BackgroundApoptosis has been recognized as a critical pathophysiological process during cerebral ischemia. The neuroprotective effect of CART on ischemic brain injury is determined. However, there is little research on the protective effect of CART on neural stem cells (NSCs).MethodsPrimary cultured rat NSCs were utilized as the research subject. In vitro oxygen glucose deprivation (OGD) treatment was employed, and NSCs were extracted from SD pregnant rats following previous experimental protocols and identified through cell immunofluorescence staining. The appropriate concentration of CART affecting OGD NSCs was initially screened using Cell Counting Kit-8 (CCK-8) and Lactate Dehydrogenase (LDH) assays. EdU staining and Western blotting (WB) techniques were employed to assess the impact of the suitable CART concentration on the proliferation and apoptosis of OGD NSCs. Finally, Western blot analysis was conducted to investigate the cAMP-response element binding protein (CREB) pathway and expression levels of related proteins after KG-501 treatment in order to elucidate the mechanism underlying apoptosis and proliferation regulation in OGD NSCs.ResultsCCK-8 and LDH assays indicated that a concentration of 0.8 nM CART may be the optimal concentration for modulating the proliferation of OGD NSCs. Subsequently, cellular immunofluorescence and EdU detection experiments further confirmed the findings obtained from CCK-8 analysis. Western blot analysis of apoptosis-related protein expression also demonstrated that an appropriate concentration of CART could suppress the apoptosis of OGD NSCs. Finally, Western blotting was conducted to examine the CREB pathway and related protein expression after treatment with KG-501, revealing that an appropriate concentration of CART regulated both apoptosis and proliferation in OGD NSCs through CREB signaling.ConclusionThe concentration of CART at 0.8 nM may be deemed appropriate for inhibiting apoptosis and promoting proliferation in OGD NSCs in vitro. The mechanism maybe through activating the CREB pathway.

To investigate the correlation the correlation between residual cholesterol (RC) and increased carotid intima-media thickness(cIMT) in non-diabetic individuals. This study included 1786 non-diabetic individuals who underwent carotid ultrasound. RC was calculated based on total cholesterol (TC), LDL-C, and high density lipoprotein cholesterol (HDL-C). The subjects were divided into the cIMT thickening group (cIMT ≥ 0.1 cm) and non-thickening group (cIMT < 0.1 cm) groups based on cIMT, binary logistic regression with different models and receiver operating characteristic (ROC) curves were adopted to evaluate the predictive ability of RC in cIMT. Of the research participants , their median age was 55 (49–51) years, 1121 (63

To investigate the role of ultrasound-targeted microbubbles in the homing effect of bone marrow-derived mesenchymal stem cells (BMSCs) and in the therapeutic efficacy of BMSCs on the ischemic stroke. A middle cerebral artery occlusion (MCAO) model was induced by plug wire preparation. Seventy-two hours after MCAO, the treatment of BMSCs with ultrasound-targeted microbubble was assessed via modified neurological severity score (mNSS), infarct volumes, and cerebral edema. In addition, immunofluorescence was performed to analyze the homing effect of BMSCs with ultrasound-targeted microbubble. We find that BMSCs with ultrasound-targeted microbubble (BMMSCs with ultrasound-targeted microbubble [USMM] group) could significantly ameliorate mNSS, infarct volumes, and cerebral edema of MCAO compared with phosphate buffer saline group, BMSCs alone group (BMSC group), and BMSCs with Ultrasound group (Ultrasound group). Immunofluorescence analysis demonstrated that ultrasound-targeted microbubbles promoted the accumulation of BMSCs in rat MCAO brains. Our findings demonstrated that ultrasound-targeted microbubble could be an effective approach for the accumulation of BMSCs on ischemic stroke, and further improved the therapeutic efficacy of BMSCs on MCAO.

