Docosahexaenoic acid protects against ischemic stroke in diabetic mice by inhibiting inflammatory responses and apoptosis.

This study was to explore whether docosahexaenoic acid (DHA) protects against ischemic stroke in diabetic mice and its mechanisms. DHA was administered to mice and its effects on stroke outcomes in type 1 diabetes mellitus were assessed 24 h and 3 days post-reperfusion using RNA sequencing, flow cytometry, multiplex immunoassays, and western-blotting analysis. In diabetic mice, DHA administration post-ischemic stroke significantly reduced cerebral infarct size, brain edema, and neurological impairments.

Intersection of Aging and Particulate Matter 2.5 Exposure in Real World: Effects on Inflammation and Endocrine Axis Activities in Rats.

Exposure to particulate matter 2.5 (PM2.5) is detrimental to multiple organ systems.

Corrigendum to "Engineering exosomes and their application in cardiovascular field: Bibliometric analysis from 2002 to 2022" [Heliyon 9(8) (August 2023) e18809].

[This corrects the article DOI: 10.1016/j.heliyon.

Cerebral Glucose Metabolism and Potential Effects on Endoplasmic Reticulum Stress in Stroke.

Ischemic stroke is an extremely common pathology with strikingly high morbidity and mortality rates. The endoplasmic reticulum (ER) is the primary organelle responsible for conducting protein synthesis and trafficking as well as preserving intracellular Ca2 homeostasis. Mounting evidence shows that ER stress contributes to stroke pathophysiology.

Neuroprotective Effects of Pharmacological Hypothermia on Hyperglycolysis and Gluconeogenesis in Rats after Ischemic Stroke.

Stroke is a leading threat to human life. Metabolic dysfunction of glucose may play a key role in stroke pathophysiology. Pharmacological hypothermia (PH) is a potential neuroprotective strategy for stroke, in which the temperature is decreased safely.

Extracellular vesicles enclosed-miR-421 suppresses air pollution (PM )-induced cardiac dysfunction via ACE2 signalling.

Air pollution, via ambient PM is a big threat to public health since it associates with increased hospitalisation, incidence rate and  mortality of cardiopulmonary injury. However, the potential mediators of pulmonary injury in PM -induced cardiovascular disorder are not fully understood. To investigate a potential cross talk between lung and heart upon PM exposure, intratracheal instillation in vivo, organ culture ex vivo and human bronchial epithelial cells (Beas-2B) culture in vitro experiments were performed respectively.

Effect of Bariatric Surgery on Metabolic Diseases and Underlying Mechanisms.

Obesity is a highly prevalent public health concern, attributed to multifactorial causes and limited in treatment options. Several comorbidities are closely associated with obesity such as the development of type 2 diabetes mellitus (T2DM), cardiovascular and cerebrovascular diseases, and nonalcoholic fatty liver disease (NAFLD). Bariatric surgery, which can be delivered in multiple forms, has been remarked as an effective treatment to decrease the prevalence of obesity and its associated comorbidities.

Non-coding RNA basis of muscle atrophy.

Muscle atrophy is a common complication of many chronic diseases including heart failure, cancer cachexia, aging, etc. Unhealthy habits and usage of hormones such as dexamethasone can also lead to muscle atrophy. However, the underlying mechanisms of muscle atrophy are not completely understood.

Targets identified from exercised heart: killing multiple birds with one stone.

Cardiovascular diseases (CVDs) are a major cause of mortality worldwide, which are mainly driven by factors such as aging, sedentary lifestyle, and excess alcohol use. Exercise targets several molecules and protects hearts against many of these physiological and pathological stimuli. Accordingly, it is widely recognized as an effective therapeutic strategy for CVD.

An inhibitory and beneficial effect of chlorpromazine and promethazine (C + P) on hyperglycolysis through HIF-1α regulation in ischemic stroke.

Background: After ischemic stroke, the increased catabolism of glucose (hyperglycolysis) results in the production of reactive oxygen species (ROS) via nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX). A depressive or hibernation-like effect of C + P on brain activity was reported to induce neuroprotection. The current study assesses the effect of C + P on hyperglycolysis and NOX activation.

Phosphoenolpyruvate Carboxykinase (PCK) in the Brain Gluconeogenic Pathway Contributes to Oxidative and Lactic Injury After Stroke.

To demonstrate the role of the rate-limiting and ATP-dependent gluconeogenic enzyme phosphoenolpyruvate carboxykinase (PCK) in oxidative and lactic stress and the effect of phenothiazine on PCK after stroke, a total of 168 adult male Sprague Dawley rats (3 months old, 280-300 g) underwent 2-h intraluminal middle cerebral artery occlusion (MCAO) and reperfusion for 6, 24, 48 h, or 7 days. Phenothiazine (chlorpromazine and promethazine (C+P)) (8 mg/kg) and 3-mercaptopicolinic acid (3-MPA, a PCK inhibitor, 100 μM) were administered at reperfusion onset. The effects of phosphoenolpyruvate, 3-MPA, or PCK knockdown were studied in neuronal cultures subjected to oxygen/glucose deprivation.

Apolipoprotein E polymorphism carriers exhibit objective cognitive deficits: a single center trial.

Objective: To assess the correlation between objectively measured cognitive function and apolipoprotein E polymorphism within one geographic region.

Methods: 61 patients, aged 55-90 years old, were enrolled in a memory clinic at the Beijing Luhe Hospital affiliated with Capital Medical University from September 2016 to September 2018. At this center, they were evaluated with neuropsychological scales to assess their memory and other aspects of cognitive function.

