Intervertebral disc degeneration (IDD) is a natural problem linked to the inflammation. Higenamine exerts multiple pharmacological properties in inflammation-related disorders. Our study aimed to explore the function of higenamine on interleukin (IL)-1β-caused apoptosis of human nucleus pulposus cells (HNPCs). Cell apoptosis was investigated by TUNEL and flow cytometry. Apoptosis-related biomarkers were determined by qRT-PCR or Western blotting. The protein in the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling was measured by Western blotting. We found that higenamine showed little effect on cell apoptosis, but mitigated IL-1β-caused apoptosis in a dose-dependent pattern. Higenamine attenuated IL-1β-induced decrease of Bcl-2 and increase of Bax and cleaved caspase-3. Higenamine did not affect the reactive oxygen species (ROS) level and the PI3K/Akt signaling, but attenuated IL-1β-induced ROS production and inhibition of the PI3K/Akt signaling. IL-1β repressed the activation of the PI3K/Akt pathway, but ROS inhibition using N-acetylcysteine (NAC) rescued this pathway. The PI3K/Akt signaling suppression using LY294002 reversed the inhibitive effect of higenamine on IL-1β-caused apoptosis, and this effect was weakened by ROS inhibition. In conclusion, higenamine attenuates IL-1β-caused apoptosis of HNPCs via ROS-mediated PI3K/Akt pathway.

椎间盘退变 (IDD) 是与炎症相关的自然问题。Higenamine 在炎症相关疾病中发挥多种药理学特性。本研究旨在探讨去甲乌药碱对白细胞介素（IL）-1β引起的人髓核细胞（HNPCs）凋亡的作用。通过TUNEL和流式细胞术研究细胞凋亡。通过 qRT-PCR 或蛋白质印迹确定细胞凋亡相关的生物标志物。通过蛋白质印迹测量磷脂酰肌醇 3-激酶 (PI3K)/蛋白激酶 B (Akt) 信号传导中的蛋白质。我们发现去甲乌药胺对细胞凋亡几乎没有影响，但以剂量依赖性模式减轻了 IL-1β 引起的细胞凋亡。Higenamine 减弱了 IL-1β 诱导的 Bcl-2 减少以及 Bax 和切割的 caspase-3 的增加。Higenamine 不影响活性氧 (ROS) 水平和 PI3K/Akt 信号传导，但减弱了 IL-1β 诱导的 ROS 产生和对 PI3K/Akt 信号传导的抑制。IL-1β 抑制 PI3K/Akt 通路的激活，但使用 ROS 抑制N-乙酰半胱氨酸 (NAC) 挽救了这一途径。使用 LY294002 的 PI3K/Akt 信号抑制逆转了去甲乌药碱对 IL-1β 引起的细胞凋亡的抑制作用，而这种作用因 ROS 抑制而减弱。总之，去甲乌龙胺通过 ROS 介导的 PI3K/Akt 通路减弱 IL-1β 引起的 HNPCs 细胞凋亡。