中文摘要：

目的研究环维黄杨星D（cyclovirobuxineD，Cvb．D）对阿霉素（doxorubicin，DOX）所致小鼠心脏毒性的影响。方法52只C57小鼠分为4组（n：12）：正常对照组（Contr01）、Cvb．D组、DOX组和Cvb．D＋DOX组，每天灌胃给予Cvb—D（1mg／kg）或生理盐水，连续给药4d，第5天单次腹腔注射DOX（15mekg）或生理盐水。心肌组织切片进行Masson’S染色，光镜下观察各组小鼠心肌组织纤维化改变；测定血清乳酸脱氢酶（LDH）、肌酸激酶（CK）水平及组织Caspase-3活性；采用末端标记TUNEL法检测各组心肌细胞凋亡情况；利用Westernblot法检测Bcl-2和Bax蛋白表达水平及其比值。结果与正常对照组相比，Cvb—D预处理可明显抑制DOX引起的体质量下降（P〈0．05）以及心肌纤维化等组织形态学改变，显著抑制DOX引起的LDH、CK及Caspase-3活性升高（P〈0．05），缓解DOX引起的心肌细胞凋亡，并显著提高DOX诱导的Bcl-2／Bax蛋白表达比值降低（P〈0．05）。结论Cvb．D对DOX心脏毒性具有保护作用，并能够改善DOX引起的细胞凋亡。

英文摘要：

Objective To observe the effect of cyclovirobuxine D （Cvb-D） on mice suffered from doxorubicin （DOX）-induced cardiotoxicity. Methods Adult C57 mice were randomly divided into four groups （n = 12） including a control group, a Cvb-D group, a DOX group and a Cvb-D ＋ DOX group. Mice were given Cvb-D （1 mg/kg） intragastrically once a day for 4 consecutive days, followed by a single intraper- itoneal injection of DOX （15 mg/kg） or saline, and the body weight was recorded thereafter. Four days later, the serum levels of creatine kinase （CK） and lactate dehydrogenase （LDH） and the activity of myocardial caspase-3 were determined, and cardiac tissue sections were stained with Masson＇ s trichrome to observe the morphology of myoeardium. Apoptotie cells in cardiac tissues were observed by TUNEL assay. The protein expression levels of Bcl-2 and Bax were determined by Western blotting, and the ratio of Bcl-2/Bax was calcu- lated. Results Cvb-D administered alone had no obvious effect on mice as compared with the control group. Pretreatment with Cvb-D significantly rescued DOX-induced decrease of body weight in mice （P 〈 0.05）, and alleviated myocardial fibrosis. Cvb-D significantly inhibited DOX-induced increase in serum levels of LDH and CK and caspase-3 activity （P 〈 0. 05 ） in cardiac tissues, and relieved DOX-induced myocardial apoptosis. Cvb-D also improved the ratio of Bcl-2/Bax expression decreased by DOX. Conclusion Cvb-D has a protec- tive effect against DOX-induced cardiotoxicity possibly by inhibiting cell apoptosis.