1 Department of Food and Nutrition, Chungnam National University , Daejon, Korea.
J Med Food. 2014 Feb;17(2):226-35. doi: 10.1089/jmf.2013.2951. Epub 2014 Jan 24.
Water extracts of deer bone, called nokgol in Korean, and deer antlers have been traditionally used as anti-aging medicines. Deer antler extract is known to possess various activities, including anti-aging or anti-amnesic activity. However, there are no reports about the neuroprotective effect of deer bone extract (DBE). The objective of this study was to examine the neuroprotective effect of DBE on glutamate-induced cell death of mouse hippocampal cells (HT-22 cells) and to elucidate the mode of neuroprotective action of DBE. In this study, HT-22 cells was pretreated with DBE before stimulation with glutamate, and then, the effects of DBE on cell viability, oxidative stress markers, and MAP kinases were determined. Separately, the effect of DBE on H₂O₂ or amyloid beta peptide (1-42) (Aβ₁₋₄₂)-induced cytotoxicity of HT-22 cells was evaluated. DBE protected HT-22 cells from glutamate-induced cell death and prevented the increase in lactate dehydrogenase leakage in HT-22 cells. DBE also prevented glutamate-induced oxidative stress, as indicated by increased reactive oxygen species and lipid peroxidation as well as by decreases in glutathione (GSH) levels and GSH peroxidase activity. In addition, DBE inhibited glutamate-induced activation of c-Jun N-terminal kinases (JNK), p38, and extracellular signal-regulated kinase, indicators of oxidative stress-induced cell death. Furthermore, DBE also protected against H₂O₂ and Aβ₁₋₄₂-induced cytotoxicity. These results suggest that DBE may be a useful functional agent for the prevention against neurodegenerative disorders involving oxidative stress.
鹿骨的水提取物,在韩语中称为 nokgol,以及鹿角一直被传统上用作抗衰老药物。已知鹿角提取物具有多种活性,包括抗衰老或抗健忘活性。然而,没有关于鹿骨提取物 (DBE) 的神经保护作用的报道。本研究的目的是研究 DBE 对谷氨酸诱导的小鼠海马细胞 (HT-22 细胞) 死亡的神经保护作用,并阐明 DBE 的神经保护作用模式。在这项研究中,在用谷氨酸刺激之前,用 DBE 预处理 HT-22 细胞,然后确定 DBE 对细胞活力、氧化应激标志物和 MAP 激酶的影响。另外,还评估了 DBE 对 H₂O₂或淀粉样β肽 (1-42) (Aβ₁₋₄₂) 诱导的 HT-22 细胞毒性的影响。DBE 可保护 HT-22 细胞免受谷氨酸诱导的细胞死亡,并防止 HT-22 细胞中乳酸脱氢酶漏出增加。DBE 还可防止谷氨酸诱导的氧化应激,如活性氧和脂质过氧化增加以及谷胱甘肽 (GSH) 水平和 GSH 过氧化物酶活性降低所表明的那样。此外,DBE 抑制了谷氨酸诱导的 c-Jun N-末端激酶 (JNK)、p38 和细胞外信号调节激酶的激活,这些是氧化应激诱导的细胞死亡的标志物。此外,DBE 还可防止 H₂O₂和 Aβ₁₋₄₂诱导的细胞毒性。这些结果表明,DBE 可能是预防涉及氧化应激的神经退行性疾病的有用功能剂。