Chen Jie, Hou Chen, Chen Xin, Wang Dong, Yang Pinglin, He Xijing, Zhou Jinsong, Li Haopeng
Department of Orthopaedic Surgery, Second Affiliated Hospital of Medical School of Xi'an Jiaotong University, Xi'an, Shaanxi 710004, P.R. China.
Department of Geriatric Neurology, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi 710068, P.R. China.
Mol Med Rep. 2016 Sep;14(3):2321-7. doi: 10.3892/mmr.2016.5513. Epub 2016 Jul 13.
Cannabidiol, a major component of marijuana, protects nerves, and exerts antispasmodic, anti-inflammatory and anti‑anxiety effects. In the current study, the protective effect of cannabidiol was observed to prevent hydrogen peroxide (H2O2)‑induced apoptosis, inflammation and oxidative stress in nucleus pulposus cells. Nucleus pulposus cells were isolated from rats and cultured in vitro, and H2O2 was used to construct the nucleus pulposus cell model. Cell viability of the nucleus pulposus cells was assessed using a 3‑(4,5-dimethylthiazol-2-yl)-2,5‑diphenyltetrazolium bromide assay. The ratio of apoptotic cells, and caspase‑3 or cyclooxygenase‑2 (COX‑2) mRNA expression was analyzed by annexin V‑fluorescein isothiocyanate/propidium‑iodide staining and reverse transcription‑quantitative polymerase chain reaction, respectively. The quantities of interleukin (IL)‑1β and interleukin‑6 were measured using a series of assay kits. B-cell lymphoma 2 (Bcl‑2) and inducible nitric oxide synthase (iNOS) protein expression levels were analyzed using western blotting. The present study identified that cannabidiol enhanced cell viability and reduced apoptosis in H2O2‑treated nucleus pulposus cells in vitro using a lumbar disc herniation (LDH) model. In addition, cannabidiol reduced caspase‑3 gene expression and augmented the Bcl‑2 protein expression levels in the nucleus pulposus cells following H2O2 exposure. Pre‑treatment with cannabidiol suppressed the promotion of COX‑2, iNOS, IL‑1β and IL‑6 expression in the nucleus pulposus cells following H2O2 exposure. Taken together, these results suggest that cannabidiol potentially exerts its protective effect on LDH via the suppression of anti‑apoptosis, anti‑inflammation and anti‑oxidative activities in nucleus pulposus cells.
大麻二酚是大麻的主要成分，具有保护神经的作用，并能发挥解痉、抗炎和抗焦虑功效。在本研究中，观察到大麻二酚具有保护作用，可预防过氧化氢（H2O2）诱导的髓核细胞凋亡、炎症和氧化应激。从大鼠中分离出髓核细胞并进行体外培养，使用H2O2构建髓核细胞模型。采用3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐法评估髓核细胞的活力。分别通过膜联蛋白V-异硫氰酸荧光素/碘化丙啶染色和逆转录-定量聚合酶链反应分析凋亡细胞比例以及半胱天冬酶-3或环氧化酶-2（COX-2）mRNA表达。使用一系列检测试剂盒测量白细胞介素（IL）-1β和白细胞介素-6的量。采用蛋白质印迹法分析B细胞淋巴瘤-2（Bcl-2）和诱导型一氧化氮合酶（iNOS）蛋白表达水平。本研究通过腰椎间盘突出症（LDH）模型证实，大麻二酚可提高体外培养的经H2O2处理的髓核细胞的活力并减少其凋亡。此外，大麻二酚可降低H2O2处理后髓核细胞中半胱天冬酶-3基因的表达，并提高Bcl-2蛋白的表达水平。大麻二酚预处理可抑制H2O2处理后髓核细胞中COX-2、iNOS、IL-1β和IL-6表达的上调。综上所述，这些结果表明大麻二酚可能通过抑制髓核细胞的抗凋亡、抗炎和抗氧化活性，对腰椎间盘突出症发挥保护作用。
