RESUMO
Objective To investigate the correlation between cerebral microbleeds (CMBs ) and cognitive impairment in patients with chronic cerebral ischemia. Methods From January 2015 to January 2017, patients with chronic cerebral ischemia admitted to the Department of Neurology, the Second Hospital of Hebei Medical University were divided into CMBs positive group and CMBs negative group according to the findings of susceptibility weighted imaging. Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment (MoCA) were used to compare the cognitive function of both groups of patients and analyze the effects of different parts of CMBs on cognitive function. They were divided into cognitive impairment group and non-cognitive impairment group according to MoCA scores. Multivariate logistic regression analysis was used to determine the independent risk factors for cognitive impairment. Results A total of 96 patients were enrolled, aged 45-83 years, 32 were females (33. 3％) and 64 were males (66. 7％). There were 51 patients (53. 1％) in the CMBs positive group, and 45 (46. 9％) in the CMBs negative group, there were 33 patients (34. 4％) in the cognitive impairment group and 63 (65. 6％) in the non-cognitive impairment group. In the CMBs positive group, 10 patients had lobar CMBs, 29 had deep brain and infratentorial CMBs, and 12 had mixed CMBs. Multivariate logistic regression analysis showed that age (odds ratio [OR] 1. 115, 95％ confidence interval [CI] 1. 030-1. 207; P = 0. 007), the number of CMBs (OR 1. 254, 95％ CI 1. 064-1. 479; P = 0. 007), Fazekas scale score (OR 2. 697, 95％ CI 1. 012-7. 185; P = 0. 047), and multiple lacunar infarction ( OR 7. 103, 95％ CI 1. 248- 40. 424; P = 0. 027 ) were the independent risk factors for cognitive impairment. Compared with the CMBs negative group, the rates of cognitive impairment and dementia in the CMBs positive group were higher. The total MoCA score, visual space and execution function, attention, and delayed recall scores were significantly lower (all P < 0. 05). Each cognitive domain score in the lobar CMBs group were significantly lower than that in the non-lobar CMBs group (all P < 0. 05). There was no significant difference in each cognitive domain score between deep and infratentorial CMBs group and that of the non-deep and infratentorial CMBs group (all P > 0. 05). The visual space and execution function, attention, and delayed recall in the mixed CMBs group were significantly lower than those in the non-mixed CMBs group (all P < 0. 05). Conclusion CMBs (especially lobar CMBs) may cause a decline in overall cognitive function, even dementia in patients with chronic cerebral ischemia, and they are most closely related to visual space and executive function, attention, and delayed recall.
RESUMO
Objective To explore the effects of luteolin on cognition function in pentylenetetrazol (PTZ)-induced epileptic rats and related mechanism.Methods Fifty male SD rats were randomly divided into a normal control group(n=8), a model group(n=12), and groups of 25, 50 mg/kg luteolin(both ofn=11), as well as 100 mg/kg luteolin group(n=8). Those rats were given different doses of luteolin (25, 50 and 100 mg/kg, daily, intragastric administration) for 36 consecutive days. Similarly, rats of the normal control group and the model group were given 0.5% sodium carboxymethyl cellulose suspension liquid via intragastric administration. Thirty minutes later, a model of epilepsy was induced using PTZ (40 mg/kg, daily) via intraperitoneal injection except the control group. Learning and memory of rats were evaluated by Morris water maze and novel objective recognition trials(including escape latency and recognition index). The levels of CaM and CaMPK were determined by ELISA methods, and expression of Ras proteins in the hippocampus were detected by Western Blot.Results Compared with the model group, luteolin treatment groups significantly shorten the escape latency(28.51 ± 3.84 s, 19.77 ± 5.41 s, 14.86 ± 2.76 svs. 37.08 ± 5.18 s) in the Morris water maze, and increased recognition index(18.77% ± 2.02%, 25.06% ± 4.32%, 31.92% ± 2.65%vs. 13.87% ± 2.14%) in the novel objection trial(P<0.05 orP<0.01). Meanwhile, CaM(140.33 ± 13.52 ng/L, 124.26 ± 9.97 ng/L, 113.52 ± 11.57 ng/Lvs. 158.36 ± 10.68 ng/L) and CaMPK(8.25 ± 1.37 ng/ml, 7.69 ± 0.84 ng/ml, 6.74 ± 0.93 ng/mlvs. 9.87 ± 1.02 ng/ml) were significantly decreased(P<0.05 orP<0.01). What’s more, the expression of Ras proteins(0.99 ± 0.08, 0.76 ± 0.07, 0.52 ± 0.07vs. 1.58 ± 0.12) was obviously decreased compared with the model group(P<0.05 orP<0.01).Conclusion Luteolin could effectively improve the cognition dysfunction of epileptic rats, and the mechanism might be relevant to regulate the CaM-CaMPK signaling pathway via down-regulation of CaM, CaMPK, as well as Ras protein.