Department of Animal Science and Technology, National Taiwan University, Taipei 106, Taiwan.
Department of Optometry, Asia University, Taichung 413, Taiwan; Department of Medical Research, China Medical University Hospital, China Medical University, Taichung 404, Taiwan.
Poult Sci. 2020 May;99(5):2819-2832. doi: 10.1016/j.psj.2019.12.060. Epub 2020 Mar 20.
Our patented protease A-digested crude chalaza hydrolysates (CCH) show antioxidant abilities in vitro. The prophylactic effects of CCH on cognitive dysfunction and brain oxidative damages were investigated via a D-galactose (DG)-injected mouse model in this study. Fifty-four mice were randomly divided into the following: (1) CON, 0.1 mL 0.9% saline (subcutaneous injection [SC] on the back)+distilled water (oral gavage); (2) DG, 100 mg/kg BW/day D-galactose (Bio-Serv Co., Flemington, NJ, USA) (SC on the back)+distilled water (oral gavage); (3) DG_LCH, 100 mg/kg BW/day D-galactose (SC on the back) + 50 mg CCH/kg BW/day in 0.1 ml distilled water (oral gavage); (4) DG_MCH, 100 mg/kg BW/day D-galactose (SC on the back) + 100 mg CCH/kg BW/day (oral gavage); (5) DG_HCH, 100 mg/kg BW/day D-galactose (SC on the back) + 200 mg CCH/kg BW/day (oral gavage); (6) DG_AG, 100 mg/kg BW/day D-galactose (SC on the back) + 100 mg aminoguanidine hydrochloride/kg BW/day (oral gavage). The experiment lasted for 84 D. CCH, containing antioxidant-free amino acids and anserine, restored (P < 0.05) DG-injected memory injury in the Morris water maze test and attenuated the neuronal degenerations and nucleus shrinkages in the dentate gyrus area. CCH supplementation also reduced amyloid β-peptide protein levels and accumulation of advanced glycation end products (AGE) in the brain of DG-injected mice, whereas the brain antioxidant capacity was reversed (P < 0.05) by supplementing CCH. Furthermore, AGE receptor (RAGE), NFκb, IL-6, and TNF-α gene expressions were downregulated (P < 0.05) by supplementing CCH. Therefore, CCH show prophylactic effects on the development of oxidative stress-induced cognitive dysfunction.
我们的专利蛋白酶 A 消化的粗卵黄囊水解物 (CCH) 在体外显示出抗氧化能力。本研究通过 D-半乳糖 (DG) 注射小鼠模型研究了 CCH 对认知功能障碍和大脑氧化损伤的预防作用。54 只小鼠随机分为以下几组：(1)CON，0.1ml 0.9%生理盐水 (背部皮下注射 [SC])+蒸馏水 (灌胃)；(2)DG，100mg/kg BW/day D-半乳糖 (美国新泽西州 Flemington 的 Bio-Serv Co.)(背部 SC)+蒸馏水 (灌胃)；(3)DG_LCH，100mg/kg BW/day D-半乳糖 (背部 SC)+50mg CCH/kg BW/day 溶于 0.1ml 蒸馏水中 (灌胃)；(4)DG_MCH，100mg/kg BW/day D-半乳糖 (背部 SC)+100mg CCH/kg BW/day (灌胃)；(5)DG_HCH，100mg/kg BW/day D-半乳糖 (背部 SC)+200mg CCH/kg BW/day (灌胃)；(6)DG_AG，100mg/kg BW/day D-半乳糖 (背部 SC)+100mg 盐酸氨基胍/kg BW/day (灌胃)。实验持续 84 天。CCH 含有抗氧化的游离氨基酸和肌肽，可恢复 (P < 0.05) DG 注射引起的 Morris 水迷宫试验中的记忆损伤，并减轻齿状回区神经元变性和核萎缩。CCH 补充还降低了 DG 注射小鼠大脑中淀粉样β肽蛋白水平和晚期糖基化终产物 (AGE) 的积累，而补充 CCH 则逆转了大脑抗氧化能力 (P < 0.05)。此外，补充 CCH 下调了 AGE 受体 (RAGE)、NFκb、IL-6 和 TNF-α 基因的表达 (P < 0.05)。因此，CCH 对氧化应激诱导的认知功能障碍的发展具有预防作用。
