Microfluidics-enabled mesenchymal stem cell derived Neuron like cell membrane coated nanoparticles inhibit inflammation and apoptosis for Parkinson's Disease.

Parkinson's disease (PD) is the second largest group of neurodegenerative diseases, and its existing drug treatments are not satisfactory. Natural cell membrane drugs are used for homologous targeting to enhance efficacy. In this study, microfluidic electroporation chip prepared mesenchymal stem cell-derived neuron-like cell membrane-coated curcumin PLGA nanoparticles (MM-Cur-NPs) was synthesized and explored therapeutic effect and mechanism in PD.

Spatial Transcriptomics: A Powerful Tool in Disease Understanding and Drug Discovery.

Recent advancements in modern science have provided robust tools for drug discovery. The rapid development of transcriptome sequencing technologies has given rise to single-cell transcriptomics and single-nucleus transcriptomics, increasing the accuracy of sequencing and accelerating the drug discovery process. With the evolution of single-cell transcriptomics, spatial transcriptomics (ST) technology has emerged as a derivative approach.

Scutellarin activates IDH1 to exert antitumor effects in hepatocellular carcinoma progression.

Isochlorate dehydrogenase 1 (IDH1) is an important metabolic enzyme for the production of α-ketoglutarate (α-KG), which has antitumor effects and is considered to have potential antitumor effects. The activation of IDH1 as a pathway for the development of anticancer drugs has not been attempted. We demonstrated that IDH1 can limit glycolysis in hepatocellular carcinoma (HCC) cells to activate the tumor immune microenvironment.

Organ-on-a-chip meets artificial intelligence in drug evaluation.

Drug evaluation has always been an important area of research in the pharmaceutical industry. However, animal welfare protection and other shortcomings of traditional drug development models pose obstacles and challenges to drug evaluation. Organ-on-a-chip (OoC) technology, which simulates human organs on a chip of the physiological environment and functionality, and with high fidelity reproduction organ-level of physiology or pathophysiology, exhibits great promise for innovating the drug development pipeline.

Chemical profile and antioxidant activity of bidirectional metabolites from and as assessed using response surface methodology.

This study aimed to establish a bidirectional fermentation system using and to promote the transformation and utilization of the synthesized antioxidant metabolites from fermentation supernatant. The effect of fermentation conditions on the total phenolic content was investigated using response surface methodology in terms of three factors, including temperature (22-28°C), pH (6-8), and inoculum size (2-8%, v/v). The optimized fermentation parameters were: 28°C, pH 8, and an inoculum size of 2%, which led to a maximum total phenolic content of 314.

Desmin Correlated with Cx43 May Facilitate Intercellular Electrical Coupling during Chronic Heart Failure.

Desmin is one of five major intermediate filament proteins in cardiomyocytes. Desmin contributes to the maintenance of healthy muscle. The desmin content in cardiomyocytes directly affects the long-term prognosis of patients with heart failure, and lack of desmin leads to myocyte contractile dysfunction.

Artemisinin suppresses myocardial ischemia-reperfusion injury via NLRP3 inflammasome mechanism.

Artemisinin is known for its pharmaceutical effect against malaria and received increased attention for its other potential function. Mounting evidence suggest that artemisinin could also exert cardioprotective effects while the understanding of its regulatory mechanism is still limited. This study is designed to investigate the role of artemisinin in myocardial ischemia/reperfusion (I/R) injury and the involvement of NLRP3 inflammasome.

The role of desmin alterations in mechanical electrical feedback in heart failure.

Aim: Mechanoelectric feedback (MEF) was related to malignant arrhythmias in heart failure (HF). Desmin is a cytoskeleton protein and could be involved in MEF as a mechanoelectrical transducer. In this study, we will discuss the role of desmin alterations in mechanical electrical feedback in heart failure and its mechanisms.

Histone demethylase JARID1B regulates proliferation and migration of pulmonary arterial smooth muscle cells in mice with chronic hypoxia-induced pulmonary hypertension via nuclear factor-kappa B (NFkB).

Chronic hypoxia-induced pulmonary hypertension (PH) is a disorder that is characterized by increased pulmonary arterial pressure resulting from lung diseases or shortage of oxygen in the body. Excess proliferation of pulmonary vascular cells such as pulmonary artery endothelial cells (PAECs) and pulmonary artery smooth muscle cells (PASMCs) plays a critical role in the pathogenesis of PH. Recent evidence indicates that, in addition to genetic predisposition and environmental factors, epigenetic mechanisms play a pivotal role in etiology of PH.

A case study of ciliary detachment with primary pulmonary hypertension.

Purpose: To introduce a case of ciliary detachment with primary pulmonary hypertension (PPH).

Methods: The clinical manifestations of a case of ciliary detachment with PPH were addressed by comprehensive examination including ultrasound biological microscope (UBM), intraocular pressure, color fundus photographs, fluorescence fundus angiography (FFA). In addition, echocardiography is used to measure primary pulmonary pressure.

Streptomycin inhibits electrophysiological changes induced by stretching of chronically infarcted rat hearts.

Objective: To investigate stretch-induced electrophysiological changes in chronically infarcted hearts and the effect of streptomycin (SM) on these changes in vivo.

Methods: Sixty Wistar rats were divided randomly into four groups: a control group (n=15), an SM group (n=15), a myocardial infarction (MI) group (n=15), and an MI+SM group (n=15). Chronic MI was obtained by ligating the left anterior descending branch (LAD) of rat hearts for eight weeks.

