β-caryophyllene alleviates cerebral ischemia/ reperfusion injury in mice by activating autophagy.
10.19540/j.cnki.cjcmm.20191112.402
- Author:
Jiang-Yan RAO
1
;
Qian WANG
1
;
Yu-Chun WANG
1
;
Fei XIANG
1
;
Xiao-Cui TIAN
1
;
Dao-Hang LIU
1
;
Zhi DONG
1
Author Information
1. Chongqing Key Laboratory of Biochemistry and Molecular Pharmacology Chongqing 400016, China Department of Pharmacy, School of Chongqing Medical University Chongqing 400016, China.
- Publication Type:Journal Article
- Keywords:
autophagy;
beclin1;
cerebral ischemia-reperfusion injury;
neuroprotection;
β-caryophyllene
- MeSH:
Animals;
Autophagy;
Brain Ischemia/drug therapy*;
Infarction, Middle Cerebral Artery;
Male;
Mice;
Mice, Inbred C57BL;
Polycyclic Sesquiterpenes/therapeutic use*;
Random Allocation;
Reperfusion Injury/drug therapy*
- From:
China Journal of Chinese Materia Medica
2020;45(4):932-936
- CountryChina
- Language:Chinese
-
Abstract:
Cerebral ischemia-reperfusion(I/R) injury is an important cause of acute ischemic stroke. Timely elimination of damaged proteins and organelles by regulating autophagy during cerebral ischemia-reperfusion plays an important role in relieving brain damage. In order to investigate whether β-caryophyllene(BCP) could protect neurons from cerebral I/R injury by regulating auto-phagy, C57 BL/6 J male mice were randomly divided into sham operation group, model group, and drug-administered group. After intra-gastric administration was given for 5 days, the middle cerebral artery occlusion(MCAO) model was established by suture method. Twenty four hours after surgery, the infarct volume and neurological function were assessed; the pathological changes of cortical tissue were observed by HE staining; Western blot was used to detect the expression of autophagy-related proteins beclin1, p62, LC3 B and apoptosis-related protein Bcl-2; immunofluorescence was used to observe the expression of LC3 B in the ischemic cortex. The autophagy of cortical tissue in the ischemic area was observed by transmission electron microscopy. The experimental results showed that as compared with the model group, the BCP pretreatment significantly reduced the neurological deficit, decreased the percentage of cerebral infarction volume, reduced the death of brain tissue cells in the ischemic area, up-regulated the expression of beclin1, LC3 B and Bcl-2 protein, down-regulated p62 protein expression, and significantly increased the number of autophagosomes in the cortical tissue of the ischemic area. It was finally determined that BCP could protect neurons from cerebral ischemia-reperfusion injury by activating autophagy.
