Picroside II Exerts a Neuroprotective Effect by Inhibiting mPTP Permeability and EndoG Release after Cerebral Ischemia/Reperfusion Injury in Rats

被引：32
作者：
Li, Shan [1 ]
Wang, Tingting [1 ]
Zhai, Li [1 ]
Ge, Keli [2 ]
Zhao, Jun [2 ]
Cong, Weihong [3 ]
Guo, Yunliang [1 ]
机构：
[1] Qingdao Univ, Shandong Prov Collaborat Innovat Ctr Neurodegener, Taishan Scholars Construct Project Excellent Inno, Inst Cerebrovasc Dis,Affiliated Hosp, Qingdao 266003, Peoples R China
[2] Qingdao Univ, Med Coll, Inst Integrat Med, Qingdao 266021, Peoples R China
[3] China Acad Chinese Med Sci, Xiyuan Hosp, Beijing 100091, Peoples R China
来源：
JOURNAL OF MOLECULAR NEUROSCIENCE | 2018年 / 64卷 / 01期
基金：
中国国家自然科学基金;
关键词：
PicrosideII; Ischemia/reperfusion; Mitochondrial permeability transition pore; Voltage-dependent anion channel 1; Endonuclease G; CELL-DEATH; ENDONUCLEASE-G; CYTOCHROME-C; VDAC1; OLIGOMERIZATION; TRANSITION; MITOCHONDRIA; ISCHEMIA; INVOLVEMENT; APOPTOSIS; PROTEIN;
D O I：
10.1007/s12031-017-1012-z
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Mitochondrial membrane permeability is closely related to cerebral ischemia/reperfusion (I/R) injury. This paper explored the neuroprotective effect of picroside II (Picr), which inhibits the permeability of mitochondrial permeability transition pore (mPTP) and endonuclease G (EndoG) release from mitochondria into cytoplasm after cerebral I/R in rats. After 2 h of cerebral ischemia and 24 h of reperfusion in rats with different intervention measures, the neurobehavioral function, infarction volume, and reactive oxygen species (ROS) content in brain tissues were observed by modified neurological severity scale (mNSS), triphenyl tetrazolium chloride (TTC) staining, and enzyme-linked immunosorbent assay, respectively. The permeability of mPTP was assayed using spectrophotometry. The morphology and apoptotic cells of brain tissues were observed by hematoxylin-eosin staining and terminal deoxynucleotidyl transferase dUTP nick end labeling assay, respectively. The expressions of EndoG and voltage-dependent anion channel 1 (VDAC1) were determined by immunohistochemical assay and western blot. The Picr group exhibited clear decreases in mNSS scores, ROS content, number of apoptotic cells, mPTP permeability and expression of VDAC1, and EndoG in cytoplasm and nuclei, and the morphology of brain tissue was improved as compared with the model group (P < 0.05). Picr could attenuate cerebral I/R injury by downregulating the expression of VDAC1 and decreasing the permeability of mPTP, thereby inhibiting EndoG release from mitochondria into cytoplasm.
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收藏
页码：144 / 155
页数：12
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