Ischemia-induced brain damage leads to apoptosis like delayed neuronal death in selectively vulnerable regions, which could further result in irreversible damages. Previous studies have demonstrated that neurons in the CA1 area of hippocampus are particularly sensitive to ischemic damage. Atorvastatin (ATV) has been reported to attenuate cognitive deficits after stroke, but precise mechanism for neuroprotection remains unknown. Therefore, the aims of this study were to investigate the neuroprotective mechanisms of ATV against ischemic brain injury induced by cerebral ischemia reperfusion. In this study, four-vessel occlusion model was established in rats with cerebral ischemia. Rats were divided into five groups: sham group, I/R group, I/R+ATV group, I/R+ATV+LY, and I/R+SP600125 group. Cresyl violet staining was carried out to examine the neuronal death of hippocampal CA1 region. Immunoblotting was used to detect the expression of the related proteins. Results showed that ATV significantly protected hippocampal CA1 pyramidal neurons against cerebral I/R. ATV could increase the phosphorylation of protein kinase B (Akt1) and nNOS, diminished the phosphorylation of JNK3 and c-Jun, and further inhibited the activation of caspase-3. Whereas, all of the aforementioned effects of ATV were reversed by LY294002 (an inhibitor of Akt1). Furthermore, pretreatment with SP600125 (an inhibitor of JNK) diminished the phosphorylation of JNK3 and c-Jun, and further inhibited the activation of caspase-3 after cerebral I/R. Taken together, our results implied that Akt-mediated phosphorylation of nNOS is involved in the neuroprotection of ATV against ischemic brain injury via suppressing JNK3 signaling pathway that provide a new experimental foundation for stroke therapy.
Objective: To predict the risk factors of progressive and non-progressive stroke by the transcranial Doppler ultrasound information technology and the analysis of the comparative examination results. Methods: A total of 180 patients with ischemic stroke (IS) treated in the Neurology Department were included as the research objects. The Scandinavian Stroke Scale (SSS) was used to score the neurological functions of patients, and the patients were then divided into the progressive group (group P) and the non-progressive group (group NP). The carotid ultrasound examination was performed on the grouped patients, and the support vector machine (SVM) regression algorithm was used to classify the data obtained by the ultrasound examinations. The differences between the results of both groups were analyzed and discussed, as well as the carotid lesions and plaques. Results: The plaque detection rate was 96.7% in group P and 75.8% in group NP. In group P, the detection rate of the single plaque was 8.3%, and the detection rate of multiple plaques was 88.3%. In group NP, the detection rate of the single plaque was 19.2%, and the detection rate of multiple plaques was 56.7%. Besides, statistical differences existed between both groups (P < 0.01). Carotid plaques in both groups were mainly distributed in common carotid artery (CA), bifurcation, internal CA, and external CA. Of all the biochemical indexes and CPS, the fasting plasma glucose (FPS), low density lipoprotein-cholesterol, lipoprotein (a), homocysteine, C-reactive protein, and fibrinogen had positive correlations. The major risk factors for the formation of vulnerable carotid plaques were increased levels of lipoprotein (a), homocysteine, and C-reactive protein. Conclusion: The pathogenesis of progressive and non-progressive stroke was closely related to vulnerable plaque. The vulnerable plague was a factor indicating the risk of progressing to early stroke. Besides, the formation of vulnerable plaques was closely correlated to the increase of lipoprotein (a), homocysteine, and C-reactive protein levels.
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