Tang Hongmei, Lu Daxiang, Pan Rui, Qin Xuebin, Xiong Huangui, Dong Jun
Department of Pathophysiology, Key Lab of State Administration of Traditional Chinese Medicine, Medical College of Jinan University, Guangdong, Guangzhou, China.
Life Sci. 2009 Jul 3;85(1-2):1-10. doi: 10.1016/j.lfs.2009.03.013. Epub 2009 Apr 5.
Human immunodeficiency virus-1 (HIV-1)-associated dementia (HAD) is a significant consequence of HIV infection. Although highly active antiretroviral therapy (HAART) has dramatically decreased HIV-1 load in acquired immune deficiency syndrome (AIDS) patients, HAART does not completely protect against the development of HAD, therefore novel strategies for the prevention and treatment are urgently needed. In this study, we chose curcumin which has a neuroprotective role and tested the effect against neuron damage induced by HIV-1gp120 V3 loop peptide.
Rats were given 150 ng gp120 V3 peptide by intracerebroventricular (ICV) infusion for 3 days to establish the cognitive dysfunction model. After recovery from the surgery, the rats in treatment groups were given curcumin by intragastric infusion for 2 weeks. Subsequently, we used the Morris water maze test, long-term potentiation (LTP) recording, biochemical measurement of oxidative damage, Nissl staining, and BDNF immunostaining to evaluate the neuropathological changes and the effect of curcumin on rats.
Our results documented that the gp120 V3 peptide induced impairment of spatial learning and memory, inhibited LTP in the CA1 region of the hippocampus, and mediated oxidative stress and neuronal injury. These impairments were ameliorated by intragastric infusion of curcumin.
These results suggested that dietary supplementation of curcumin may be a potential therapeutic strategy for the treatment and/or prevention of HAD.
人类免疫缺陷病毒1型(HIV-1)相关痴呆(HAD)是HIV感染的一个重要后果。尽管高效抗逆转录病毒疗法(HAART)已显著降低了获得性免疫缺陷综合征(AIDS)患者体内的HIV-1载量,但HAART并不能完全预防HAD的发生,因此迫切需要新的预防和治疗策略。在本研究中,我们选择了具有神经保护作用的姜黄素,并测试了其对HIV-1 gp120 V3环肽诱导的神经元损伤的作用。
通过脑室内(ICV)注射150 ng gp120 V3肽,连续3天,建立大鼠认知功能障碍模型。术后恢复后,治疗组大鼠通过胃内灌注给予姜黄素,持续2周。随后,我们使用莫里斯水迷宫试验、长时程增强(LTP)记录、氧化损伤的生化检测、尼氏染色和脑源性神经营养因子(BDNF)免疫染色来评估神经病理变化以及姜黄素对大鼠的影响。
我们的结果表明,gp120 V3肽诱导空间学习和记忆障碍,抑制海马CA1区的LTP,并介导氧化应激和神经元损伤。胃内灌注姜黄素可改善这些损伤。
这些结果表明,饮食中补充姜黄素可能是治疗和/或预防HAD的一种潜在治疗策略。