Protective Effects of Ginsenoside Rb1 against Blood-Brain Barrier Damage Induced by Human Immunodeficiency Virus-1 Tat Protein and Methamphetamine in Sprague-Dawley Rats
Protective Effects of Ginsenoside Rb1 against Blood-Brain Barrier Damage Induced by Human Immunodeficiency Virus-1 Tat Protein and Methamphetamine in Sprague-Dawley Rats
复制标题
人参皂苷 Rb1 对人类免疫缺陷病毒 1 Tat 蛋白和甲基苯丙胺所致 Sprague-Dawley 大鼠血脑屏障损伤的保护作用
DOI：
10.1142/s0192415x18500283
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发表时间：
2018-01-01
影响因子：
5.7
通讯作者：
Zeng, Xiaofeng
中科院分区：
文献类型：
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作者：
Li, Juan;Zeng, Bairui;Zeng, Xiaofeng
虽然抗逆转录病毒疗法有助于改善感染人类免疫缺陷病毒1（HIV-1）的个人的生活，但这些患者通常仍患有HIV-1相关的神经认知障碍，这可能导致神经认知障碍甚至痴呆，并继续影响他们的生活质量。HIV-1患者滥用甲基苯丙胺可能导致HIV相关神经认知障碍，因为甲基苯丙胺和HIV-1蛋白质（如转录反式激活因子）可协同损害血脑屏障（BBB）。在这项研究中，我们的目的是检查甲基苯丙胺和HIV-1达特蛋白对血脑屏障功能的影响，并确定是否GsRb 1（GsRb 1）在保护血脑屏障中发挥作用。Sprague-Dawley大鼠分为4组。实验组接受甲基苯丙胺和HIV-1达特蛋白或两者联合治疗，对照组接受生理盐水或GsRb 1预处理。记录各组的氧化应激相关因子、紧密连接（TJ）蛋白、血脑屏障通透性和形态学变化。结果显示，甲基苯丙胺+达特组在超微结构水平、氧化应激相关因子、TJ蛋白和血脑屏障通透性水平均出现显著变化，提示HIV-1达特和甲基苯丙胺协同作用严重损害血脑屏障功能。然而，与甲基苯丙胺+Tat治疗组相比，GsRh 1治疗组的丙二醛水平和BBB渗透性较低，氧化应激相关因子超氧化物歧化酶和谷胱甘肽较高，表明GsRh 1可以保护BBB免受HIV-1的毒性作用。达特和甲基苯丙胺。这些结果表明，GsRb 1可能为HIV相关神经认知障碍或其他神经退行性疾病患者提供潜在的治疗选择。
Although antiretroviral therapy has helped to improve the lives of individuals infected with human immunodeficiency virus 1 (HIV-1), these patients are often still afflicted with HIV-1-associated neurocognitive disorders, which can lead to neurocognitive impairment and even dementia, and continue to hamper their quality of life. Methamphetamine abuse in HIV-1 patients poses a potential risk for HIV-associated neurocognitive disorders, because methamphetamine and HIV-1 proteins such as transactivator of transcription can synergistically damage the blood-brain barrier (BBB). In this study, we aimed to examine the effects of methamphetamine and HIV-1 Tat protein on the blood-brain barrier function and to determine whether ginsenoside Rb1 (GsRb1) plays a role in protecting the BBB. Sprague-Dawley rats were divided into four groups. The experimental groups received methamphetamine and HIV-1 Tat protein or both and the control group received saline or GsRb1 pretreatment. Oxidative stress-related factors, tight junction (TJ) proteins, blood-brain barrier permeability, and morphological changes were recorded in each group. The results showed that the group treated with Methamphetamine+Tat showed a significant change at the ultrastructural level and in the levels of oxidative stress-related factors, TJ proteins, and BBB permeability, suggesting that the BBB function was severely damaged by HIV-1 Tat and methamphetamine synergistically. However, malondialdehyde levels and BBB permeability were lower and the oxidative stress-related factors superoxide dismutase and glutathione were higher in the GsRb1-treated group than in the Methamphetamine+Tat-treated group, indicating that GsRb1 can protect the BBB against the toxic effects of HIV-1 Tat and methamphetamine. These results show that GsRb1 may offer a potential therapeutic option for patients with HIV-associated neurocognitive disorders or other neurodegenerative diseases.