PDF(Pubmed)
Abstract：
UNASSIGNED: Acrylamide (ACR) is a neurotoxic agent whose damage could be attenuated by antioxidants administration. Crocetin is a saffron-derived antioxidant that has neuroprotective effects. This study evaluates the protective effects of trans-sodium crocetinate (TSC) and its water-soluble derivative, Bis-N-(N-methylpyprazinyl) crocetinate (BMPC) against ACR neurotoxicity.
UNASSIGNED: PC12 cells were treated with TSC and BMPC (1.95, 3.9, 7.81, 15.62, 31.25, 62.5, 125, 250, 500, and 1000 μM) for 24 hr. ACR was then added at a concentration of 6.5 mM (IC50), and cell viability was assessed by 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide. In the in vivo study, male Wistar rats were treated with ACR (50 mg/kg, intraperitoneal (i.p.)) for 11 days alone or in combination with TSC and BMPC (2.5, 5, and 10 mg/kg, i.p.) or vitamin E (200 IU/kg, i.p.). Motor impairments were then evaluated. The cerebral cortex of sacrificed rats was taken for the malondialdehyde (MDA) and glutathione (GSH) levels measurement.
UNASSIGNED: In vitro studies showed that TSC at a concentration of 7.81 μM and BMPC at concentrations of 3.9, 7.81, and 15.62 μM exhibited the lowest toxicity in acrylamide administration. In the in vivo study, pretreatment with 2.5, 5, and 10 mg/kg of TSC ameliorated behavioral impairments, but BMPC could not attenuate them. GSH and MDA were improved by 2.5, 5, and 10 mg/kg TSC and 2.5 mg/kg BMPC.
UNASSIGNED: TSC and BMPC administration improved behavioral index and oxidative stress injuries in Wistar rats exposed to ACR through MDA reduction and GSH content enhancement in the cerebral cortex.
UNASSIGNED: PC12 cells were treated with TSC and BMPC (1.95, 3.9, 7.81, 15.62, 31.25, 62.5, 125, 250, 500, and 1000 μM) for 24 hr. ACR was then added at a concentration of 6.5 mM (IC50), and cell viability was assessed by 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide. In the in vivo study, male Wistar rats were treated with ACR (50 mg/kg, intraperitoneal (i.p.)) for 11 days alone or in combination with TSC and BMPC (2.5, 5, and 10 mg/kg, i.p.) or vitamin E (200 IU/kg, i.p.). Motor impairments were then evaluated. The cerebral cortex of sacrificed rats was taken for the malondialdehyde (MDA) and glutathione (GSH) levels measurement.
UNASSIGNED: In vitro studies showed that TSC at a concentration of 7.81 μM and BMPC at concentrations of 3.9, 7.81, and 15.62 μM exhibited the lowest toxicity in acrylamide administration. In the in vivo study, pretreatment with 2.5, 5, and 10 mg/kg of TSC ameliorated behavioral impairments, but BMPC could not attenuate them. GSH and MDA were improved by 2.5, 5, and 10 mg/kg TSC and 2.5 mg/kg BMPC.
UNASSIGNED: TSC and BMPC administration improved behavioral index and oxidative stress injuries in Wistar rats exposed to ACR through MDA reduction and GSH content enhancement in the cerebral cortex.
摘要：
■丙烯酰胺（ACR）是一种神经毒性剂，其损害可以通过抗氧化剂的施用来减轻。藏红花素是一种藏红花衍生的抗氧化剂，具有神经保护作用。本研究评估了反式-克罗西汀钠（TSC）及其水溶性衍生物的保护作用，双-N-(N-甲基吡嗪基)色胺酸盐(BMPC)抗ACR神经毒性。
用TSC和BMPC(1.95、3.9、7.81、15.62、31.25、62.5、125、250、500和1000μM)处理PC12细胞24小时。然后加入浓度为6.5mM(IC50)的ACR,通过3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四唑溴化物评估细胞活力。在体内研究中，雄性Wistar大鼠用ACR治疗(50mg/kg，腹膜内（i.p.）单独或与TSC和BMPC（2.5、5和10mg/kg，i.p.）或维生素E（200IU/kg，i.p.）。然后评估运动障碍。取大鼠大脑皮层进行丙二醛(MDA)和谷胱甘肽(GSH)水平测定。
体外研究表明，浓度为7.81μM的TSC和浓度为3.9、7.81和15.62μM的BMPC在丙烯酰胺施用中表现出最低的毒性。在体内研究中，用2.5、5和10mg/kg的TSC预处理可改善行为障碍，但是BMPC不能减弱它们。GSH和MDA被2.5、5和10mg/kgTSC和2.5mg/kgBMPC改善。
■TSC和BMPC给药通过减少MDA和提高大脑皮层中GSH含量来改善暴露于ACR的Wistar大鼠的行为指数和氧化应激损伤。
用TSC和BMPC(1.95、3.9、7.81、15.62、31.25、62.5、125、250、500和1000μM)处理PC12细胞24小时。然后加入浓度为6.5mM(IC50)的ACR,通过3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四唑溴化物评估细胞活力。在体内研究中，雄性Wistar大鼠用ACR治疗(50mg/kg，腹膜内（i.p.）单独或与TSC和BMPC（2.5、5和10mg/kg，i.p.）或维生素E（200IU/kg，i.p.）。然后评估运动障碍。取大鼠大脑皮层进行丙二醛(MDA)和谷胱甘肽(GSH)水平测定。
体外研究表明，浓度为7.81μM的TSC和浓度为3.9、7.81和15.62μM的BMPC在丙烯酰胺施用中表现出最低的毒性。在体内研究中，用2.5、5和10mg/kg的TSC预处理可改善行为障碍，但是BMPC不能减弱它们。GSH和MDA被2.5、5和10mg/kgTSC和2.5mg/kgBMPC改善。
■TSC和BMPC给药通过减少MDA和提高大脑皮层中GSH含量来改善暴露于ACR的Wistar大鼠的行为指数和氧化应激损伤。
