Relationship between NLRP3 activation level of inflammasome and the change of cognitive functions in patients with acute ischemic stroke / 中华行为医学与脑科学杂志

Objective:To investigate the relationship between the activation level of Nod-like receptor pyrin domain-containing 3 (NLRP3) inflammasome and the change of cognitive functions in patients with acute ischemic stroke.Methods:A total of 88 patients with acute ischemic stroke in Department of Neurology from October 2018 to July 2020 were selected as case group and 100 healthy physical examinees were selected as control group.Peripheral blood of the case group and the control group was collected, and peripheral blood mononuclear cells (PBMCs) were isolated by centrifugation.Then the NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC), Caspase-1 and interleukin-1β (IL-1β) expression were detected by Western blot.The cognitive function of patients with acute ischemic stroke was detected by Montreal Cognitive Assessment (MoCA). The differences in expression levels of NLRP3, ASC, Caspase-1 and IL-1β were compared between the case group and the control group.Pearson correlation analysis was used to analyze the correlation between expression levels of NLRP3, ASC, Caspase-1, IL-1β and MoCA score.Logistic multivariate regression was used to analyze the relationship between expression levels of NLRP3, ASC, caspase-1, IL-1β and the cognitive dysfunction.Results:(1)Western blot results showed that NLRP3, ASC, Caspase-1 and IL-1β expressions in PBMCs cells in the case group were higher than those in the control group (all P<0.05). (2)The expression level of NLRP3 in stroke patients with hypertension, hyperlipidemia, National Institutes of Health Stroke Scale (NIHSS) score ≥ 8 points was significantly higher than that in patients without hypertension, hyperlipidemia and NIHSS score<8 points ( P<0.05); (3)The incidence of cognitive dysfunction in the case group was 34.09% (30/88). The MoCA scores of the cognitive dysfunction group and the non-cognitive dysfunction group were 20 (24, 28) and 27 (26, 28) points respectively, and the difference between the groups was statistically significant ( P<0.05); (4)Pearson correlation analysis showed that NLRP3, ASC, caspase-1 and IL-1β expression in PBMCs cells were negatively correlated with MoCA scores ( r=-0.426, -0.396, -0.417, -0.320 respectively, all P<0.05). (5)Logistic regression analysis showed that hyperlipidemia, NIHSS scores, frontotemporal lobe infarction, and NLRP3 expression were the influencing factors for the occurrence of cognitive dysfunction (all P<0.05). Conclusion:Patients with acute ischemic stroke have high activated NLRP3 inflammasome, and its activation degree is closely related to the condition and the occurrence of cognitive dysfunction after stroke.Targeted inhibition or regulation of NLRP3 inflammasome activation may become a new idea of neuroprotection for acute ischemic stroke.

Taurine induces apoptosis in pulmonary artery smooth muscle cells / 中国中药杂志

<p><b>OBJECTIVE</b>To study the effect of taurine on apoptosis in PASMCs, and whether the death-receptor pathway act in the mechanism.</p><p><b>METHOD</b>Culture the PASMCs, and divided the cells into control, SD. Acridine orange(AO) assay and western-blot analysis on the expression of Bax, Bcl-2, Procaspase-3 and Fas were used to study the mechanism.</p><p><b>RESULT</b>A major finding of this study is that the Tau effects many apoptosis index, such as increasing the expression of Bax and Fas, decreasing the expression of Procaspase-3, and Bcl-2, accrescencing the mitochondrial depolarization, causing the nuclear shrinkage, all these datas demonstrated that Tau induced the apoptosis in pulmonary artery smooth muscle cells through mitochondrial-dependent pathway.</p><p><b>CONCLUSION</b>Tau induces the apoptosis in pulmonary artery smooth muscle cells through death-receptor.</p>

Puerarin induced apoptosis of pulmonary artery smooth muscle cell by mitochondrial pathway / 中国中药杂志

<p><b>OBJECTIVE</b>To investigate the contribution of mitochondrial pathway in the apoptosis induced by puerarin (PUE) in pulmonary artery smooth muscle cells.</p><p><b>METHOD</b>Cultured rat pulmonary artery smooth muscle cells (PASMC) were intervened by high, middle and low dose of puerarin (1.5 x 10(-3), 1.5 x 10(-4), 1.5 x 10(-5) mol x L(-1)). The change of mitochondrial membrane potential was observed. Western blot detected the expression of apoptosis-related gene Caspase-9, Bax and Bcl-2 protein.</p><p><b>RESULT</b>Compared with the control group, mitochondrial membrane potential significantly decreased in puerarin groups. Puerarin can enhance the expression of Caspase-9 and Bax protein, decrease the expression of Bcl-2 protein. Puerarin also has a concentration-dependent on the induction of PASMC.</p><p><b>CONCLUSION</b>Puerarin can induce PASMC apoptosis through mitochondrial pathway.</p>

Comparison of the effects of sevoflurane and isoflurane on intracranial pressure in neurosurgical patients / 中华麻醉学杂志

To evaluate the effects of sevoflurane and isoflurane at 1.0 minimum alveolar concentration (MAC) on intracranial pressure(ICP) in patients undergoing craniotomy.Method:Sixteen patients without pre-existing increased ICP subjected to craniotomy for pituitary adenoma or craniopharyngioma were intubated with midazolam, fentanyl and atracurium.After intubation,midazolam and atracurium were pumped intravenously for 30 min.Then,sevoflurane or isoflurane was inhaled and the patients were randomly divided into two groups:A:1.0 MAC sevoflurane:B:1.0 MAC isoflurane.In the whole procedure,PaCO_2 with an average of 5.3 kPa was maintained. ICP was measured continuously by placement of a catheter into lumbar subarachoid space.Result:Sevoflurane maintained cerebral perfusion pressure slightly better than equipotent dose of isoflurane. During sevoflurane administration at 1.0 MAC.ICP decreased slighly,then increased gradually.However,ICP remained stable in group B.Conclusion:Sevoflurane and isoflurane at 1.0 MAC,Combined with midazolam and fentanyl,can be administered safely to the patients without preexisting increased ICP.