Testosterone replacement therapy promotes angiogenesis after acute myocardial infarction by enhancing expression of cytokines HIF-1a, SDF-1a and VEGF.

In order to investigate the effects of testosterone-replacement therapy on peripheral blood stem cells and angiogenesis after acute myocardial infarction, a castrated rat acute myocardial infarction model was established by ligation of the left anterior descending coronary followed by treatment with testosterone. CD34(+) cells in myocardium and in peripheral blood after 1 and 3 days were measured by immunohistochemistry and flow cytometry, respectively. In the early phase of acute myocardial infarction, the expression levels of hypoxia-inducible factor 1a (HIF-1a), stromal cell-derived factor 1a (SDF-1a) and vascular endothelium growth factor (VEGF) in ischemic myocardium were determined by real time RT-PCR and immunohistochemistry, respectively.

Testosterone improves cardiac function and alters angiotensin II receptors in isoproterenol-induced heart failure.

Background: The renin-angiotensin-aldosterone system is known to play an important role in the pathophysiology and development of heart failure. Several studies have reported the benefits of testosterone in heart failure. However, the mechanisms of testosterone-induced effects on heart failure require further study.

Regional differential expression of TREK-1 at left ventricle in myocardial infarction.

Background: Altered membrane electrophysiology contributes to arrhythmias after myocardial infarction (MI). TREK-1 channel is essential in various physiological and pathological conditions through its regulation on resting membrane potential and voltage-dependent action potential duration.

Objectives: The aim of this study was to investigate changes in gene expression and electrophysiology of TREK-1 in the left ventricle in a MI model.

Testosterone modulation of cardiac β-adrenergic signals in a rat model of heart failure.

In this study, we examined the effects of castration and testosterone replacement on β-adrenoceptor and G protein expression in rats subjected to doxorubicin-induced heart failure. Five groups were included in this report: control, sham-castration with heart failure, castration with heart failure, castration+testosterone replacement with heart failure and castration+testosterone replacement and flutamide with heart failure. At 4 weeks post-treatment, echocardiography, hemodynamics and histopathology were assessed.

Berberine cooperates with adrenal androgen dehydroepiandrosterone sulfate to attenuate PDGF-induced proliferation of vascular smooth muscle cell A7r5 through Skp2 signaling pathway.

Platelet-derived growth factor (PDGF) is released from vascular smooth muscle cell (VSMC), after percutaneous coronary intervention and is related with neointimal proliferation and restenosis. Adrenal steroid dehydroepiandrosterone sulfate (DHEAS), the sulfated prohormone of dehydroepiandrosterone has shown remarkable biological activity against proliferation of VSMC in some animal and clinical studies. Combinations of DHEAS with other agents have also shown promising results, with acquiring more efficient effect.

Taxol inhibits stretch-induced electrophysiological alterations in isolated rat hearts with acute myocardial infarction.

Mechanosensitive channels have been determined to work as transducers of mechanoelectric feedback in the heart, which is associated with the generation of arrhythmias. Recent studies have investigated the role of the cytoskeleton in ion channels control. This study explored the ability of taxol to inhibit stretch-induced electrophysiological alterations in the ischemic myocardium.

Neuroprotective effects of testosterone upon cardiac sympathetic function in rats with induced heart failure.

The current study was designed to determine whether castration with or without testosterone replacement resulted in changes in cardiac sympathetic nerve activity in rats with heart failure induced by isoproterenol. At eight weeks post-castration, dysfunction of the cardiac sympathetic nerve system was aggravated as indicated by elevated plasma norepinephrine, reduced myocardial norepinephrine content and tyrosine hydroxylase (TH) protein. These effects of castration were reversed by testosterone replacement, as indicated by decreased plasma norepinephrine, increased myocardial norepinephrine and density of TH-labeled nerve fibers, as well as by an upregulated expression of myocardial TH protein.

Testosterone deprivation by castration impairs expression of voltage-dependent potassium channels in rat aorta.

In this study, we explored the effects of testosterone deprivation on the expression of voltage-dependent potassium (Kv) channels in vascular smooth muscle cells (VSMCs) in rats. Six months after mature male Wistar rats were castrated, functional and posttranscriptional alterations of voltage-dependent potassium channels were detected using isometric tension measurement, whole-cell patch-clamp and western blot analysis. Constriction of aortic artery rings in response to 4-aminopyridine was significantly decreased 6 months after castration.

[Effect of phalloidin on electrophysiological changes induced by stretch of myocardial infarcted hearts in rats].

The present study aimed to explore whether the stretch of ischemic myocardium could modulate the electrophysiological characteristics via mechanoelectric feedback (MEF), as well as the effect of phalloidin on the electrophysiological changes. Thirty-two Wistar rats were randomly divided into 4 groups: control group (n=9), phalloidin group (n=7), myocardial infarction (MI) group (n=9), MI + phalloidin group (n=7). The acute myocardial infarction (AMI) was conducted by ligation of the left anterior descending (LAD) coronary artery for 30 min in isolated rat heart.

The effect of streptomycin on stretch-induced electrophysiological changes of isolated acute myocardial infarcted hearts in rats.

Aims: To explore whether the stretch of ischaemic myocardium could modulate the electrophysiological characteristics, especially repolarization via mechanoelectric feedback (MEF), as well as the effect of streptomycin (SM) on these changes. Methods Thirty-six wistar rats were randomly divided into four groups: control group (n = 9), SM group (n = 9), myocardial infarction (MI) group (n = 9), and MI + SM group (n = 9). After perfused on Langendorff, the isolated hearts were stretched for 5s by a ballon inflation of 0.