大蒜多糖对阿霉素所致小鼠心脏毒性的拮抗作用

Inhibitory effect of Garlic Polysaccharide on adriamycin-induced cardiotoxicity in mice

目的研究大蒜多糖(GP)对中毒性心肌炎的拮抗作用并探讨其机制.方法建立小鼠阿霉素(ADR)中毒性心肌炎模型,测定血清、心肌多项生化指标,并观察心肌结构变化.结果 ADR(3 mg·kg-1ip, qod×7)可致小鼠血清肌酸激酶(CK)、乳酸脱氢酶(LDH)、谷草转氨酶(GOT)和诱导型一氧化氮合酶(iNOS)活力升高(P<0.01),同时心肌超氧化物歧化酶(SOD)活力下降而丙二醛(MDA)含量升高(P<0.01),线粒体水肿明显.GP(0.75～3.0 g·kg-1 ig, qd×15)能逆转ADR所致的上述改变,表现为剂量相关性降低血清CK、LDH、GOT 和iNOS活力,增加心肌SOD活力和降低MDA含量,尤其以GP大剂量组作用明显(P<0.05或P<0.01).光镜和电镜结果也证实了GP的保护作用.结论 GP能拮抗阿霉素所致的小鼠中毒性心肌炎,其作用机制与增强心肌SOD活力和抗心肌脂质过氧化有关.

Aim To study the inhibitory effects and its mechanis ms of Garlic Polysaccharide (GP) on adriamycin(ADR)-induced cardiotoxicity in mic e.Mehtod ADR was injected intraperitoneally to induce myocardiu m injury model in mice. The activities of several serum and heart tissue enzymes were measured. With scanning electron microscope, the cardiac ultrastructural c hanges were examined.Results ADR (3 mg·kg -1 ip, qod×7) induced severe myocardial damages with the increasing activities of creatine kin ase (CK), lactate dehydrogenase (LDH), glutamic oxaloacetic transaminase (GOT) a nd inducible nitric oxide synthase (iNOS) (P<0.01). ADR increased myocardia l malondialdehyde (MDA) content, while decreased the superoxide dismutase (SOD) activities (P<0.01). It also caused mitochondrion edema at ultrastructural levels. GP (0.75～3.0 g·kg -1 ig, qd×15) relieved these damages. GP dec reased the activities of serum CK, LDH, GOT and iNOS. It also increased SOD acti vities and depressed MDA content in a dose-dependent manner. Especially, the ex tent of ADR-induced myocardial damage was markedly reduced by high dose of GP ( P<0.05 or P<0.01). The changes of myocardial pathological and ultrastr uctural damages were improved by GP. Conclusion These observati ons highlight the antioxidative property of GP and its cytoprotective action aga inst ADR-induced cardiotoxity.