Ischemic stroke causes dysfunction of ventricular motile cilia and induces cerebral edema

Acta Universitatis Medicinalis Anhui 2022 01 v.57 47-52     font:big middle small

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Authors:Zhao Yujie; Zhang Ling; Ma Lan; Teng Zengguang; Jia Jinxin; Cao Xiaolu

Keywords:cerebral ischemia-reperfusion;cerebral edema;ependymal cells;motile cilia;SPAG6

DOI:10.19405/j.cnki.issn1000-1492.2022.01.010

〔Abstract〕 Objective To investigate the effect of motile cilia of ependymal cells on cerebral edema induced by ischemic stroke. Methods SD rats(n=60)were randomly divided into sham group and ischemia-reperfusion model group. In the model group, a 2 h reperfusion 24 h model of ischemia was constructed by the method of suture. The Longa′s-5 point method and the 2, 3, 5-triphenyltetrazolium chloride(TTC) staining were used to assess neurological function and the cerebral infarction volume, respectively. The dry and wet weight method was used to measure brain water content. The morphological changes of motile cilia were observed by HE staining and scanning electron microscope(SEM). The level of SPAG6 expressed in tissues with motile cilia was measured by Western blot. Immunofluorescence was used to detect the structure of motile cilia and the expression distribution of SPAG6 in brain. Results Compared with the sham group, the infarct volume and neurological function score of the model group increased significantly, and the brain edema was obvious(P<0.05). HE staining and SEM results showed that the brain tissue structure of the sham group was tight and regular and the ependymal cell nucleus was round and full. The motile cilia in sham group were arranged orderly and the structure was complete. The brain tissue structure of the model group was loose and the ependymal cell nucleus was wrinkled、condensed and dyed. A large number of necrotic cells were generated, and the structure of motile cilia was disordered. The number and density of motile cilia were significantly reduced, and the arrangement was disordered. Western blot results showed that the total protein content of SPAG6 in the model group was higher than that in the sham group, but the results were not statistically different. Immunofluorescence results showed that compared with the sham group, the length of motile cilia in the model group was significantly shorter(P<0.05). The fluorescence intensity of SPAG6 in the model group was higher than that in the sham group, but the results were not statistically different. Compared with the sham group, the average fluorescence intensity of SPAG6 in ependymal cells of the model group significantly increased, and the difference was statistically significant(P<0.05); and cerebral ischemia-reperfusion injury reduced the expression of SPAG6 fluorescence in the cilia(P<0.05). Conclusion Cerebral ischemia-reperfusion down-regulates the expression of SPAG6 in motile cilia of ependymal cells, resulting in abnormal structure and dysfunction of motile cilia, and subsequent brain edema injury.