神经保护
瘦素
缺血
细胞凋亡
免疫印迹
脑梗塞
生物
磁共振成像
灵长类动物
梗塞
内科学
内分泌学
医学
神经科学
放射科
生物化学
心肌梗塞
基因
肥胖
作者
Cheng Ge,Deng Yan-xian,Zhipeng Zhou,Junxiong Yu,Huiyang Zhang,Xianfeng Wang,Xiaotian Li
标识
DOI:10.1080/10495398.2021.1920424
摘要
The purpose of this study was to evaluate the neuroprotective effect of leptin on a non-human primate model of cerebral ischemia. A total of 39 Guangxi macaques were used to establish the primate cerebral-ischemia model. HE staining was used to evaluated the pathological changes. Moreover, magnetic resonance imaging was used for the detection of embolic area. The measurements of behavior observation and cerebral infarction area were also performed. They all received autologous thrombus operation. Furthermore, western blot and RT-PCR were also used to detect the protein and mRNA expression levels of apoptosis-related factors. Our results showed that leptin could reduce the volume of cerebral infarction by about 35%. Behavioral defects can be significantly improved. In addition, mid-term and long-term behavioral deficiencies had been significantly improved by leptin. Moreover, leptin significantly decreased the expression levels of caspase-3 and Bax, and increased the expression levels of Bcl-2. In conclusion, leptin has neuroprotective effects on cerebral ischemia by effectively reducing the volume of cerebral infarction.
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