Department of Medical Laboratory Technology, Faculty of Applied Medical Sciences, King Abdulaziz University, Jeddah 21589, Saudi Arabia.
Biomolecules. 2021 Jan 27;11(2):165. doi: 10.3390/biom11020165.
High-fat diet (HFD) is a major problem causing neuronal damage. Thymoquinone (TQ) could regulate oxidative stress and the inflammatory process. Hence, the present study elucidated the significant role of TQ on oxidative stress, inflammation, as well as morphological changes in the cerebellum of rats with HFD. Rats were divided into three groups as (1) control, (2) saturated HFD for eight weeks and (3) HFD supplementation (four weeks) followed by TQ 300 mg/kg/day treated (four weeks). After treatment, blood samples were collected to measure oxidative stress markers glutathione (GSH), malondialdehyde (MDA), superoxide dismutase (SOD), and inflammatory cytokines. Furthermore, neuronal morphological changes were also observed in the cerebellum of the rats. HFD rats show higher body weight (286.5 ± 7.4 g) as compared with the control group (224.67 ± 1.78 g). TQ treatment significantly ( < 0.05) lowered the body weight (225.83 ± 13.15 g). TQ produced a significant ( < 0.05) reduction in cholesterol, triglycerides, high-density lipoprotein (HDL), and low-density lipoprotein (LDL). The antioxidative enzymes significantly reduced in HFD rats (GSH, 1.46 ± 0.36 mol/L and SOD, 99.13 ± 5.41 µmol/mL) as compared with the control group (GSH, 6.25 ± 0.36 mol/L and SOD, 159.67 ± 10.67 µmol/mL). MDA was increased significantly in HFD rats (2.05 ± 0.25 nmol/L) compared to the control group (0.695 ± 0.11 nmol/L). Surprisingly, treatment with TQ could improve the level of GSH, MDA, and SOD. TQ treatment significantly ( < 0.05) reduced the inflammatory markers as compared with HFD alone. TQ treatment minimizes neuronal damage as well as reduces inflammation and improves antioxidant enzymes. TQ can be considered as a promising agent in preventing the neuronal morphological changes in the cerebellum of obese populations.
高脂肪饮食(HFD)是导致神经元损伤的主要问题。百里醌(TQ)可以调节氧化应激和炎症过程。因此,本研究阐明了 TQ 对 HFD 大鼠小脑氧化应激、炎症和形态变化的重要作用。大鼠分为三组:(1)对照组,(2)饱和 HFD 喂养 8 周,(3)HFD 喂养 4 周后补充 TQ(300mg/kg/天)治疗 4 周。治疗后,采集血样测量氧化应激标志物谷胱甘肽(GSH)、丙二醛(MDA)、超氧化物歧化酶(SOD)和炎症细胞因子。此外,还观察了大鼠小脑神经元形态变化。HFD 大鼠体重(286.5±7.4g)明显高于对照组(224.67±1.78g)。TQ 治疗显著降低体重(225.83±13.15g)。TQ 显著降低胆固醇、甘油三酯、高密度脂蛋白(HDL)和低密度脂蛋白(LDL)。与对照组相比,HFD 大鼠的抗氧化酶(GSH,1.46±0.36mol/L 和 SOD,99.13±5.41µmol/mL)显著降低(<0.05)。HFD 大鼠 MDA 明显升高(2.05±0.25nmol/L),而对照组 MDA 水平(0.695±0.11nmol/L)。令人惊讶的是,TQ 治疗可改善 GSH、MDA 和 SOD 水平。与单独 HFD 组相比,TQ 治疗显著降低了炎症标志物。TQ 治疗可减轻神经元损伤,减少炎症,改善抗氧化酶。TQ 可作为预防肥胖人群小脑神经元形态变化的有前途的药物。