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目的:研究蝎毒纤溶活性肽(SVFAPs)对大鼠神经元低糖低氧/复氧损伤的影响,探讨药物发挥神经保护作用的可能机制。方法:建立原代培养的大鼠皮层神经元的低糖低氧/复氧(OGD/R)模型,采用四唑蓝(MTT)法和乳酸脱氢酶(LDH)释放法检测细胞活力;检测细胞上清液中丙二醛(MDA)和一氧化氮(NO)含量、超氧化物歧化酶(SOD)活性;Hoechst染色和DNA片段法检测细胞凋亡;W estern b lot法检测PARP蛋白的表达。结果:经OGD/R损伤后细胞活力明显下降,细胞上清液中MDA、NO升高,SOD降低;出现凋亡典型的形态学特征,PARP蛋白表达下降;蝎毒纤溶活性肽(2～8mg/L)可不同程度提高低糖低氧/复氧后神经元的活力,降低细胞上清液MDA和NO含量,提高SOD活性。改善凋亡相关的细胞核形态学改变,并且减少凋亡特征性DNA片段化的发生,降低细胞凋亡率,保持PARP的完整性。结论:蝎毒纤溶活性肽对低糖低氧/复氧损伤的神经元具有保护作用,其机制可能与抗氧化和减轻细胞凋亡有关。
Objective: To investigate the effects of scorpion venom fibrinolytic active peptides (SVFAPs) on neuronal hypoxia / reoxygenation injury in rats and to explore the possible mechanisms by which drugs can exert neuroprotective effects. Methods: Primary hypoxic hypoxia / reoxygenation (OGD / R) model of rat cortical neurons was established. Cell viability was measured by MTT assay and LDH release assay. The content of malondialdehyde (MDA) and nitric oxide (NO) and the activity of superoxide dismutase (SOD) in the supernatant were measured. The apoptosis of cells was detected by Hoechst staining and DNA fragmentation. The expression of PARP protein was detected by Western blot . Results: The viability of cells after OGD / R injury was significantly decreased, the content of MDA and NO in the supernatant of the cells increased, and the content of SOD decreased. The morphological features of apoptosis were typical and the expression of PARP protein was decreased. 8mg / L) could increase the activity of neurons in hypoxia / hypoxia / reoxygenation groups to a certain extent, reduce the content of MDA and NO in cell supernatant and increase the activity of SOD. Improve apoptosis-related nuclear morphological changes, and reduce the occurrence of apoptotic DNA fragmentation, reduce the rate of apoptosis and maintain the integrity of PARP. CONCLUSION: Scorpion venom fibrinolytic active peptide can protect neurons from hypoxia / reoxygenation hypoxia injury, and its mechanism may be related to anti-oxidation and reducing apoptosis.