School of Pharmacy, Anhui Medical University, 81 Meishan Road, Hefei 230032, China; The Key Laboratory of Anti-inflammatory and Immune Medicine, Ministry of Education, Anhui Medical University, Hefei, China; Anhui Provincial Laboratory of Inflammatory and Immune Disease, Anhui Institute of Innovative Drugs, Hefei, China.
School of Pharmacy, Anhui Medical University, 81 Meishan Road, Hefei 230032, China; The Key Laboratory of Anti-inflammatory and Immune Medicine, Ministry of Education, Anhui Medical University, Hefei, China; Anhui Provincial Laboratory of Inflammatory and Immune Disease, Anhui Institute of Innovative Drugs, Hefei, China.
Biochem Pharmacol. 2023 Nov;217:115846. doi: 10.1016/j.bcp.2023.115846. Epub 2023 Oct 5.
Melatonin (MLT) is ahormonal substance reported with various pharmacological activities.Based on its effects of neuroprotection and metabolic regulation, the aim of the present study is to investigate its potential effect on palmitic acid (PA)-induced cell injuries and glucolipid metabolic dysfunction and explore the possible mechanism. Briefly, HT-22 cells were challenged with PA (0.1 mM, 24 h) and treated with MLT (10-10 mol/L). Cell proliferation, lipid accumulation and glucose consumption were detected. The protein expression of key molecular involved with the function of synaptic plasticity and circadian rhythms were measured via western blotting, and the expression of Map-2, MT1A, MT1B and Bmal1 were measured via immunofluorescence staining. The results showed that MLT could alleviate the neurotoxicity induced by PA, as indicated by the increased cell proliferation, enhanced fluorescence intensity of Map-2, and decreased lipid deposition and insulin resistance. Moreover, treatment of MLT could reverse the imbalanced expression of p-Akt, p-ERK, Synapsin I, Synaptotagmin I, BDNF, MT1B, Bmal1, and Clock in PA-induced HT-22 cells. These results suggested a remarkably neuroprotective effect of MLT against PA-induced cell injury and glucolipid metabolic dysfunction, the mechanism of which might be involved in the regulation of synaptic plasticity and circadian rhythms.
褪黑素（MLT）是一种具有多种药理活性的激素物质。基于其神经保护和代谢调节作用，本研究旨在探讨其对棕榈酸（PA）诱导的细胞损伤和糖脂代谢功能障碍的潜在作用，并探讨其可能的机制。简而言之，用 PA（0.1 mM，24 h）处理 HT-22 细胞，并给予 MLT（10-10 mol/L）处理。检测细胞增殖、脂质积累和葡萄糖消耗。通过 Western blot 检测与突触可塑性和昼夜节律功能相关的关键分子的蛋白表达，通过免疫荧光染色检测 Map-2、MT1A、MT1B 和 Bmal1 的表达。结果表明，MLT 可减轻 PA 诱导的神经毒性，表现为细胞增殖增加、Map-2 荧光强度增强、脂质沉积减少和胰岛素抵抗减轻。此外，MLT 处理可逆转 PA 诱导的 HT-22 细胞中 p-Akt、p-ERK、Synapsin I、Synaptotagmin I、BDNF、MT1B、Bmal1 和 Clock 的失衡表达。这些结果表明 MLT 对 PA 诱导的细胞损伤和糖脂代谢功能障碍具有显著的神经保护作用，其机制可能涉及调节突触可塑性和昼夜节律。
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