The alpha2-adrenergic receptor agonist clonidine protects against cerebral ischemia/reperfusion induced neuronal apoptosis in rats.

Apoptosis is the crucial pathological mechanism following cerebral ischemic injury. Our previous studies demonstrated that clonidine, one agonist of alpha2-adrenergic receptor (α2-AR), could attenuate cerebral ischemic injury in a rat model of middle cerebral artery occlusion/reperfusion (MCAO/R). However, it's unclear whether clonidine exerts neuroprotective effects by regulating neuronal apoptosis. In this study, we elucidated whether clonidine can exert anti-apoptotic effects in cerebral ischemic injury, and further explored the possible mechanisms. Neurological deficit score was measured to evaluate the neurological function. TTC staining was used for the measurement of brain infarct size. Hematoxylin-Eosin (HE) staining was applied to examine the cell morphology. TUNEL and DAPI fluorescent staining methods were used to analyze the cell apoptosis in brain tissue. Fluorescence quantitative real-time PCR was performed to assess the gene expression of Caspase-3 and P53. Western blotting assay was applied to detect the protein expression of Caspase-3 and P53. The results showed that clonidine improved neurological function, reduced brain infarct size, alleviated neuronal damage, and reduced the ratio of cell apoptosis in the brain with MCAO/R injury. moreover, clonidine down-regulated the gene and protein expression of Caspase-3 and P53 which were over-expressed after MCAO/R injury. Whereas, yohimbine (one selective α2-AR antagonist) mitigated the anti-apoptosis effects of clonidine, accompanied by reversed gene and protein expression changes. The results indicated that clonidine attenuated cerebral MCAO/R injury via suppressing neuronal apoptosis, which may be mediated, at least in part, by activating α2-AR.

ICGA combined with EP monitoring in microclipping of cerebral aneurysms.

Cerebral aneurysm is one of the common cerebrovascular diseases in neurosurgery, and rupture of cerebral aneurysm is the most important cause of spontaneous subarachnoid hemorrhage. How to precisely clip the aneurysm has been a topic worth discussing, so the authors explore the value of ICGA combined with electrophysiological monitoring in the microclipping of cerebral aneurysms. Using the method of retrospective analysis of cases, 661 patients with cerebral aneurysms admitted to the Department of Neurosurgery, Zhongnan Hospital of Wuhan University, from 2021.8 to 2022.10 were studied, 390 patients with aneurysm clipping were included, and patients with Hunt-Hess classification ≥ 4 were excluded, and whether to use ICGA combined with EP in microclipping of the ruptured and unruptured aneurysm in pterional approach was investigated at the time of discharge, respectively. The MRS and total hospital days were compared to investigate the value of ICGA combined with EP in the microclipping of cerebral aneurysms. All 390 patients enrolled in the group had successful aneurysm clipping, 178 patients were screened for ruptured aneurysm pterional approach and 120 patients for unruptured aneurysm pterional approach access; the MRS at discharge was significantly lower in the ICGA combined with EP group than in the no-EP group for ruptured aneurysm pterional approach microclipping (p < 0.001), and the mean number of days in hospital was significantly lower (p < 0.01). Patients in the ICGA combined with EP group in microclipping of unruptured aneurysms with pterional approach also had significantly lower MRS at discharge compared with patients in the ICGA alone group (p < 0.001), with no statistically significant difference in the mean number of days in hospital (p = 0.09). In open cerebral aneurysm microclipping, ICGA combined with EP monitoring for both ruptured and unruptured aneurysms can effectively reduce the false-negative rate of ICGA, significantly reduce the incidence of postoperative neurological deficits, and shorten the total hospital stay to some extent. ICGA combined with EP monitoring may be an effective means to reduce the rate of false clipping of the penetrating vessels and to avoid stenosis or occlusion of the aneurysm-carrying artery and is worth promoting in microclipping of cerebral aneurysms except for Hunt-Hess ≥ 4.