Houttuynia cordata Thunb-derived extracellular vesicle-like particles alleviate ischemic brain injury by miR159a targeting ACSL4 to suppress ferroptosis.

Introduction: Neuroprotective agents for acute ischemic stroke often fall short in efficacy due to the blood-brain barrier challenges, lack of target specificity, and limited effectiveness. Recently, plant-derived extracellular vesicle-like particles (EVLP) have shown promise in their multifaceted functions.

Objectives: The neuroprotective advantages that EVLP produced from Houttuynia cordata Thunb against cerebral ischemia/reperfusion injury are investigated.

[Method for Simultaneous Quantifying Five Types of Microplastics by Tubular Furnace Pyrolysis-thermal Desorption-gas Chromatography-mass Spectrometry].

A susceptible method has been established to simultaneously quantify five types of microplastics greater than 0.22 μm across various environmental matrices, namely, polyethylene （PE）, polypropylene （PP）, polystyrene （PS）, polyvinyl chloride （PVC）, and polyethylene terephthalate （PET）. In detail, five types of microplastics were completely pyrolyzed within a tubular furnace.

Maintaining moderate levels of hypochlorous acid promotes neural stem cell proliferation and differentiation in the recovery phase of stroke.

JOURNAL/nrgr/04.03/01300535-202503000-00029/figure1/v/2024-06-17T092413Z/r/image-tiff It has been shown clinically that continuous removal of ischemia/reperfusion-induced reactive oxygen species is not conducive to the recovery of late stroke. Indeed, previous studies have shown that excessive increases in hypochlorous acid after stroke can cause severe damage to brain tissue.

Walp (Maca)-derived extracellular vesicles ameliorate depression by promoting 5-HT synthesis via the modulation of gut-brain axis.

Depression is a common and debilitating condition for which effective treatments are needed. Walp (Maca) is a plant with potential medicinal effects in treating depression. Recently, there has been growing interest in plant-derived extracellular vesicles (EVs) due to their low toxicity and ability to transport to human cells.

Peroxynitrite-Triggered Carbon Monoxide Donor Improves Ischemic Stroke Outcome by Inhibiting Neuronal Apoptosis and Ferroptosis.

Cerebral ischemia-reperfusion injury produces excessive reactive oxygen and nitrogen species, including superoxide, nitric oxide, and peroxynitrite (ONOO). We recently developed a new ONOO-triggered metal-free carbon monoxide donor (PCOD585), exhibiting a notable neuroprotective outcome on the rat middle cerebral artery occlusion model and rendering an exciting intervention opportunity toward ischemia-induced brain injuries. However, its therapeutic mechanism still needs to be addressed.

Melatonin alleviates Hg toxicity by modulating redox homeostasis and the urea cycle in moss.

Mercury (Hg) is a highly toxic metal and can cause severe damage to many organisms under natural conditions. As an effective free radical scavenger and antioxidant, Melatonin (MT) has played important protective roles in alleviating oxidative damage caused by environmental cues including heavy metal stress in plants. However, the detailed mechanisms of melatonin in alleviating Hg toxicity still remain unclear in plants.

Exosome-based drug delivery systems for the treatment of diabetes and its complications: current opinion.

Diabetes medication is based on controlling blood glucose and delaying the onset of related complications and is not a complete cure for diabetes. Conventional drug therapy fails to stop progressive islet β cell failure in diabetic patients. Recent studies have shown that "exosome-based therapy" holds great promise in treating diabetes and its complications.

Ischemic accumulation of succinate induces Cdc42 succinylation and inhibits neural stem cell proliferation after cerebral ischemia/reperfusion.

Ischemic accumulation of succinate causes cerebral damage by excess production of reactive oxygen species. However, it is unknown whether ischemic accumulation of succinate affects neural stem cell proliferation. In this study, we established a rat model of cerebral ischemia/reperfusion injury by occlusion of the middle cerebral artery.

Exosome-Like Nanoparticles Exert Neuroprotective Effects Against Ischemic Brain Injury Inhibiting Matrix Metalloproteinase 9 and Activating the AKT/GSK3β Signaling Pathway.

Plant exosome-like nanoparticles (ELNs) have shown great potential in treating tumor and inflammatory diseases, but the neuroprotective effect of plant ELNs remains unknown. In the present study, we isolated and characterized novel ELNs from (MC) and investigated their neuroprotective effects against cerebral ischemia-reperfusion injury. In the present study, MC-ELNs were isolated by ultracentrifugation and characterized.

-Derived Extracellular Vesicles-Like Nanovesicles Protect Cardiomyocytes Against Radiation Injury via Attenuating DNA Damage and Mitochondria Dysfunction.

