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Study on protection against β-amyloid peptide toxicity with oral administration of medicinal herbs

机译:口服药对β-淀粉样肽毒性的保护作用研究

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Seonghyangjeongkisan has been used as a therapeutic agent for cerebral disease in Korea, but its effectiveness in Alzheimer's disease is not well known. In this study, we examined whether Seonghyangjeongkisan could protect against amyloid β-induced cytotoxicity in neuroblastoma cells and the brain. Seonghyangjeongkisan rescued amyloid β-induced cytotoxicity dose dependently and reduced amyloid β-induced apoptosis and reactive oxygen species. Injection of mice with amyloid β impaired performance on the passive avoidance task, but Seonghyangjeongkisan markedly improved memory impairment in mice, with it being more effective than tacrine treatment in mice. Moreover, the activation of stress-related kinases such as extracellular signal-regulated kinase, c-Jun NH2-terminal kinase, and p38 was suppressed, and the phosphorylation of τ protein, which is known as a marker of Alzheimer's disease, was also suppressed by Seonghyangjeongkisan treatment in the hippocampus. These results demonstrate that Seonghyangjeongkisan reduces amyloid β-induced toxicity in the brain, suggesting that it may be a useful complementary therapy against Alzheimer's disease.
机译:在韩国,Seonghyangjeongkisan已被用作脑部疾病的治疗剂,但其在阿尔茨海默氏病中的功效尚不为人所知。在这项研究中,我们研究了Seonghyangjeongkisan是否可以预防淀粉样β诱导的神经母细胞瘤细胞和大脑的细胞毒性。 Seonghyangjeongkisan依赖性地挽救了淀粉样β诱导的细胞毒性,并减少了淀粉样β诱导的细胞凋亡和活性氧。注射淀粉样蛋白β的小鼠在被动回避任务上的表现受损,但Seonghyangjeongkisan显着改善了小鼠的记忆障碍,比他克林治疗小鼠更有效。此外,抑制了与压力相关的激酶的激活,例如细胞外信号调节激酶,c-Jun NH2末端激酶和p38的激活,并且也抑制了被称为阿尔茨海默氏病标志物的τ蛋白的磷酸化。通过Seonghyangjeongkisan治疗海马体。这些结果表明,Seonghyangjeongkisan减少了淀粉样β诱导的脑毒性,这表明它可能是对抗阿尔茨海默氏病的有用补充疗法。

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