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目的:观察藁本内酯对H_2O_2诱导的B16黑素瘤细胞氧化损伤的保护作用并探讨其可能机制。方法:以H_2O_2诱导B16黑素瘤细胞氧化损伤为模型,并以藁本内酯进行干预,采用MTT法测细胞活力,酶标仪检测乳酸脱氢酶(LDH)漏出量,流式细胞术测细胞凋亡率、线粒体膜电位(△Ψm)和细胞内游离钙离子浓度。结果:与H_2O_2诱导的B16黑素瘤细胞比较,应用藁本内酯(5、10、20μmol·L~(-1))处理的B16黑素瘤细胞活力和△Ψm明显提高,LDH漏出量明显减少,细胞凋亡率和细胞内游离钙离子浓度明显降低,差异均具有统计学意义(P<0.05)。结论:藁本内酯对H_2O_2诱导的B16黑素瘤细胞氧化损伤具有保护作用,其作用机制可能通过恢复线粒体功能、抑制细胞凋亡有关。
OBJECTIVE: To observe the protective effect of ligustilide against oxidative damage of B16 melanoma cells induced by H 2 O 2 and its possible mechanism. Methods: Oxidative damage of B16 melanoma cells was induced by H2O2 and ligustilide was used as a model. Cell viability was measured by MTT assay. LDH leakage was detected by microplate reader. Flow cytometry Apoptosis rate, mitochondrial membrane potential (△ Ψm) and intracellular free calcium concentration. Results: Compared with H 2 O 2 -induced B16 melanoma cells, the viability and △ ψm of B16 melanoma cells treated with ligustilide (5, 10 and 20 μmol·L -1) were significantly increased, and the leakage of LDH was significantly Decrease, apoptosis rate and intracellular free calcium concentration were significantly decreased, the differences were statistically significant (P <0.05). CONCLUSION: ligustilide can protect H 2 O 2 -induced B16 melanoma cells from oxidative damage, and its mechanism may be related to the restoration of mitochondrial function and inhibition of apoptosis.