Filtered air intervention reduces inflammation and hypothalamus-pituitary-adrenal axis activation in adult male and female rats after PM 2.5 exposure.

Previous studies have indicated that particulate matter 2.5 (PM2.5) exposure stimulates systemic inflammation and activates the hypothalamus-pituitary-adrenal (HPA) axis, both of which are associated with stroke incidence and mortality.

Reduced Apoptotic Injury by Phenothiazine in Ischemic Stroke through the NOX-Akt/PKC Pathway.

Phenothiazine treatment has been shown to reduce post-stroke ischemic injury, though the underlying mechanism remains unclear. This study sought to confirm the neuroprotective effects of phenothiazines and to explore the role of the NOX (nicotinamide adenine dinucleotide phosphate oxidase)/Akt/PKC (protein kinase C) pathway in cerebral apoptosis. Sprague-Dawley rats underwent middle cerebral artery occlusion (MCAO) for 2 h and were randomly divided into 3 different cohorts: (1) saline, (2) 8 mg/kg chlorpromazine and promethazine (C+P), and (3) 8 mg/kg C+P as well as apocynin (NOX inhibitor).

From circadian clocks to non-alcoholic fatty liver disease.

: The circadian rhythm is an integral regulator of various endocrine processes in the body, including sleep-wake cycles, hormonal regulation, and metabolism. In addition to metabolic, genetic, and environmental factors, a dysregulated circadian rhythm resulting from lifestyle changes has been implicated in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). An accumulating body of evidence also supports strong association between NAFLD and metabolic disorder, the pathogenesis of which is related to periodic fluctuations in hormonal homeostasis.

Neuroprotection by mesenchymal stem cell (MSC) administration is enhanced by local cooling infusion (LCI) in ischemia.

Objective: The present study aimed to determine if hypothermia augments the neuroprotection conferred by MSC administration by providing a conducive micro-environment.

Methods: Sprague-Dawley rats were subjected to 1.5 h middle cerebral artery occlusion (MCAO) followed by 6 or 24 h of reperfusion for molecular analyses, as well as 1, 14 and 28 days for brain infarction or functional outcomes.

Artificial Hibernation by Phenothiazines: A Potential Neuroprotective Therapy Against Cerebral Inflammation in Stroke.

Background: The inflammatory response to acute cerebral ischemia is a major factor in stroke pathobiology and patient outcome. In the clinical setting, no effective pharmacologic treatments are currently available. Phenothiazine drugs, such as chlorpromazine and promethazine, (C+P) have been widely studied because of their ability to induce neuroprotection through artificial hibernation after stroke.

Is air pollution a potential cause of neuronal injury?

: Fine particle pollution, including diesel exhaust particles (DEP), is a well-recognized and significant threat to public health. Cerebrovascular disease has been shown to be among the pathologies produced by fine particle exposure, and is thought to arise in this context through oxidative and inflammatory mechanisms. The manner by which these mechanisms interface with normal cerebral metabolism in their promotion of cerebrovascular pathogenesis, however, remains to be elucidated.

ADMET-score - a comprehensive scoring function for evaluation of chemical drug-likeness.

Chemical absorption, distribution, metabolism, excretion, and toxicity (ADMET), play key roles in drug discovery and development. A high-quality drug candidate should not only have sufficient efficacy against the therapeutic target, but also show appropriate ADMET properties at a therapeutic dose. A lot of models are hence developed for prediction of chemical ADMET properties.

PM exposure induces systemic inflammation and oxidative stress in an intracranial atherosclerosis rat model.

Objectives: Exposure to airborne particle (PM ) is a risk factor for intracranial atherosclerosis (ICA). Because of the established role of systemic inflammation and oxidative stress by PM , we determined whether these processes account for PM -mediated ICA, and also whether omega-3 fatty acid (O3FA) dietary supplementation could attenuate them.

Methods: Adult Sprague-Dawley rats were exposed to filtered air (FA) or PM and fed either a normal chow diet (NCD) or a high-cholesterol diet (HCD), administered with or without O3FA (5 mg/kg/day by gavage) for 12 weeks.

PM2.5 induces liver fibrosis via triggering ROS-mediated mitophagy.

Background: The increasing epidemic of fine particulate matter (PM2.5) is a serious threat to human health. It induces the occurrence of liver fibrosis, but its molecular mechanism is not yet clear.

Efficacy of neuromuscular electrical stimulation in improving the negative psychological state in patients with cerebral infarction and dysphagia.

Objective To observe the improvement of negative affect disorders in patients with cerebral infarction and dysphagia by neuromuscular electrical stimulation. Methods One hundred and twelve patients with cerebral infarction and dysphagia were selected and randomized into treatment (n = 59) and control (n = 53) groups. Similar swallowing function was found in both groups before treatment: (1) Water-drinking test in the treatment group proved swallowing function Level III in 24 cases, Level IV in 22 cases and Level V in 13 cases; (2) in the control group, swallowing function was Level III in 21 cases, Level IV in 20 cases and Level V in 12 cases.

MiR-146a regulates PM -induced inflammation via NF-κB signaling pathway in BEAS-2B cells.

Exposure to particulate matter (PM) leads to kinds of cardiopulmonary diseases, such as asthma, COPD, arrhythmias, lung cancer, etc., which are related to PM-induced inflammation. We have found that PM (aerodynamics diameter <2.