The aim of this study was to investigate the protective effect of sulforaphane (SFN) on 1-methyl-4-phenyl pyridine ion (MPP+)-induced cytotoxicity and to investigate its possible mechanisms. Methods: PC12 cell toxicity induced by MPP+ served as a cell model of Parkinson's diseases. The cell culture + experiments were divided into four groups based on the different treatments, namely, vehicle control, SFN, MPP+ and SFN pretreatment plus MPP+. Cell viability and apoptosis were examined by MTT assay and flow cytometry, respectively. Expressions of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase 1 (HO-1) and nicotinamide quinone oxidoreductase 1 (NQO1) were detected using western blotting. Results: MPP+ reduced the survival rate of PC12 cells in a dose- and time-dependent manner. After 24-h treatment with 500 µmol/l MPP+, the survival rate of PC12 cells decreased to 58.2±0.03% of that in the control groups. Under the same conditions MPP+ resulted in significant apoptosis of PC12 cells (apoptosis rate: 30.4±0.6%). However, SFN pretreatment significantly attenuated the cell damage induced by MPP+. Furthermore, it was demonstrated that SFN reversed the reduction of Nrf2, HO-1 and NQO1 expression induced by MPP+. Conclusion: SFN may protect PC12 cells from MPP+-induced damage via activating the Nrf2-ARE (antioxidant responsive element) pathway.

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Atraumatic convexity subarachnoid hemorrhage (c-SAH) concomitant with large artery atherosclerosis (LAA) stroke has been rarely discussed in the literature. Our aim in this study is to characterize the clinical and neuroradiological features of patients with LAA stroke and c-SAH. A retrospective study from a single institution was performed between January 2016 and June 2020. Only patients diagnosed with c-SAH and LAA stoke were included in this study. The clinical presentation and neuroimaging finding were summarized by our experienced neurologists. In total, 12 patients (8 men, 4 women), ranging in age from 45 to 75 years, were identified. All of them had cardiovascular risk factors and hypertension was the commonest (50%). Almost all patients presented hemiparesis (91.7%). Other clinical presentations included, dysarthria (41.7%), hemianesthesia (33.3%), facial palsy (33.3%), aphasia (16.7%), and cognitive impairment (8.3%). Internal border-zone (IBZ) infarction and cortical border-zone (CBZ) infarction occurred in 12 and 3 patients, respectively. c-SAH might occurred in different cortical sulcis. Percentages of frontal lobe, parietal lobe and fronto-parietal lobe were 41.7% (n = 5), 25% (n = 3) and 25% (n = 3), respectively. All ischemic lesions were ipsilateral to the sites of c-SAH. High-grade atherosclerotic stenosis of large artery was detected in all patients. The M1 segment of middle cerebral artery (MCA) is the second most common atherosclerotic artery after internal carotid artery (ICA). Our data suggest that LAA stroke is always ipsilateral to the site of c-SAH. Severe atherosclerotic changes can also been seen in the M1 segment of MCA apart from extracranial ICA. Moreover, border zone infarction may be a specific form of infarct when c-SAH is confronted with LAA stroke.

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