姜黄素和硼酸对淀粉样β（1-42）诱导的神经退行性损伤的影响。
Effects of Curcumin and Boric Acid Against Neurodegenerative Damage Induced by Amyloid Beta (1-42).
机构信息
Department of Medical Biochemistry, Faculty of Medicine, Duzce University, Duzce, Turkey.
Department of Medical Biochemistry, Faculty of Medicine, Eskisehir Osmangazi University, Eskisehir, Turkey.
出版信息
Biol Trace Elem Res. 2021 Oct;199(10):3793-3800. doi: 10.1007/s12011-020-02511-2. Epub 2020 Nov 25.
Synaptosomes are used as an ex vivo model in the investigation of neuronal transmission and neurodegenerative processes. In this study, we aimed to determine the protective effects of boric acid (BA) and curcumin, which have antioxidant and anti-inflammatory properties, on Aβ1-42 induced neurodegenerative damage. Synaptosomes obtained from the rat cerebral cortex were divided into five groups: control, 10 μM Aβ1-42, 10 μM Aβ1-42 + 25 mM BA, 10 μM Aβ1-42 + 10 μM curcumin, and 10 μM Aβ1-42 + 25 mM BA+10 μM curcumin. Synaptosomes treated with Aβ1-42 caused a significant decline in synaptophysin levels and increase in malondialdehyde (MDA) levels, acetylcholinesterase (AChE) activities, DNA fragmentation values, and nitric oxide (NO) levels compared with the control group (P < 0.01). Synaptosomes treated with BA showed a significant reduction in MDA and NO levels against Aβ1-42 exposure (P < 0.01). In addition, curcumin treatment has been found to cause a significant reduction in AChE activities and MDA levels in synaptosomes (P < 0.05). Co-administration of BA and curcumin on synaptosomes exposed to Aβ1-42 resulted in a significant decrease in DNA fragmentation values, MDA levels, and AChE activities. Curcumin and BA + curcumin combination showed an enhancement in synaptophysin levels of Aβ1-42-induced synaptosomes (P < 0.01). The results showed that BA and curcumin had protective effects on rat brain synaptosomes against Aβ1-42 exposure. BA and curcumin treatment can have abilities to prevent the alterations of the cholinergic system and inhibit oxidative stress in the cerebral cortex synapses of Aβ1-42 exposed.
突触体被用作研究神经元传递和神经退行性过程的体外模型。在这项研究中，我们旨在确定硼酸（BA）和姜黄素的保护作用，它们具有抗氧化和抗炎特性，对 Aβ1-42 诱导的神经退行性损伤。从大鼠大脑皮质中分离出的突触体分为五组：对照组、10 μM Aβ1-42、10 μM Aβ1-42+25 mM BA、10 μM Aβ1-42+10 μM 姜黄素和 10 μM Aβ1-42+25 mM BA+10 μM 姜黄素。与对照组相比，用 Aβ1-42 处理的突触体导致突触小体蛋白水平显著下降，丙二醛（MDA）水平、乙酰胆碱酯酶（AChE）活性、DNA 片段化值和一氧化氮（NO）水平显著增加（P<0.01）。与 Aβ1-42 暴露相比，BA 处理组的 MDA 和 NO 水平显著降低（P<0.01）。此外，姜黄素处理可导致 Aβ1-42 暴露的突触体 AChE 活性和 MDA 水平显著降低（P<0.05）。在 Aβ1-42 暴露的突触体上同时给予 BA 和姜黄素可导致 DNA 片段化值、MDA 水平和 AChE 活性显著降低。姜黄素和 BA+姜黄素联合治疗可提高 Aβ1-42 诱导的突触体中突触小体蛋白的水平（P<0.01）。结果表明，BA 和姜黄素对 Aβ1-42 暴露的大鼠脑突触体具有保护作用。BA 和姜黄素治疗可防止 Aβ1-42 暴露的大脑皮质突触中胆碱能系统的改变，并抑制氧化应激。
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