Cerebral venous sinus thrombosis (CVST) is a rare ischemic cerebrovascular disease. The aim of this retrospective observational study was to investigate the risk factors for complication of cerebral venous sinus thrombosis by seizures and to explore the impact of such seizures on clinical outcomes. Patients with cerebral venous sinus thrombosis with or without epileptic seizures were retrospectively analyzed and compared in terms of clinical variables, causative factors, clinical presentation, and imaging data. In all, 69 patients with cerebral venous sinus thrombosis were enrolled in this study, 32 (46.38%) of whom had experienced secondary seizures. Compared with those with no seizures, significantly more patients with secondary seizures had hemiplegia (37.50 vs. 15.63%; P = 0.020), bleeding (29.40 vs. 10.81%; P = 0.047), lesions involving the frontal (31.25 vs. 10.81%; P = 0.023) and temporal lobe (43.75 vs. 8.11%; P = 0.005), and thrombosis in the superior sagittal sinus (65.63 vs. 40.54%; P = 0.036). Multivariate logistic regression analysis showed focal neurological deficits (P = 0.004, odds ratio = 5.16, 95% CI 1.99-15.76) and thrombosis of the superior sagittal sinus (P = 0.039, odds ratio = 0.13, 95% CI 0.04-0.37) were independent risk factors for secondary seizures in patients with cerebral venous sinus thrombosis. In addition, mortality rate (9.38 vs. 5.41%; P = 0.469) and 90-day excellent prognosis rate (81.25 vs. 86.47%; P = 0.793) did not differ significantly between patients with and without epileptic seizures. The presence of focal neurological deficits and thrombosis of the superior sagittal sinus are independent risk factors for secondary seizures in patients with cerebral venous sinus thrombosis, whereas mortality and 90-day prognosis have no correlation with secondary seizures.

Objective:To explore the protective effects and mechanism of Peroxisome proliferative activated receptor-γ activation of auxiliary factor 1 Alpha(PGC-1α) on injured neurons induced by oxygen-glucose deprivation(OGD) in embryonic mice.Methods: Cortical neurons cultured for 7 days were randomly divided into four groups:normal control group,oxygen-glucose deprivation group(OGD);OGD + PGC-1α overexpression plasmid group(overexpression group) and OGD +no-load plasmid group(no-loa d group).Overexpression group and the no-load group pretreatment with PGC-1α overexpression plasmid and no-load plasmid respectively before OGD treatment.24 hours after OGD,cell survival rate was detected by MTT(Methylthiazolyldiphenyl-tetrazolium bromide),observe the expression of PGC-1α was using Western blot technology,and the flow cytometry was used to monitor the content of Reactive Oxygen Species(ROS).Results:Compared with the normal control group,the cell survival rate in OGD group decreased(P<0.01),the survival rate was increased in overexpression group due to pretreatment of PGC-1α overexpression plasmid,which was compared with OGD group and no-load group with a significant difference(P<0.01).The ROS of OGD groups were significantly higher than that of the normal group(P<0.01);the content of ROS was decreased in overexpression group,and was significantly lower than that of the OGD group and no-load group(P<0.01).Conclusion:The study indicated that PGC-1α can significantly reduce the ROS content of oxygen-glucose deprivation neurons and improve its survival rate,to protect the neurons.

Stroke, of which about 87% is ischemic stroke, constitutes one of the main causes of morbidity, disability, and mortality worldwide. Ischemic brain injury has complex pathological mechanisms. Considerable evidence has been collected over the last few years suggesting that oxidative stress associated with excessive production of reactive oxygen species is a fundamental mechanism of brain damage in stroke and reperfusion after stroke. Oxidative stress is an important trigger of neuronal apoptosis in ischemic stroke. In this current study, it was found that cocaine-regulated and amphetamine-regulated transcript 55-102 (CART55-102) inhibited oxygen-induced and glucose deprivation (OGD)-induced neurotoxicity in a dose-dependent manner. The peak dose of CART55-102 was 0.4 nmol/l. In addition, the level of intracellular reactive oxygen species was decreased in OGD-treated neurons in the presence of 0.4 nmol/l CART55-102. Mitochondrial membrane potential (ΔΨm) and mtDNA mRNA expressions were increased in OGD-treated neurons in the presence of 0.4 nmol/l CART55-102. The current study suggests that CART55-102, by inhibiting oxidative stress, may be developed into therapeutic agents for ischemic stroke.

Cocaine and amphetamine regulated transcript（CART） peptides are endolaous neurotrans mitters with important roles in a number of physiological and pathological processes in vivo. Many studies suggested that CART is widely distributed in the central nervous system, and it has some central protective effects. This article reviews the recent progress in research on the protective effect of CART on cerebral ischemia and its mechanisms. Key words: Cocaine- And Amphetamine-Regulated Transcript Protein; Brain Ischemia; NeuroprotectiveA~ts