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鹿茸多肽通过激活神经营养因子和 SDF1/CXCR4 轴改善大鼠缺氧缺血性脑病。

Pilose antler polypeptides ameliorates hypoxic-ischemic encephalopathy by activated neurotrophic factors and SDF1/CXCR4 axis in rats.

机构信息

College of Biotechnology and Bioengineering, Zhejiang University of Technology, Hangzhou 310014, China.

College of Pharmaceutical Science, Zhejiang University of Technology, Hangzhou 310014, China.

出版信息

Acta Biochim Biophys Sin (Shanghai). 2018 Mar 1;50(3):254-262. doi: 10.1093/abbs/gmy005.

DOI:10.1093/abbs/gmy005
PMID:29385398
Abstract

Hypoxic-ischemic encephalopathy (HIE) is a complex condition which is associated with high mortality and morbidity. However, few promising treatments for HIE exist. In the present study, the central objective was to identify the therapeutic effect of pilose antler polypeptides (PAP) on HIE in rats. Sprague-Dawley (SD) rats (14 days old) were used and divided into three groups, including control group, hypoxic-ischemia (HI) group and PAP group. After 21 days of treatment, locomotor activity was improved in PAP-treated rats, brain atrophy was decreased and cerebral edema was mitigated to some extent. Real-time quantitative polymerase chain reaction (RT-qPCR) analysis indicated that PAP administration decreased the expressions of inflammatory cytokines and apoptosis genes in hippocampus compared with HI group. Furthermore, the mRNA expressions of genes related to neurotrophic factors were significantly increased in the hippocampus. In addition, the expressions of oxidative stress markers were all down-regulated after PAP administration. Moreover, PAP up-regulated both the mRNA and protein levels of SDF1 and CXCR4, which may activate the SDF1/CXCR4 axis to moderate brain injury. These results suggest that PAP may be potentially used in the treatment of HIE.

摘要

缺氧缺血性脑病(HIE)是一种复杂的疾病,与高死亡率和高发病率相关。然而,目前针对 HIE 的治疗方法有限。本研究的主要目的是探讨鹿茸多肽(PAP)对 HIE 大鼠的治疗作用。选用 14 日龄 Sprague-Dawley(SD)大鼠,分为对照组、缺氧缺血(HI)组和 PAP 组。治疗 21 天后,PAP 治疗组大鼠的运动活动能力得到改善,脑萎缩减轻,脑水肿在一定程度上得到缓解。实时定量聚合酶链反应(RT-qPCR)分析表明,与 HI 组相比,PAP 给药可降低海马中炎症细胞因子和凋亡基因的表达。此外,海马中与神经营养因子相关的基因表达显著增加。此外,PAP 给药后,氧化应激标志物的表达均下调。此外,PAP 上调了 SDF1 和 CXCR4 的 mRNA 和蛋白水平,可能通过激活 SDF1/CXCR4 轴来调节脑损伤。这些结果表明,PAP 可能具有治疗 HIE 的潜力。

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