刺五加皂苷改善过氧化氢诱导的新生大鼠心肌细胞氧化损伤

Liang Qiming, Qu Shaochun, Yu Xiaofeng, Xu Huali, Sui Dayun

Department of Pharmacology, School of Pharmaceutical Sciences, Jilin University, Changchun 130021, China.

Zhongguo Zhong Yao Za Zhi. 2009 Oct;34(19):2489-93.

OBJECTIVE

To investigate the effect of Acanthopanax senticosus saponins (ASS) on oxidative damage induced by hydrogen peroxide (H2O2 ) in cardiomyocytes.

METHOD

The cardiomyocytes were induced to oxidative damaged by exposed to H2O2. We evaluated the level of oxidative injury through morphology change, the survival rate, the activity of lactate dehydrogenase (LDH) and the content of cellular malondialdehyde (MDA). The activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and the content of reductive glutathione (GSH) of cardiomyocytes were also determined.

RESULT

When the cardiomyocytes were exposed to H2O, (50, 100, 200 micromol x L(-1)) for deigned time, the percentage of survival cells was down significantly (P < 0.01 or P < 0.001), and the activity of LDH and the content of MDA were increased markedly (P < 0.05, P < 0.01 or P < 0.001). These results show that the cells were subjected to oxidative damage. Treatment with ASS (600 mg x L(-1)) prior to H2O2 exposure could increase cell viability significantly, lessen cardiomyocyte morphological damaged change, and decrease LDH activity (1687.40 +/- 97.51) U x mL(-1) in media and cellular MDA content (16.50 +/- 2.66) nmol x mg(-1) markedly (P < 0.01 and P < 0.05). Furthermore, the activities of SOD (89.55 +/- 6.93) U x mg(-1), GSH-Px (845.87 +/- 63.76) mU x mg(-1), CAT (93.07 +/- 10.40) U x mg(-1) and the content of GSH (8.91 +/- 1.06) micromol x mg(-1) of cardiomyocytes were also raised by 600 mg x L(-1) l ASS (P < 0.05).

CONCLUSION

Taken together, the study implicate that ASS protects cardiomyocytes against oxidative-stress injury induced by H2O2 through reduction of lipid peroxidation and enhancement of the activity of antioxidant defense.

目的

研究刺五加皂苷（ASS）对过氧化氢（H2O2）诱导的心肌细胞氧化损伤的影响。

方法

通过暴露于H2O2诱导心肌细胞发生氧化损伤。我们通过形态学变化、存活率、乳酸脱氢酶（LDH）活性和细胞丙二醛（MDA）含量来评估氧化损伤程度。同时还测定了心肌细胞中超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）、过氧化氢酶（CAT）的活性以及还原型谷胱甘肽（GSH）的含量。

结果

当心肌细胞暴露于不同浓度（50、100、200 μmol·L-1）的H2O2一定时间后，存活细胞百分比显著下降（P < 0.01或P < 0.001），LDH活性和MDA含量显著增加（P < 0.05、P < 0.01或P < 0.001）。这些结果表明细胞受到了氧化损伤。在H2O2暴露前用ASS（600 mg·L-1）处理可显著提高细胞活力，减轻心肌细胞形态损伤变化，并显著降低培养基中LDH活性（1687.40±97.51）U·mL-1和细胞MDA含量（16.50±2.66）nmol·mg-1（P < 0.01和P < 0.05）。此外，600 mg·L-1的ASS还可使心肌细胞中SOD（89.55±6.93）U·mg-1、GSH-Px（845.87±63.76）mU·mg-1、CAT（93.07±10.40）U·mg-1的活性以及GSH（8.91±1.06）μmol·mg-1的含量升高（P < 0.05）。