Apelin-13 Attenuates Traumatic Brain Injury-Induced Damage by Suppressing Autophagy

被引:92
作者
Bao, Hai-Jun [1 ]
Zhang, Lin [1 ]
Han, Wen-Can [1 ]
Dai, Ding-Kun [2 ]
机构
[1] Xuzhou Med Coll, Dept Pathol, 209 Tongshan Rd,Xuzhou Yunlong Town, Xuzhou, Peoples R China
[2] Peoples Hosp Subei, Dept Forens Identificat, Yangzhou, Peoples R China
基金
美国国家科学基金会;
关键词
Apelin-13; Traumatic brain injury (TBI); Autophagy; CONTROLLED CORTICAL IMPACT; TRANSCRIPTION FACTOR NRF2; SELECTIVE AUTOPHAGY; TISSUE DISTRIBUTION; CELL-DEATH; P62/SQSTM1; RECEPTOR; PEPTIDE; APJ; P62;
D O I
10.1007/s11064-014-1469-x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
The adipocytokine apelin is a peptide, Apelin and its receptor are abundantly expressed in the nervous and cardiovascular systems. Previous studies had found apelin-13 reduces brain injuries and postischemic cerebral edema through blocking programmed cell death, Apelin-13 is also able to inhibit glucose deprivation induced cardiomyocyte autophagy in a concentration dependent fashion. To observe the effect of Apelin-13 on the brain injury induced by traumatic brain injury (TBI), and explore the effect of Apelin-13 on autophagy in TBI, We performed The neurological test, and the numbers of TBI-induced neural cell death were also counted by propidium iodide labeling. At last, the autophagy associated proteins LC3, Beclin-1, Bcl-2, p62 were also assessed with western-blotting. Compared with saline vehicle groups, the neural cell death, lesion volume, and neural dysfunction were attenuated by apelin-13 after TBI. In additionally, Apelin-13 also reversed TBI induced downregulation of LC3, Beclin-1, Bcl-2, p62 expression, compared with saline vehicle groups, at 24 and 48 h post TBI. Apelin-13 attenuates TBI induced brain damage by suppressing autophagy. All these results revealed that Apelin-13 suppressed autophagy. The autophagy may be involved in the mechanism of Apelin-13 rescue the subsequent damaged neuron in TBI.
引用
收藏
页码:89 / 97
页数:9
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