Department of Neurology, the First People's Hospital of Changzhou, The Third Affiliated Hospital of Soochow University, Changzhou, China.
Hum Exp Toxicol. 2023 Jan-Dec;42:9603271231220610. doi: 10.1177/09603271231220610.
Ginsenoside Rk1, a novel ginsenoside isolated from red ginseng, has anti-inflammatory and anti-tumor activities. This study was designed to elucidate the role of RK1 in an 1-methyl-4-phenylpyridinium (MPP) cell model and an 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) of Parkinson's disease (PD). The grasping test, pole-climbing test, and rotarod test were performed to measure the effects of RK1 on MPTP-induced motor disorders. The expression of tyrosine hydroxylase (TH) and IBA-1 were evaluated by western blotting. CCK-8 and flow cytometry assays were utilized to assess cell viability and apoptosis. Reactive oxygen species (ROS), Lactate dehydrogenase (LDH), and superoxide dismutase (SOD) were detected to analyze the effects of RK1 on oxidative stress. The levels of inflammatory cytokines were evaluated by enzyme-linked immunosorbent assay (ELISA). The results showed that RK1 allayed motor deficit elicited by MPTP in a mouse model. RK1 administration augmented tyrosine hydroxylase (TH) expression in the brain striatum and substantia nigra (SN) of MPTP-treated mice. Moreover, RK1 pretreatment promoted viability and suppressed apoptosis in MPP-induced PC-12 cells. Further, RK1 also attenuated MPP-stimulated oxidative stress and inflammatory response in PC-12 cells. Besides, RK1 augmented the level of SIRT3, and SIRT3 deletion counteracted RK1-induced repression on MPP-elicited apoptosis, oxidative stress, and inflammatory response in PC-12 cells via modulating the Nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway. RK1 might exert neuroprotective effects against MPP/MPTP-induced neurotoxicity via activating SIRT3-mediated Nrf2/HO-1 signaling. RK1 might be a promising candidate against PD.
人参皂苷 Rk1 是从红参中分离得到的一种新型人参皂苷，具有抗炎和抗肿瘤活性。本研究旨在阐明 RK1 在 1-甲基-4-苯基吡啶（MPP）细胞模型和 1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）帕金森病（PD）中的作用。通过抓握试验、爬杆试验和旋转棒试验来测量 RK1 对 MPTP 诱导的运动障碍的影响。通过 Western blot 评估酪氨酸羟化酶（TH）和 IBA-1 的表达。CCK-8 和流式细胞术检测用于评估细胞活力和凋亡。检测活性氧（ROS）、乳酸脱氢酶（LDH）和超氧化物歧化酶（SOD）来分析 RK1 对氧化应激的影响。通过酶联免疫吸附测定（ELISA）评估炎症细胞因子的水平。结果表明，RK1 减轻了 MPTP 诱导的小鼠模型中的运动缺陷。RK1 给药增强了 MPTP 处理小鼠大脑纹状体和黑质（SN）中的酪氨酸羟化酶（TH）表达。此外，RK1 预处理可促进 MPP 诱导的 PC-12 细胞活力并抑制其凋亡。此外，RK1 还减轻了 MPP 刺激的 PC-12 细胞中的氧化应激和炎症反应。此外，RK1 增加了 SIRT3 的水平，并且 SIRT3 的缺失通过调节核因子红细胞 2 相关因子 2（Nrf2）/血红素加氧酶-1（HO-1）通路拮抗 RK1 诱导的对 MPP 诱导的凋亡、氧化应激和炎症反应的抑制作用。RK1 通过激活 SIRT3 介导的 Nrf2/HO-1 信号通路可能对 MPP/MPTP 诱导的神经毒性发挥神经保护作用。RK1 可能是治疗 PD 的有前途的候选药物。
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