Department of Biochemistry and Molecular Biology, Faculty of Medicine, Universitas Indonesia, Jakarta, 10430, Indonesia.
Center of Hypoxia and Oxidative Stress Studies, Faculty of Medicine, Universitas Indonesia, Jakarta, 10430, Indonesia.
Sci Rep. 2024 Jan 5;14(1):603. doi: 10.1038/s41598-024-51221-5.
In this study, the potential neuroprotective ability of coriander seeds (Coriandrum sativum L.) ethanolic extract (CSES) as a neuroprotectant agent in the brains of high-fat diet-induced obese rats was analyzed. The study investigated how CSES impacts oxidative stress markers (i.e., malondialdehyde/MDA, glutathione/GSH and catalase), inflammation marker (i.e., Interleukin-6/IL-6), cellular senescence markers (i.e., senescence-associated β-galactoside/SA-β-Gal activity and p16), brain damage marker (i.e., Neuron-specific Enolase/NSE), and neurogenesis markers (i.e., mature Brain-derived Neurotropic Factor/BDNF, pro-BDNF, and mature/pro-BDNF ratio). Male adult Wistar rats were fed a high-fat diet and given CSES once daily, at 100 mg/kg body weight, for 12 weeks. CSES significantly reduced MDA concentration (p = < 0.001), SA-β-Gal activity (p = 0.010), and increased GSH concentration (p = 0.047) in the brain of obese rats; however, the decrease of IL-6, NSE, and p16 as well as the increase of catalase specific activity and BDNF expression were not significant. Moreover, the mature/pro-BDNF ratio was significantly higher in the brains of non-obese rats, both given the control diet and the high-fat diet compared to the control. Our results suggest that obese rats benefited from consuming CSES, showing improved oxidative stress levels, reduced cellular senescence and increased endogenous antioxidants, making CSES a potential neuroprotective agent.
在这项研究中,分析了芫荽籽(Coriandrum sativum L.)乙醇提取物(CSES)作为高脂饮食诱导肥胖大鼠脑部神经保护剂的潜在神经保护能力。研究调查了 CSES 如何影响氧化应激标志物(即丙二醛/MDA、谷胱甘肽/GSH 和过氧化氢酶)、炎症标志物(即白细胞介素-6/IL-6)、细胞衰老标志物(即衰老相关β-半乳糖苷/SA-β-Gal 活性和 p16)、脑损伤标志物(即神经元特异性烯醇化酶/NSE)和神经发生标志物(即成熟的脑源性神经营养因子/BDNF、pro-BDNF 和成熟/pro-BDNF 比值)。雄性成年 Wistar 大鼠喂食高脂肪饮食,并每天给予 CSES,剂量为 100mg/kg 体重,持续 12 周。CSES 可显著降低肥胖大鼠大脑中 MDA 浓度(p<0.001)、SA-β-Gal 活性(p=0.010),并增加 GSH 浓度(p=0.047);然而,IL-6、NSE 和 p16 的降低以及过氧化氢酶比活和 BDNF 表达的增加并不显著。此外,与对照组相比,无论是给予对照饮食还是高脂饮食,非肥胖大鼠的大脑中成熟/pro-BDNF 比值均显著升高。我们的研究结果表明,肥胖大鼠受益于食用 CSES,表现出改善的氧化应激水平、减少的细胞衰老和增加的内源性抗氧化剂,使 CSES 成为一种有潜力的神经保护剂。