠随机分为正常对照组、Dox模型组、Dox+MT组.免疫组织化学法检测NF-κB的活性,分光光密度法检测心肌组织中一氧化氮(NO)含量和诱导型一氧化氮合酶(iNOS)活性,TUNEL法检测心肌细胞凋亡.结果 与正常对照组相比,NF-κB在Dox模型组显著活化,MT可抑制NF-κB的激活(P<0.05);与正常对照组相比,Dox组NO含量、iNOS活性和心肌细胞凋亡率显著升高(P<0.05),MT干预后均显著降低.结论 NF-κB参与心肌氧化应激损伤,促进心肌细胞凋亡.MT可抑制NF-κB活化,减少自由基的生成,抑制心肌细胞凋亡,对Dox心肌病具有保护作用.
目的 探討NF-κB在多柔比星(Dox)心肌病中的作用及褪黑素(MT)的榦預作用.方法 30隻雄性SD大鼠隨機分為正常對照組、Dox模型組、Dox+MT組.免疫組織化學法檢測NF-κB的活性,分光光密度法檢測心肌組織中一氧化氮(NO)含量和誘導型一氧化氮閤酶(iNOS)活性,TUNEL法檢測心肌細胞凋亡.結果 與正常對照組相比,NF-κB在Dox模型組顯著活化,MT可抑製NF-κB的激活(P<0.05);與正常對照組相比,Dox組NO含量、iNOS活性和心肌細胞凋亡率顯著升高(P<0.05),MT榦預後均顯著降低.結論 NF-κB參與心肌氧化應激損傷,促進心肌細胞凋亡.MT可抑製NF-κB活化,減少自由基的生成,抑製心肌細胞凋亡,對Dox心肌病具有保護作用.
목적 탐토NF-κB재다유비성(Dox)심기병중적작용급퇴흑소(MT)적간예작용.방법 30지웅성SD대서수궤분위정상대조조、Dox모형조、Dox+MT조.면역조직화학법검측NF-κB적활성,분광광밀도법검측심기조직중일양화담(NO)함량화유도형일양화담합매(iNOS)활성,TUNEL법검측심기세포조망.결과 여정상대조조상비,NF-κB재Dox모형조현저활화,MT가억제NF-κB적격활(P<0.05);여정상대조조상비,Dox조NO함량、iNOS활성화심기세포조망솔현저승고(P<0.05),MT간예후균현저강저.결론 NF-κB삼여심기양화응격손상,촉진심기세포조망.MT가억제NF-κB활화,감소자유기적생성,억제심기세포조망,대Dox심기병구유보호작용.
OBJECTIVE To investigate the effect of NF-κB on cardiomyopathy induced by doxorubicin(Dox) in rats and the effect of melatonin(MT). METHODS Thirty male Sprague-Dawley rats were randomly divided into 3 groups: normal control group; Dox model group; Dox+MT group. The content of nitric oxide (NO) and the activity of inducible nitric oxide synthase (iNOS) in cardiac tissues were examined by spectrophotography method; the activity of NF-κB in myocardial cell was observed by immunohistochemistry method; the apoptosis information of myocardial cell was detected by TUNEL method. RESULTS There was significant difference in activity of NF-κB between normal control and the Dox model group. MT could inhibit the activation of NF-κB(P＜0.05). There was significant difference in the content of NO and the activity of iNOS between normal control and Dox model group, MT could decrease content of NO and the activity of iNOS(P＜0.05); apoptotic rate in Dox model group was significantly increased compared with that in normal control group, MT could significantly decrease myocardial cell apoptosis (P＜0.05). CONCLUSION The activation of NF-κB plays an important role in cardiomyopathy induced by Dox, NF-κB seems to increase the activity of iNOS, and then significantly increase the content of NO in cardiac muscle; NF-κB possibly enhances myocardial cell apoptosis in cardiomyopathy induced by Dox. MT may inhibit the activation of NF-κB, and prevent excessive oxidative stress and suppress myocardial cell apoptosis, MT has protective effect against cardiomyopathy induced by Dox.
