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首页> 外文期刊>Biochemical Pharmacology >Dietary polyphenols protect dopamine neurons from oxidative insults and apoptosis: investigations in primary rat mesencephalic cultures.
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Dietary polyphenols protect dopamine neurons from oxidative insults and apoptosis: investigations in primary rat mesencephalic cultures.

机译：饮食中的多酚可保护多巴胺神经元免受氧化损伤和细胞凋亡：在原代大鼠中脑培养物中的研究。

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摘要

Naturally occurring polyphenols have the potential to prevent oxidative damage in various pathophysiological conditions. Various members of the flavonoid family were investigated to determine if they could protect mesencephalic dopamine (DA) neurones from injury and reduce apoptosis produced by oxidative stressors. Primary mesencephalic cultures were sensitive to oxidative insults (hydrogen peroxide, 4-hydroxynonenal, rotenone, 6-hydroxydopamine and N-methyl-4-phenyl-1,2,3,6-tetrahydropyridinium hydrochloride (MPP(+))) which produced concentration-dependent decreases in cellular viability across an apoptotic-necrotic continuum of injury. Flavonoids (catechin, quercetin, chrysin, puerarin, naringenin, genestein) protected mesencephalic cultures from injury by MPP(+), which was shown by DNA fragmentation studies and tyrosine hydroxylase (TH) immunocytochemistry of DA neurones to occur by apoptosis. Catechin also reduced injury produced by hydrogen peroxide, 4-hydroxynonenal, rotenone and 6-hydroxydopamine as shown by increases in cellular viability and [(3)H]DA uptake. When the neuroprotection of catechin against MPP(+)-induced injury was compared to that produced by the caspase-3 inhibitor, Z-DVED-FMK, both reduced DNA fragmentation and the injury patterns of TH-positive neurones. These data demonstrate the neuroprotective abilities of flavonoids which are able to attenuate the apoptotic injury of mesencephalic DA neurones. Since these DA neurones are under oxidative stress in Parkinsonism, our findings suggest that flavonoids could provide benefits along with other anti-oxidant therapies in Parkinson's disease.
机译：天然存在的多酚具有在各种病理生理条件下防止氧化损伤的潜力。研究了类黄酮家族的各种成员，以确定它们是否可以保护中脑多巴胺（DA）神经元免受损伤并减少氧化应激源产生的细胞凋亡。原发性中脑培养对氧化损伤（过氧化氢，4-羟基壬醛，鱼藤酮，6-羟基多巴胺和N-甲基-4-苯基-1,2,3,6-四氢吡啶鎓盐酸盐（MPP（+）））敏感凋亡的坏死连续性损伤过程中，细胞活力的依赖依赖性降低。黄酮类化合物（儿茶素，槲皮素，chrysin，葛根素，柚皮素，genestein）可保护中脑培养物免受MPP（+）的损伤，DNA片段化研究和DA神经元酪氨酸羟化酶（TH）免疫细胞化学表明，黄酮类化合物是通过凋亡发生的。儿茶素还减少了过氧化氢，4-羟基壬烯醛，鱼藤酮和6-羟基多巴胺产生的损伤，如细胞活力和[（3）H] DA摄取增加所表明。当将儿茶素对MPP（+）诱导的损伤的神经保护作用与caspase-3抑制剂Z-DVED-FMK产生的神经保护作用进行比较时，可减少DNA片段化和TH阳性神经元的损伤模式。这些数据证明了类黄酮的神经保护能力，其能够减轻中脑DA神经元的凋亡损伤。由于这些DA神经元在帕金森病中处于氧化应激状态，因此我们的发现表明，类黄酮可与帕金森氏病中的其他抗氧化剂疗法一起提供益处。

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