Inhibition of p-caveolin1 attenuates neurological injury induced by cerebral ischemia-reperfusion in rats

Abstract

Objective To explore the mechanism of phosphorylation of caveolin1 (Cav1) in neurological injury after cerebral ischemia-reperfusion in rats. Methods The rats were randomly divided into sham group, model group and inhibitor group(PP2). Neurological function was evaluated by modified neurological deficit score (mNSS) neurobehavioral score, cerebral infarction volume was evaluated by triphenyltetrazolium chloride (TTC) staining, histomorphology after cerebral ischemia-reperfusion was evaluated by Nissl staining, and apoptosis of peri-infarcted tissue was detected by Tunel staining. Western blot and immunofluorescence were used to detect the protein expression of p-Cav1, glial fibrillary acidic protein (GFAP) and ion calcium binding junction molecule 1 (Iba1) in the tissue around cerebral infarction. Results Compared with the sham operation group, there were significantly increased mNSS score, volume of cerebral infarction, number of apoptotic cells and expression of p-Cav1, GFAP and Iba1 in the model group,while the number of Nissl corpuscles decreased. The inhibitor PP2 reduced the changes of the above-mentioned indexes and protect the neurological function of rats with cerebral ischemia-reperfusion injury. Conclusions Inhibition of p-Cav1 may improve the neurological function after cerebral ischemia-reperfusion in rats with potential mechanism of inhibiting glial cell activation and interaction.

Keywords

• cerebral ischemia-reperfusion|astrocytes|microglia|caveolin 1