Objective:To explore the mechanism of gypenoside ⅩⅦ against cerebral ischemia/reperfusion (I/R) through nuclear factor erythroid 2-related factor 2/antioxidant responsive element (Nrf2/ARE) signaling pathway.Methods:Forty SPF Sprague Dawley (SD) rats were randomly divided into sham operated group, I/R model group, 25, 50 and 100 mg/kg gypenoside ⅩⅦ groups ( n = 8). Gypenoside ⅩⅦ groups were administered 25, 50 or 100 mg/kg (0.01 mL/g) gypenoside ⅩⅦ by intragastric administration for 14 days; the other two groups received the same dose of saline. Rat cerebral I/R model was established by modified line bolt method; rats in the sham operated group underwent the same procedure without producing substantial embolization. After 24 hours of reperfusion, the neurological deficit scores of the rats in each group were assessed. Rat abdominal aortic whole blood was collected and the serum reactive oxygen species (ROS), heme oxygenase-1 (HO-1), γ-glutamylcysteine synthase (γ-GCS), superoxide dismutase (SOD), quinone NADH oxidoreductase 1 (NQO1), and malondialdehyde (MDA) were detected. Then whole brain tissue was harvested and penumbra tissue was isolated from cerebral cortex, the general condition of rat brain tissue and the volume of cerebral infarction were evaluated, the histopathological changes in the brain were observed under light microscopy, the mRNA expressions of Nrf2 and Keap1 were measured by real-time fluorescent quantitative polymerase chain reaction (RT-qPCR), the protein expressions of Nrf2 and Keap1 were determined by Western blotting. Results:After 24 hours of reperfusion, compared with the sham operated group, the score of neurological deficit and infarct volume were significantly increased, the NQO1, SOD and γ-GCS levels in serum were significantly decreased, MDA, HO-1 and ROS levels in serum were significantly increased, the Nrf2 and Keap1 mRNA and protein expressions in the ischemic penumbra were significantly increased in rats from I/R model group. Compared with the I/R model group, the neurological deficit scores (1.50±0.53, 1.37±0.52 vs. 2.75±0.46) and brain infarct volume [(19.8±5.1)%, (21.4±6.4)% vs. (42.3±5.8)%] were significantly reduced, serum NQO1, SOD, HO-1 and γ-GCS were significantly increased [NQO1 (ng/L): 186.05±10.38, 220.75±16.22 vs. 131.36±5.95, SOD (kU/L): 63.23±5.30, 72.70±8.62 vs. 36.75±6.55, HO-1 (ng/L): 60.57±7.93, 60.35±4.72 vs. 42.72±4.95, γ-GCS (kU/L): 8.81±0.53, 8.72±0.69 vs. 6.80±0.56], serum MDA and ROS levels were significantly reduced [MDA (μmol/L): 5.94±0.66, 5.61±0.53 vs. 10.88±1.34, ROS (kU/L): 69.11±4.23, 67.12±4.52 vs. 104.43±7.54], the mRNA and protein expressions of Nrf2 and Keap1 in the ischemic penumbra were significantly increased in rats from 50 mg/kg and 100 mg/kg gypenoside ⅩⅦ groups [Nrf2 mRNA (2 -△△Ct): 1.90±0.13, 2.13±0.18 vs. 1.48±0.11, Keap1 mRNA (2 -△△Ct): 1.78±0.11, 1.85±0.10 vs. 1.43±0.10, Nrf2/β-actin: 0.73±0.04, 0.79±0.03 vs. 0.60±0.03, Keap1/β-actin: 0.71±0.01, 0.76±0.03 vs. 0.61±0.01], all the comparative differences were statistically significant (all P < 0.01); 25 mg/kg gypenoside ⅩⅦ had no significant effect. Conclusion:Gypenoside ⅩⅦ (50 mg/kg and 100 mg/kg) may play a role in anti-cerebral I/R injury by regulating NQO1, SOD, HO-1, γ-GCS, ROS and MDA through Nrf2/ARE signaling pathway.

Aim To investigate the relationship between carotid artery perivascular fat density and carotid artery stenosis,prognosis.Methods A total of 209 consecutive patients with extracranial internal carotid artery stenosis in Taizhou Central Hospital(Taizhou University Affiliated Hospital)were retrospectively included from January 2017 to Janu-ary 2021.The carotid artery perivascular fat density in the narrowest axial layer and in the same contralateral axial layer was evaluated by computed tomography angiography.Clinical data of patients were collected.The stenosis was graded according to the guidelines.Symptomatic carotid stenosis was determined according to the medical history.The patients were followed up for one year.Results Carotid artery perivascular fat density was 4.2％higher on the stenosis side than those on the opposite side(P＜0.001).The fat density increased with the stenosis severity.On the stenosis side,carotid artery perivascular fat density was 6.25％higher in symptomatic patients than that in asymptomatic patients(P=0.015).In asymptomatic patients,perivascular fat density in patients with stenosis related cerebrovascular events oc-curred within 1 year was 12.4％higher than that in patients without related cerebrovascular events(P=O.017),and the difference remained after adjusting the clinical parameters by Logistic regression analysis(OR=1.060,95％CI:1.006～1.117,P=0.028).Conclusions Carotid artery perivascular fat density is positively correlated with the degree of ca-rotid stenosis.Patients with symptomatic carotid artery stenosis or recurrent related ischemic cerebrovascular outcome e-vents have higher carotid artery perivascular fat density.

Objective To explore the predictive value of cognitive function trend after ACI for the recurrence risk of cerebral infarction.Methods A total of 256 ACI patients admitted to our hospi-tal from January 2021 to December 2023 were enrolled retrospectively.Based on their MoCA score at 3 months after onset,they were assigned into 96 cases of no PSCI,51 cases of improved PSCI,17 cases of delayed PSCI and 92 cases of persistent PSCI.According to the results of MoCA at 2 weeks after onset,they were divided into 133 cases of PSCI group and 123 cases of non-PSCI group.The clinical data of the ACI patients were compared between the two groups,and their cog-nitive function trends were analyzed.Results Advanced age,and larger proportions of female,du-al antiplatelet therapy and PSQI＞5 were observed in the PSCI group than the non-PSCI group(P＜0.05,P＜0.01).There were significant differences in the incidences of recurrence and poor prognosis in the ACI patients with different cognitive function trends(P＜0.01).The persistent PSCI was associated with the increased risk of recurrence of cerebral infarction and poor prognosis(P＜0.05).The AUC value of persistent PSCI in predicting the recurrence and poor prognosis of cerebral infarction was 0.703(95％CI:0.631-0.767)and 0.595(95％CI:0.521-0.666),respec-tively.Conclusion Persistent PSCI can be used as a predictor of recurrence of cerebral infarction,and it also increases the risk of cognitive dysfunction in ACI patients.