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提高多糖对利血平诱导的抑郁小鼠的活性。

Improving Activity of Polysaccharide on Depressive Mice Induced by Reserpine.

作者信息

Zhao Rui, Master Bing Qiu, Master Baoling Ma, Cai Yaping

机构信息

Department of Pharmaceutical Engineering, College of Life Science & Biotechnology, Heilongjiang August First Land Reclamation University, Daqing High-Tech Industrial Development Zone, 163319, P. R. China.

Department of Gastroenterology, Heilongjiang Province Hospital, 82 Zhongshan Road, Harbin, 150036, P. R. China.

出版信息

Iran J Pharm Res. 2019 Summer;18(3):1556-1565. doi: 10.22037/ijpr.2019.1100763.

Abstract

Depressive disorder will be the second highest disease burden worldwide, which will impair life quality, reduce productivity, and increase disability and mortality. polysaccharide (LBP) is the main active fraction purified from The aim of this study was to evaluate the potential therapeutic effects of LBP on depressive mice induced by reserpine, as well as the relevant mechanisms. The antidepressant effect of LBP was investigated by open field test (OFT), forced swimming test (FST), tail suspension test (TST), and antagonism of reserpine hypothermia and ptosis in mice. In addition, we examined the oxidative status and antioxidation power of striatum in both control and depressive mice with or without LBP treatment. To explore the mechanism of LBP on regulating antioxidants in the depressive mice, we detected the expression level of Bcl-2 and poly (ADP ribose) polymerase (PARP) in striatum of mice by western blotting. The results showed that administration with LBP for 4 consecutive weeks significantly increased locomotor activity, reduced the duration of immobility, and antagonized hypothermia and ptosis in mice induced by reserpine. Also, LBP treatment was able to reduce the lipid peroxidation (LPO) production, and enhance the antioxidation effect of the striatum in depressive mice. Furthermore, LBP inhibited the decreased extent of the apoptotic suppressors, Bcl-2 and PARP, which were markedly decreased after treatment with reserpine. The above results indicated that LBP possess antidepressant activities, probably via its powerful antioxidative properties and then decreased the apoptosis of striatum neuron.

摘要

抑郁症将成为全球第二大疾病负担,它会损害生活质量、降低生产力,并增加残疾率和死亡率。多糖(LBP)是从[具体来源未给出]中纯化得到的主要活性成分。本研究的目的是评估LBP对利血平诱导的抑郁小鼠的潜在治疗作用及其相关机制。通过旷场试验(OFT)、强迫游泳试验(FST)、悬尾试验(TST)以及对小鼠利血平诱导的体温过低和眼睑下垂的拮抗作用来研究LBP的抗抑郁作用。此外,我们检测了在有或没有LBP治疗的对照小鼠和抑郁小鼠纹状体中的氧化状态和抗氧化能力。为了探究LBP调节抑郁小鼠抗氧化剂的机制,我们通过蛋白质免疫印迹法检测了小鼠纹状体中Bcl-2和聚(ADP核糖)聚合酶(PARP)的表达水平。结果表明,连续4周给予LBP可显著增加小鼠的运动活性,减少不动时间,并拮抗利血平诱导的小鼠体温过低和眼睑下垂。此外,LBP治疗能够降低脂质过氧化(LPO)的产生,并增强抑郁小鼠纹状体的抗氧化作用。此外,LBP抑制了凋亡抑制因子Bcl-2和PARP的降低程度,利血平处理后它们显著降低。上述结果表明,LBP具有抗抑郁活性,可能是通过其强大的抗氧化特性,进而减少纹状体神经元的凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4434/6934982/f8f6c212d410/ijpr-18-1556-g001.jpg

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