Prediction of prognosis in patients with ischemic stroke combined with type 2 diabetes mellitus based on serum total bilirubin levels.

Serum bilirubin levels may have therapeutic benefits in oxidative stress-related diseases, but their role in stroke remains unclear. This study aimed to investigate the relationship between serum bilirubin levels on admission and clinical outcomes in ischemic stroke patients. We prospectively collected data from consecutive ischemic stroke admissions. Serum total bilirubin (TBIL) and direct bilirubin levels on admission were measured. Stroke severity at admission was assessed using the National Institutes of Health Stroke Scale, and functional status at discharge was evaluated using the modified Rankin scale. Among 180 patients, lower TBIL levels were observed in all 3 groups, with the mild group (7.89 ±â€…2.12 µmol/L) having lower levels than the moderate group (8.01 ±â€…2.12 µmol/L) and the severe group (9.12 ±â€…2.12 µmol/L). Although TBIL levels were initially associated with stroke severity, this relationship did not hold after adjusting for confounding factors. Serum bilirubin levels appear to be related to stroke severity but not independently associated with outcomes in ischemic stroke patients. Further research is needed to understand the underlying mechanisms of this relationship. There is a strong correlation between serum bilirubin levels and the severity and prognosis of ischemic stroke in patients with type 2 diabetes. Therefore, early control of serum TBIL and direct bilirubin is crucial for the treatment and prognosis of ischemic stroke in patients with type 2 diabetes.

NLRP3 inflammasome inhibitor ameliorates ischemic stroke by reprogramming the phenotype of microglia/macrophage in a murine model of distal middle cerebral artery occlusion.

Stroke is one of the leading causes of death and disability worldwide. NLRP3 inflammasome has an essential role in the neuropathology of stroke. Recent studies report that shifting the microglial M1 phenotype to the M2 phenotype protects against ischemic stroke. In the present study, the precise effects of Tranilast, a NLPR3 inflammasome inhibitor, on stroke were evaluated. We established a murine model of distal middle cerebral artery occlusion (dMCAO) and administered Tranilast to dMCAO-induced stroke mice. The NLRP3 level, caspase 1 activity, and infarct volume stroke mice were measured. The sensorimotor function, pro-inflammatory cytokine production, and M1/M2 marker expression were measured. The M1 phenotype was induced by treatment of BV2 microglia with lipopolysacharide and interferon γ, and these BV-2 cells were further treated with Tranilast. The expression of CD16 and CD206 was monitored. dMCAO increased the NLRP3 expression and enhanced caspase 1 activity. Tranilast treatment significantly decreased the infarct volume, improved sensorimotor function, and suppressed the production of inflammatory cytokines in stroke mice. Moreover, Tranilast decreased the M1 marker level while promoting the expression of M2 markers. In summary, our findings suggest that Tranilast ameliorates ischemic stroke through stimulating M2 polarization of microglia.

Betaine protects rats against ischemia/reperfusion injury-induced brain damage.

Brain ischemia and reperfusion (I/R) injury may lead to a poor prognosis for ischemic stroke, which could be alleviated by antioxidants with diminished oxidative stress. Betaine is a natural nutrient found in beetroot and seafood to improve cognitive performance in the elderly. The present study investigated whether betaine could protect the brain from I/R injury. Results showed that betaine treatment could reduce H2O2-induced cell death in the PC12 cell line. Pretreatment with betaine reduced the brain infarct volume and neuronal apoptosis in a rat I/R injury model induced by 2-h middle cerebral artery occlusion (MCAO). Biochemical analyses indicated that betaine treatment decreased proinflammatory cytokine production and reduced oxidative stress after I/R injury. Betaine increased the expression of antioxidative enzymes, such as glutathione peroxidase 4 (Gpx4) and superoxide dismutase 1 (Sod1), and antioxidative nonenzymatic genes, such as 3-mercaptopyruvate sulfurtransferase (Mpst), methionine sulfoxide reductases b1 (Msrb1), and Msrb2. These data suggest that betaine exerts a neuroprotective effect in I/R injury through enzymatic and nonenzymatic antioxidative systems and anti-inflammatory mechanisms.NEW & NOTEWORTHY These data suggested that betaine exerted a neuroprotective effect in I/R injury through enzymatic and nonenzymatic antioxidative systems.

Effects of an evidence-based nursing intervention on neurological function and serum inflammatory cytokines in patients with acute cerebral infarction: A randomized controlled trial.

