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目的:研究北虫草小分子肽影响大鼠心肌细胞线粒体生物酶活性的作用机制,为北虫草的进一步提升利用提供科学的理论和实验依据。方法:建立大鼠心肌细胞线粒体H_2O_2/Fe~(2+)自由基生成损伤模型,采用紫外分光度计法测定细胞色素C氧化酶(CCO)与超氧化物岐化酶(SOD)活力,化学分析法检测ATP酶和磷脂酶A2(PLA2)活力。结果:与对照组比较,CCO和ATPase活力:H_2O_2/Fe~(2+)损伤组和小分子肽组分别为[(10.33±3.76)、(21.49±3.18)和(18.90±4.51)、(37.64±2.33)与(22.64±4.47)和(40.17±4.12)];PLA2和SOD活力:H_2O_2/Fe~(2+)损伤组和小分子肽组分别为[(98.48±27.6)、(30.02±3.44)和(18.78±14.61)、(35.04±2.11)与(22.84±12.26)、(37.82±3.82)];差异性显著,P<0.05。结论:在大鼠心肌细胞线粒体H_2O_2/Fe~(2+)自由基生成损伤模型中,北虫草蛋白源小分子肽能够降低H_2O_2和金属离子对酶系的损伤,提高CCO、ATPase和SOD活力,保护线粒体膜结构、呼吸链电子传递系统和氧化磷酸化体系等生物功能的完整性。
OBJECTIVE: To study the mechanism of action of Cordyceps small peptide on myocardial mitochondrial enzyme activity in rat myocardial cells, and provide scientific theoretical and experimental basis for the further promotion and utilization of Cordyceps militaris. Methods: The model of mitochondrial H 2 O 2 / Fe 2+ production in rat myocardial cells was established. The activity of cytochrome C oxidase (CCO) and superoxide dismutase (SOD) were measured by ultraviolet spectrophotometer. The chemical The ATPase and phospholipase A2 (PLA2) activities were assayed by the assay. RESULTS: Compared with the control group, the activities of CCO and ATPase in H 2 O 2 / Fe 2+ group and small peptide group were (10.33 ± 3.76), (21.49 ± 3.18) and (18.90 ± 4.51) and (37.64 ± 2.33) and (22.64 ± 4.47) and (40.17 ± 4.12) respectively. The activity of PLA2 and SOD in the H 2 O 2 / Fe 2+ group and the small peptide group were (98.48 ± 27.6) and (30.02 ± 3.44 ) And (18.78 ± 14.61), (35.04 ± 2.11) and (22.84 ± 12.26) and (37.82 ± 3.82) respectively. The difference was significant (P <0.05). CONCLUSION: In the mitochondrial H 2 O 2 / Fe 2+ free radical generation injury model of rat myocardial cells, small molecule peptides from Cordyceps militaris can reduce the damage of enzymes and increase the activity of CCO, ATPase and SOD by H 2 O 2 and metal ions, Protects the integrity of biological functions such as mitochondrial membrane structure, respiratory chain electron transport system and oxidative phosphorylation system.