更新于：2024-11-01

CB x HIV-1 tat

更新于：2024-11-01

基本信息

关联

项与 CB x HIV-1 tat 相关的药物

CS-TATI-1

靶点

CB x HIV-1 tat

作用机制

CB激动剂 [+1]

在研机构

Cannabis Science, Inc.

原研机构

Cannabis Science, Inc.

在研适应症

HIV感染 [+1]

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 CB x HIV-1 tat 相关的临床结果

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100 项与 CB x HIV-1 tat 相关的转化医学

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0 项与 CB x HIV-1 tat 相关的专利（医药）

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项与 CB x HIV-1 tat 相关的文献（医药）

2024-01-01·Brain Research

Effects of acute Δ9-tetrahydrocannabinol on behavior and the endocannabinoid system in HIV-1 Tat transgenic female and male mice

Article

作者: Peace, Michelle R ; Yadav-Samudrala, Barkha J ; Ramineni, Shreya ; Jiang, Wei ; Fitting, Sylvia ; Poklis, Justin L ; Dodson, Hailey ; Gorman, Benjamin L ; Wallace, E Diane

Cannabis use is highly prevalent especially among people living with HIV (PLWH). Activation of the anti-inflammatory and neuroprotective endocannabinoid system by phytocannabinoids, i.e. Δ⁹-tetrahydrocannabinol (THC), has been proposed to reduce HIV symptoms. However, THC's effects on HIV-related memory deficits are unclear. Using HIV-1 Tat transgenic mice, the current study investigates acute THC effects on various behavioral outcomes and the endocannabinoid system. For the rodent tetrad model, THC doses (1, 3, 10 mg/kg) induced known antinociceptive effects, with Tat induction increasing antinociceptive THC effects at 3 and 10 mg/kg doses. Only minor or no effects were noted for acute THC on body temperature, locomotor activity, and coordination. Increased anxiety-like behavior was found for females compared to males, but acute THC had no effect on anxiety. Object recognition memory was diminished by acute THC in Tat(-) females but not Tat(+) females, without affecting males. The endocannabinoid system and related lipids were not affected by acute THC, except for THC-induced decreases in CB₁R protein expression levels in the spinal cord of Tat(-) mice. Female sex and Tat induction was associated with elevated 2-AG, AEA, AA, CB₁R, CB₂R, FAAH and/or MAGL expression in various brain regions. Further, AEA levels in the prefrontal cortex of Tat(+) females were negatively associated with object recognition memory. Overall, findings indicate that acute THC exerts differential effects on antinociception and memory, dependent on sex and HIV Tat expression, potentially in relation to an altered endocannabinoid system, which may be of relevance in view of potential cannabis-based treatment options for PLWH.

2002-12-01·Journal of Biological Chemistry2区 · 生物学

The Endocannabinoid System Protects Rat Glioma Cells Against HIV-1 Tat Protein-induced Cytotoxicity

2区 · 生物学

Article

作者: Teresa Iuvone ; Menotti Ruvo ; Giuseppe Esposito ; Massimo Di Rosa ; Angelo A. Izzo ; Vincenzo Di Marzo ; Tiziana Bisogno ; Alessia Ligresti

Cannabinoids modulate nitric oxide (NO) levels in cells of the central nervous system. Here we studied the effect of cannabinoid CB(1) and CB(2) receptor agonists on the release of NO and cell toxicity induced by the human immuno-deficiency virus-1 Tat protein (HIV-1 Tat) in rat glioma C6 cells. The CB(1) and CB(2) agonist WIN 55,212-2 inhibited the expression of inducible NO synthase (iNOS) and NO release caused by treatment of C6 cells with HIV-1 Tat and interferon-gamma (IFN-gamma). The effect of WIN 55,212-2 was uniquely due to CB(1) receptors, as shown by experiments carried out with selective CB(1) and CB(2) receptor agonists and antagonists. CB(1) receptor stimulation also inhibited HIV-1 Tat + IFN-gamma-induced and NO-mediated cell toxicity. Moreover, cell treatment with HIV-1 Tat + IFN-gamma induced a significant inhibition of CB(1), but not CB(2), receptor expression. This effect was mimicked by the NO donor GSNO, suggesting that the inhibition of CB(1) expression was due to HIV-1 Tat + IFN-gamma-induced NO overexpression. HIV-1 Tat + IFN-gamma treatment also induced a significant inhibition of the uptake of the endocannabinoid anandamide by C6 cells with no effect on anandamide hydrolysis. These findings show that the endocannabinoid system, through the modulation of the l-arginine/NO pathway, reduces HIV-1 Tat-induced cytotoxicity, and is itself regulated by HIV-1 Tat.