JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES) ›› 2016, Vol. 54 ›› Issue (10): 11-15.doi: 10.6040/j.issn.1671-7554.0.2015.257

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Effects of Wnt3a on neuronal autophagy and apoptosis in early brain injury after subarachnoid hemorrhage in rats

REN Baoxin, MA Yunfeng, LIU Dianwei, LI Zhuo, JIANG Yong   

  1. Department of Neurosurgery, Jinan Central Hospital Affilicated to Shandong University, Jinan 250012, Shandong, China
  • Received:2015-03-10 Online:2016-10-10 Published:2016-10-10

Abstract: Objective To investigate the effects of Wnt3a on neuronal autophagy and apoptosis in early brain injury after subarachnoid hemorrhage(SAH)in rats. Methods A total of 75 SD male rats were randomly divided in to Sham group, SAH group and Wnt3a group. The SAH model was established by injecting autologous blood into cisterna magna. Brain was taken out after SAH at five different time points(0, 12, 24, 48, and 72 h). Western bloting was used to detect the ratio of LC3Ⅱ and LC3Ⅰ, and analyze the expressions of Beclin-1 and Caspase-3. An immunofluorescence technique was used to observe the autophagy and apoptosis of neurons. Results Western bloting results showed that in SAH group, expressions of LC3Ⅱ/Ⅰ and Beclin-1 increased after SAH and reached the peak at 24 h time point. The expressions of LC3Ⅱ and Beclin-1 in Wnt3a group were significantly higher than those in SAH group at 24 h time point(P<0.05). Caspase-3 expression, which in Wnt3a group was significantly lower than the SAH group(P<0.05), peaked at 48 h after SAH. Immunohistochemistry result showed that, compared with SAH group, the number of Beclin-1 positive neurons in Wnt3a group enhanced at 24 h while Bax positive neurons and apoptotic cells decreased at 48 h(P<0.05). Conclusion Wnt3a promotes neuronal autophagy and decreases neuronal apoptosis, which may protect the neurons.

Key words: Rats, Apoptosis, Subarachnoid hemorrhage, Wnt3a, Autophagy

CLC Number: 

  • R392.7
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