Micro RNA-122 aggravates brain parenchymal injury in mice after ischemia-reperfusionby down-regulating insulin-like growth factor type 1 receptor
10.3760/cma.j.issn.1671-8925.2018.12.004
- VernacularTitle:miR-122对脑缺血再灌注损伤小鼠的影响及其机制研究
- Author:
Bin LUO
1
;
Yujue WANG
;
Hengxing YOU
;
Zhitao PENG
;
Xiaowen LIAN
Author Information
1. 中山大学附属第八医院(深圳市福田区人民医院)神经外科
- Keywords:
Micro RNA-122;
Cerebral ischemia/reperfusion;
Insulin-like growth factor type 1 receptor
- From:
Chinese Journal of Neuromedicine
2018;17(12):1210-1216
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of micro RNA (miR)-122 on cerebral ischemia/reperfusion (I/R) injury and its mechanism in mice. Methods Thirty-six male C57BL mice were randomly divided into a sham-operated group, a model group, a miR-122 mimics group and a miR-122 inhibitor group (n=9). The miR-122 NCs, inhibitor fragments and overexpression fragments were injected into the lateral ventricles of mice from the later 3 groups; 10 min after that, middle cerebral artery I/R injury models were induced by reforming Longa method. Twenty-four h after model making, real-time fluorescent quantitative PCR (qRT-PCR) was used to detect the miR-122 and insulin like growth factor 1-receptor (IGF-1R) mRNA expressions; cell apoptosis in the peripheral region of cerebral infarction was detected by immunofluorescent staining; the volumes of cerebral infarction and brain edema were measured by TTC staining; and IGF-1R protein expression was detected by Western blotting. Results As compared with the sham-operated group, the model group had significantly increased miR-122 expression and significantly increased brain infarction volume and edema volume (P<0.05). As compared with the model group, miR-122 mimics group had significantly increased miR-122 expression and significantly increased brain infarction volume and edema volume (P<0.05), while miR-122 inhibitor group had statically decreased miR-122 expression and significantly decreased brain infarction volume and edema volume (P<0.05). The number of apoptosis of peripheral cells in the cortical infarction area of mice in the sham-operated group, model group and miR-122 mimic group became lager successively, while the number of apoptosis of peripheral cells in the cortical infarction area of mice in the miR-122 inhibitor group was smaller than that in the model group. The IGF-1R mRNA and protein expressions in the cortical infracted peripheral zone of model group were significantly decreased as compared with those in the sham-operated group (P<0.05); the IGF-1R mRNA and protein expressions in the miR-122 mimics group were significantly decreased as compared with those in the model group (P<0.05), while those in the miR-122 inhibitor group were significantly increased as compared with those in the model group (P<0.05). Conclusion MiR-122 may be involved in the regulation of cerebral I/R for brain injury by inhibition of IGF-1R pathway.
