Increased serum visfatin as a risk factor for atherosclerosis in patients with ischaemic cerebrovascular disease

<p><b>INTRODUCTION</b>The present study aimed to investigate the possible associations between serum levels of visfatin, an adipokine, and atherosclerosis in patients with ischaemic cerebrovascular disease.</p><p><b>METHODS</b>A total of 95 participants were recruited for this study. Group A comprised 35 individuals with no history of cerebrovascular disease (control group) and Group B comprised 60 patients with ischaemic cerebrovascular disease. Group B was further categorised into two subgroups based on the ultrasonographic findings of the common carotid artery intima‑media thickness (CCA‑IMT) - Group B1 consisted of 21 patients with no atherosclerosis (i.e. CCA‑IMT ≤ 0.9 mm) and Group B2 consisted of 39 patients with atherosclerosis (i.e. CCA‑IMT > 0.9 mm). The body mass index, fasting blood total cholesterol, triglycerides, high‑density lipoprotein cholesterol, low‑density lipoprotein cholesterol and glucose levels of each patient were measured. Serum visfatin levels were determined using enzyme‑linked immunosorbent assays. Visfatin levels were compared between groups, and stepwise logistic regression analysis was used to identify risk factors for atherosclerosis, including visfatin levels.</p><p><b>RESULTS</b>The mean serum visfatin level of the patients in Group B was higher than that in Group A (75.5 ± 77.80 ng/mL vs. 8.6 ± 4.69 ng/mL; p < 0.05) and the level was higher in patients from Group B2 than those from Group B1 (89.0 ± 80.68 ng/mL vs. 50.4 ± 72.44 ng/mL; p < 0.05). Multivariate regression analysis showed that CCA‑IMT values were not significantly associated with visfatin levels. However, logistic regression analysis showed that serum visfatin was an independent risk factor for atherosclerosis (odds ratio 37.80; p = 0.004).</p><p><b>CONCLUSION</b>Serum visfatin may be an independent risk factor for cerebral infarction, as high serum visfatin levels are positively associated with the underlying pathogenic mechanisms of ischaemic cerebrovascular disease.</p>

Effect of anti-epileptic, nootropic drugs on the expression of ERK2 and NCAM1 in the hippocampus changes on the epileptic rats with cognitive dysfunction / 中华行为医学与脑科学杂志

Objective To study the effect of anti-epileptic,nootropic drugs on the expression of NCAM and ERK2 in the hippocampus changes on the epileptic rats with cognitive dysfunction.Methods A total of 120Wistar rats were used.20 controls and 100 in which epilepticus with cognitive dysfunction were randomly assigned to 5 groups (n =20/group) that received daily treatments for 30 days with either (1) saline (epilepsy),(2) carbamazine (traditional anti-epileptic),(3) oxcarbazine (new anti-epileptic),(4) aniracetam (brain protective),or (5) donepezil (nootopic).Spatial learning and memory were assessed with a Morris Water Maze (MWM).Hippocampus tissue was assessed for NCAM1 and ERK-2 mRNAs by RT-PCR and proteins by immunochemistry.Results The mean escape latency of the place navigation test:EP group ((67.14 ± 7.37)s)was all higher than NS group (35.78 ± 4.84 s)and there was statistical significance (P ＜ 0.01),carbamazepine group ((81.23 ± 9.46)s) ＞ EP group((67.14 ±7.37)s) ＞ donepezi group((53.75 ±6.74) s) (P＜0.01).Immunohistochemical and RT-PCR result:carbamazepine ＜ oxcarbazepine ＜ epilepsy ＜ aniracetam ＜ donepezi group.Compared with control group,donepezil group ＞ control group (P ＜ 0.01),aniracetam group ＞ control group (P ＜ 0.05).Conclusion ERK-2 expression is decreased and NCAM 1 expression is increased in the hippocampus in the epileptic rats.Thus,both are involved in cognitive dysfunction.Carbamazepine aggravates cognitive dysfunction,whereas donepezil improves cognitive dysfunction associated with epilepsy.

Effect of songling xuemaikang pretreatment on the expression of matrix metalloproteinase-9 after focal cerebral ischemia-reperfusion in rats / 国际脑血管病杂志

Objective To investigate the effect of songling xuemaikang(SL-xmk)pretreatment on the expression of matrix metalloproteinase-9(MMP-9)after focal cerebral ischemia-reperfusion in rats.Methods A total of 45 male Sprague-Dawley rats were randomly allocated into SL-xmk pretreatment,sham operation,and normal saline control group.Preventive gavage was per-formed for 8 weeks in rats using SL-xmk(937.50 mg/kg)suspension in the SLxmk pretreatment group(n = 15);the preventive gavage was performed in rats using the equal volume of normal saline in the sham operation(n = 15)and normal saline control(n = 15)groups.At the end of the pretreatment process,a model of middle cerebral artery occlusion(MCAO)in rats was induced by suture method for 2 hours and reperfusion for 24 hours.The effects of SL-xmk pretreatment on the neurologic deficit scores after transient MCAO,brain water content,and infarct volume in rats were observed.Immunohistochemical staining was used to detect the MMP-9 immunoreactive positive cells in ischemic brain tissue.Results The neurologjc deficit scores(1.21 ± 0.25 vs.2.37 ± 0.35,P = 0.000),the brain water content (76.24% ± 7.09% vs.88.78% ± 6.57%,P = 0.000),the percentage of infarct volume (22.62% ±2.17% vs.27.84% ±3.43%,P =0.000),and the numbers of MMP-9 positive cells(16.20 ± 2.17/mm vs.20.60 ± 2.71/mm,P = 0.000)were all significantly lower than those in the control group.Conclusions SL-xmk pretreatment may significantly inhibit the expression of MMP-9 in the brain tissue of focal cerebral ischemia-reperfusion rats and reduce brain water content and infarct volume.