BACKGROUND: Acute cerebral infarction is a clinically common and critical disease which seriously endangers the life and safety of elderly patients. Evidence-based nursing is an effective way of nursing and has great significance in improving the neurological function and quality of life of patients. In China, evidence-based nursing has been highlighted and highly developed in recent decades. OBJECTIVES: This research aimed to investigate the effect of evidence-based nursing on the recovery of neurological function and serum inflammatory cytokines in patients with acute cerebral infarction. METHODS: A total of 116 patients with acute cerebral infarction were randomly divided into two groups: the control group patients (n = 58) received conventional nursing, while the intervention group patients (n = 58) received evidence-based nursing intervention. National Institutes of Health Stroke Scale (NIHSS), Fugl-Meyer assessment (FMA) and activities of daily living (ADL) scores, as well as serum TNF-α and IL-6 levels were evaluated and compared between the two groups. RESULTS: NIHSS scores in the intervention group were significantly lower than the control group. FMA and ADL scores in the intervention group were significantly higher than the control group. TNF-α and IL-6 levels in the serum of the intervention group were significantly lower than the control group. CONCLUSIONS: In conclusion, evidence-based nursing has a positive effect on the treatment of patients with acute cerebral infarction, which decreases the level of serum inflammatory cytokines and contributes to the recovery of neurological function, motor function and activities of daily living.

miR-499-5p suppresses C-reactive protein and provides neuroprotection in hypoxic-ischemic encephalopathy in neonatal rat.

Perinatal hypoxic-ischemic encephalopathy (HIE) is associated with high neonatal mortality and permanent neurologic deficit. Recent data suggested microRNAs (miRNAs) may have essential functions in the regulation of HIE. This study aims to investigate the functional role of miR-499-5p and the underlying mechanism in regulating neonatal hypoxia-ischemia (HI)-induced brain injury. Dual-luciferase reporter assay and western blotting assay were performed to investigate the relationship between miR-499-5p and C-reactive protein (CRP). TUNEL staining assay was applied to evaluate neuronal cell apoptosis in the hippocampus after administration of miR-499-5p in HIE rat model. Neurobehavioral assays were conducted to evaluate the effect of miR-499-5p on the neurological functions of rat pups with HI-induced brain injury. Our study showed that miR-499-5p regulated CRP expression in L-02 cells and rat HIE model. The miR-499-5p treatment resulted in significant reduction of neuronal cell apoptosis and the infarct size of the brain. Furthermore, administration of miR-499-5p significantly improved spatial learning ability, spatial memory, and locomotor function of rat pups with HIE. Our data demonstrated that miR-499-5p have a neuroprotective effect in HI-induced brain injury in rat pups, which suggests a potential therapeutic application of miR-499-5p in the treatment of neonatal HIE.

The Neuroprotective Effect of Steroid Receptor Coactivator-Interacting Protein (SIP) in Astrocyte Model of 1-Methyl-4-Phenylpyridinium (MPP⁺)-Induced Parkinson's Disease.

BACKGROUND The purpose of this study was to investigate the role and mechanism of steroid receptor coactivator-interacting protein (SIP) in an astrocyte model of 1-methyl-4-phenylpyridinium (MPP⁺)-induced Parkinson's disease. MATERIAL AND METHODS To perform our study, a Parkinson's disease cell model was established by treating the rat glioblastoma cell line C6 with MPP⁺. SIP was overexpressed in C6 cells using SIP-plasmid. Cell viability and apoptosis were analyzed using MTT assay and flow cytometer respectively. Tumor necrosis factor (TNF)-alpha and interleukin (IL)-1ß levels were detected using enzyme linked immunosorbent assay and quantitative reverse transcription PCR. Besides, lactate dehydrogenase (LDH) release, reactive oxygen species (ROS) production, and superoxide dismutase (SOD) enzyme activity were determined in the present study. For protein and mRNA detection, western blot assay, and qRT-PCR were performed respectively. RESULTS SIP was decreased in MPP⁺-induced C6 cells. SIP overexpression relieved MPP⁺-induced cytotoxicity of C6 cells, displayed as increased cell viability and reduced cell apoptosis and reduced LDH release. Besides, SIP inhibited MPP⁺-induced inflammatory response and oxidative stress, evidenced by decreased levels of inflammatory factors (TNF-alpha and IL-1ß), reduced ROS generation and enhanced SOD activity. Moreover, MPP⁺-induced nuclear factor-kappaB activation was inhibited by SIP overexpression. CONCLUSIONS SIP was downregulated in Parkinson's disease and it played a protective role in the development Parkinson's disease, thus may be a promising target for Parkinson's disease treatment.