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目的:研究灯盏花乙素对超氧阴离子引起的大鼠脑突触体氧化应激的保护作用。方法:采用与黄嘌呤(0.3mmol/L)和黄嘌呤氧化酶(0.02U)体系在37℃下孵育30min,建立大鼠脑突触体超氧阴离子氧化损伤模型,通过测定脂质过氧化产物丙二醛评价脂质过氧化程度,通过脂溶性荧光探针DPH的各向异性判断突触体膜的流动性,胞内钙离子的测定采用荧光光度法,以Fura 2-AM为荧光探针,测定ATP酶解释放的无机磷确定Na~+/K~+-ATP酶的活性。结果:超氧阴离子使大鼠脑突触体的脂质过氧化产物丙二醛及胞内钙离了浓度显著上升,突触体的膜流动性和Na~+/K~+-ATP酶的活性则显著下降,预先加入灯盏花乙素(25-100μmol/L)则能显著缓解超氧阴离子引起的氧化性损伤,表现为丙二醛的水平和胞内钙离子浓度下降,膜流动性增加及Na~+/K~--ATP酶活性的恢复。结论:灯盏花乙素对超氧阴离子引起的大鼠脑突触体氧化应激具有良好的保护作用。
Objective: To study the protective effect of scutellarin on oxidative stress induced by superoxide anion in rat brain synaptosomes. METHODS: Rat brain synaptosomal superoxide anion oxidative damage model was established by incubating with xanthine (0.3 mmol/L) and xanthine oxidase (0.02 U) system at 37°C for 30 min. Malondialdehyde was used to evaluate the degree of lipid peroxidation. The fluidity of the synaptosome membrane was determined by the anisotropy of lipid-soluble fluorescent probe DPH. The intracellular calcium ion was measured by fluorescence spectrometry, and Fura 2-AM was used as the fluorescent probe. , Determination of ATP enzyme explained release of inorganic phosphorus determined Na~+/K~+-ATPase activity. RESULTS: Superoxide anion increased the lipid peroxidation product malondialdehyde and intracellular calcium concentration of rat brain synaptosomes significantly, and the membrane fluidity of the synaptosomes and the Na~+/K~+-ATPase. The activity was significantly decreased. Pretreatment with scutellarin (25-100 μmol/L) significantly alleviated the oxidative damage caused by superoxide anion, showing decreased levels of malondialdehyde, decreased intracellular calcium concentration, and increased membrane fluidity. Recovery of Na~+/K~-ATPase activity. Conclusion: Scutellarin has a good protective effect on oxidative stress of rat brain synaptosomes induced by superoxide anion.