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Nicotinamide riboside rescues angiotensin II-induced cerebral small vessel disease in mice.
CNS Neuroscience & Therapeutics ( IF 4.8 ) Pub Date : 2020-01-14 , DOI: 10.1111/cns.13276
Cheng-Cheng Li 1, 2 , Wei-Xiang Chen 1 , Jie Wang 1 , Min Xia 1 , Zheng-Cai Jia 1 , Chao Guo 1 , Xiao-Qin Tang 1 , Ming-Xi Li 1 , Yi Yin 1 , Xin Liu 1 , Hua Feng 1, 3
Affiliation  

AIMS Hypertension is a leading cause of cerebral small vessel disease (CSVD). Currently, treatments for CSVD are limited. Nicotinamide riboside (NR) can protect against vascular injury and cognitive impairment in neurodegenerative diseases. In this study, the protective effects of NR against angiotensin - (Ang -)-induced CSVD were evaluated. METHODS To explore the effects of NR in CSVD, C57BL/6 mice were infused with Ang -, and NR was added to the food of the mice for 28 days. Then, short-term memory, blood-brain barrier (BBB) integrity, and endothelial function were detected. Arteriole injury and glial activation were also evaluated. RESULTS Our data showed that mice infused with Ang - exhibited decreased short-term memory function and BBB leakage due to decreased claudin-5 expression and increased caveolae-mediated endocytosis after 28 days. Furthermore, Ang - decreased the expression of α-smooth muscle actin (α-SMA) and increased the expression of proliferating cell nuclear antigen (PCNA) in arterioles and decreased the expression of neurofilament 200 (NF200) and myelin basic protein (MBP) in the white matter. These CSVD-related damages induced by Ang - were inhibited by NR administration. Moreover, NR administration significantly reduced glial activation around the vessels. CONCLUSION Our results indicated that NR administration alleviated Ang --induced CSVD by protecting BBB integrity, vascular remodeling, neuroinflammation, and white matter injury (WMI)-associated cognitive impairment.

中文翻译:

烟酰胺核糖苷可以挽救血管紧张素II引起的小鼠脑小血管疾病。

AIMS高血压是脑小血管疾病(CSVD)的主要原因。目前,CSVD的治疗方法很有限。烟酰胺核糖苷(NR)可以预防神经退行性疾病中的血管损伤和认知障碍。在这项研究中,评估了NR对血管紧张素-(Ang-)诱导的CSVD的保护作用。方法为了研究NR对CSVD的影响,向C57BL / 6小鼠注入Ang-,并将NR添加到小鼠的食物中28天。然后,检测了短期记忆,血脑屏障(BBB)完整性和内皮功能。还评估了小动脉损伤和神经胶质激活。结果我们的数据表明,注射Ang的小鼠在28天后表现出减少的短期记忆功能和BBB渗漏,这是由于claudin-5表达下降和小窝介导的内吞作用增加所致。此外,Ang-降低了小动脉中α-平滑肌肌动蛋白(α-SMA)的表达,增加了增殖细胞核抗原(PCNA)的表达,并降低了神经丝200(NF200)和髓鞘碱性蛋白(MBP)的表达。白质。这些由Ang诱导的与CSVD相关的损伤被NR抑制。此外,NR给药显着减少了血管周围的神经胶质活化。结论我们的结果表明,NR给药可通过保护BBB完整性,血管重塑,神经炎症和白质损伤(WMI)相关的认知障碍来减轻Ang诱导的CSVD。血管紧张素-降低小动脉中α平滑肌肌动蛋白(α-SMA)的表达并增加增殖细胞核抗原(PCNA)的表达,并降低白色中神经丝200(NF200)和髓鞘碱性蛋白(MBP)的表达物。这些由Ang诱导的与CSVD相关的损伤被NR抑制。此外,NR给药显着减少了血管周围的神经胶质活化。结论我们的结果表明,NR给药可通过保护BBB完整性,血管重塑,神经炎症和白质损伤(WMI)相关的认知障碍来减轻Ang诱导的CSVD。血管紧张素-降低小动脉中α平滑肌肌动蛋白(α-SMA)的表达并增加增殖细胞核抗原(PCNA)的表达,并降低白色中神经丝200(NF200)和髓鞘碱性蛋白(MBP)的表达物。这些由Ang诱导的与CSVD相关的损伤被NR抑制。此外,NR给药显着减少了血管周围的神经胶质活化。结论我们的结果表明,NR给药可通过保护BBB完整性,血管重塑,神经炎症和白质损伤(WMI)相关的认知障碍来减轻Ang诱导的CSVD。NR治疗显着减少了血管周围的胶质细胞活化。结论我们的结果表明,NR给药可通过保护BBB完整性,血管重塑,神经炎症和白质损伤(WMI)相关的认知障碍来减轻Ang诱导的CSVD。NR治疗显着减少了血管周围的胶质细胞活化。结论我们的结果表明,NR给药可通过保护BBB完整性,血管重塑,神经炎症和白质损伤(WMI)相关的认知障碍来减轻Ang诱导的CSVD。
更新日期:2020-01-15
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