目的 探討注射用益氣復脈（凍干，YQFM）對阿霉素（doxorubicin，DOX）誘導H9c2（2-1）心肌細胞毒性的保護作用。方法 H9c2（2-1）心肌細胞隨機分為對照組，模型組（終濃度為0.3 μmol/L的DOX處理細胞48 h），YQFM低、中、高劑量（125、625、3 125 μg/mL）組（提前2 h加入藥物預處理，然后加入終濃度為0.3 μmol/L的DOX處理48 h），采用CCK-8法檢測細胞活力；使用乳酸脫氫酶（LDH）和ATP試劑盒檢測細胞LDH和ATP水平；應用Hoechst 33258染色法檢測細胞凋亡；JC-1法檢測細胞線粒體膜電位；Western blotting法檢測caspase-3蛋白的表達水平。結果 與模型組比較，YQFM中、高劑量組顯著增加細胞存活率（P<0.05、0.01），低、高劑量組明顯改善細胞凋亡；低、中、高劑量組LDH活性顯著降低（P<0.05、0.01），ATP含量顯著增加（P<0.05、0.01），線粒體膜電位明顯恢復。結論 YQFM抑制DOX誘導H9c2（2-1）的細胞毒性，其作用機制可能與抑制線粒體凋亡信號通路的激活有關。

Objective To investigate the protective effect of Yiqi Fumai Lyophilized Injection (YQFM) against Doxorubicin (Dox)-induced cardiotoxicity in H9c2 (2-1). Methods H9c2 (2-1) myocardial cells were randomly divided into control group, model group (cells treated with DOX at the final concentration of 0.3 μmol/L for 48 h), YQFM low, medium and high dose (125, 625, and 3 125 g/mL) group (pretreatment with YQFM for 2 h, and then adding DOX of a final concentration of 0.3 μmol/L). Cell viability was detected with CCK-8 assay. Cells LDH and ATP levels were examined using LDH and ATP kits. Cell death was measured by Hoechst 33258 stain assay. The mitochondrial membrane potential was detected by JC-1. Caspase-3 protein expression was evaluated by Western blotting. Results Compared with model group, YQFM medium and high dose group significantly increased the cell survival rate (P < 0.05 and 0.01), low and high dose group significantly improved cell apoptosis; LDH activity of low, medium and high dose group was significantly decreased (P < 0.05 and 0.01), ATP content increased significantly (P < 0.05 and 0.01), and the mitochondrial membrane potential was restored. Conclusion YQFM inhibited DOX-induced cardiotoxicity in H9c2 (2-1), the possible mechanisms may be related to the inhibition of activation of mitochondrial apoptotic signaling pathway.

天津市中藥注射劑關鍵技術校企協(xié)同創(chuàng)新實驗室建設基金（17PTSYJC00090）