Li Di, Ren Jinwei, Du Qian, Liu Peng, Li Yong
Department of Clinical Nutrition, Peking University People's Hospital Beijing 100044, PR China.
Department of Nutrition and Food Hygiene, School of Public Health, Peking University Beijing 100191, PR China.
Am J Transl Res. 2021 Mar 15;13(3):1657-1666. eCollection 2021.
To explore the anti-hypoxic effects of oat oligopeptides (OOPs) in mice.
We randomly divided mice into six groups, including a vehicle control group, a whey protein group (0.50 g/kg), and four OOPs-treated groups (0.25, 0.50, 1.00, and 2.00 g/kg). The test substances were administered by gavage once a day for 30 days. The normobaric hypoxia, sodium nitrite toxicosis, and acute cerebral ischemia survival times were recorded. Also, the MDA content, the lactate levels, the LDH activity, and the mRNA levels of HIF-1α and VEGF in the brains were measured. We performed a whole blood cell analysis using a blood analyzer.
The OOPs significantly extended the survival times of normobaric hypoxia, sodium nitrite toxicosis, and acute cerebral ischemia. Notably, the OOPs enhanced the RBC, Hb, and Hct levels, decreased the malonaldehyde (MDA) and lactate content in the brain, enhanced the brain lactate dehydrogenase (LDH) activity, and increased the hypoxia-inducible factor 1alpha (HIF1α) mRNA and the vascular endothelial growth factor (VEGF) mRNA expression levels.
OOPs have anti-hypoxic effects, and the mechanism may involve improving the blood's oxygen carrying capacity and oxygen utilization rate minimizing the lipid peroxidation lesions, increasing the brain's ability to buffer against lactic acidosis in mice, and promoting angiogenesis and regulating the hypoxic response.
探讨燕麦寡肽（OOPs）对小鼠的抗缺氧作用。
将小鼠随机分为六组，包括溶剂对照组、乳清蛋白组（0.50 g/kg）和四个OOPs处理组（0.25、0.50、1.00和2.00 g/kg）。受试物每天灌胃给药1次，连续30天。记录常压缺氧、亚硝酸钠中毒和急性脑缺血存活时间。同时，检测脑组织中丙二醛（MDA）含量、乳酸水平、乳酸脱氢酶（LDH）活性以及缺氧诱导因子1α（HIF-1α）和血管内皮生长因子（VEGF）的mRNA水平。使用血液分析仪进行全血细胞分析。
OOPs显著延长了常压缺氧、亚硝酸钠中毒和急性脑缺血的存活时间。值得注意的是，OOPs提高了红细胞（RBC）、血红蛋白（Hb）和血细胞比容（Hct）水平，降低了脑组织中丙二醛（MDA）和乳酸含量，增强了脑乳酸脱氢酶（LDH）活性，并增加了缺氧诱导因子1α（HIF1α）mRNA和血管内皮生长因子（VEGF）mRNA表达水平。
OOPs具有抗缺氧作用，其机制可能涉及提高血液携氧能力和氧利用率，减少脂质过氧化损伤，增强小鼠脑缓冲乳酸酸中毒的能力，促进血管生成并调节缺氧反应。