Thoracic radiotherapy patients have higher risks of developing radiation-induced heart disease (RIHD). Ionizing radiation generates excessive reactive oxygens species (ROS) causing oxidative stress, while and its extract have antioxidant activity. Plant-derived extracellular vesicles (EVs) is emerging as novel therapeutic agent.

Enhanced autophagy promotes radiosensitivity by mediating Sirt1 downregulation in RM-1 prostate cancer cells.

Autophagy is a double-edged sword that affects tumor progression by promoting cell survival or death depending on different living contexts. The concrete mechanism by which autophagy modulates the efficacy of radiotherapy for prostate cancer (PC) remains unclear. We exposed RM-1 PC cells to X-ray and explored the role of autophagy in radiation injury.

Healthy Serum-Derived Exosomes Improve Neurological Outcomes and Protect Blood-Brain Barrier by Inhibiting Endothelial Cell Apoptosis and Reversing Autophagy-Mediated Tight Junction Protein Reduction in Rat Stroke Model.

Blood-brain barrier (BBB) dysfunction causing edema and hemorrhagic transformation is one of the pathophysiological characteristics of stroke. Protection of BBB integrity has shown great potential in improving stroke outcome. Here, we assessed the efficacy of exosomes extracted from healthy rat serum in protection against ischemic stroke and .

Diagnosis of mycoplasma pneumoniae by loop-mediated isothermal amplification: systematic review and meta-analysis.

Background: A novel method, termed loop-mediated isothermal amplification (LAMP), was developed by Notomi et al. (2000). Individually published results have been reported that this technology has been successfully applied to the detection of a variety of pathogens.

Golgin-160 and GMAP210 play an important role in U251 cells migration and invasion initiated by GDNF.

Gliomas are the most common malignant tumors of the brain and are characteristic of severe migration and invasion. Glial cell line-derived neurotrophic factor (GDNF) promotes glioma development process. However, the regulatory mechanisms of promoting occurrence and development of glioma have not yet been clearly elucidated.

Decreased intracellular chloride promotes ADP induced platelet activation through inhibition of cAMP/PKA instead of activation of Lyn/PI3K/Akt pathway.

Decrease of chloride concentration contributes to cardiovascular diseases, however, whether decrease of chloride concentration is involved in platelet activation remains elusive. In the present study, we found that ACI patients had lower serum chloride which would be rescued after Aspirin administration. ADP induced chloride concentration reduction in platelets.

Aggravated intestinal apoptosis by ClC-3 deletion is lethal to mice endotoxemia.

Our previous study found that ClC-3 chloride channel functioned differently in the vascular and intestinal inflammation, the loss of ClC-3 reduced vascular inflammation but exacerbated intestinal inflammation. To furtherly clarify the role of ClC-3 chloride channels in systemic inflammation, we used LPS-induced endotoxemia model to investigate the response of wild-type and ClC-3 knockout mice to systemic inflammation. The results showed that in the LPS-induced endotoxemia model, the mortality of mice with ClC-3 deletion was significantly higher than that of wild-type mice.

Cross-link regulation of precursor N-cadherin and FGFR1 by GDNF increases U251MG cell viability.

Glial cell line-derived neurotrophic factor (GDNF) is considered to be involved in the development of glioma. However, uncovering the underlying mechanism of the proliferation of glioma cells is a challenging work in progress. We have identified the binding of the precursor of N-cadherin (proN-cadherin) and GDNF on the cell membrane in previous studies.

Inhibition of Orai1-mediated Ca entry limits endothelial cell inflammation by suppressing calcineurin-NFATc4 signaling pathway.

Orai1-dependent Ca entry plays an essential role in inflammatory response through regulating T cell and macrophage activation and neutrophil infiltration. However, whether Orai1 Ca entry contributes to endothelial activation, one of the early steps of vascular inflammation, remains elusive. In the present study, we observed that knockdown of Orai1 reduced, whereas overexpression of Orai1 potentiated, TNFα-induced expression of adhesion molecules such as ICAM-1 and VCAM-1 in HUVECs, and subsequently blocked adhesion of monocyte to HUVECs.

MiRNAs Mediate GDNF-Induced Proliferation and Migration of Glioma Cells.

Background/aims: Glial cell line-derived neurotrophic factor (GDNF) is an important factor promoting invasive glioma growth. This study was performed to reveal a unique mechanism of glioma cell proliferation and migration.

Methods: Human U251 glioma cells were used to screen the optimal GDNF concentration and treatment time to stimulate proliferation and migration.

SOS response and its regulation on the fluoroquinolone resistance.

Bacteria can survive fluoroquinolone antibiotics (FQs) treatment by becoming resistant through a genetic change-mutation or gene acquisition. The SOS response is widespread among bacteria and exhibits considerable variation in its composition and regulation, which is repressed by LexA protein and derepressed by RecA protein. Here, we take a comprehensive review of the SOS gene network and its regulation on the fluoroquinolone resistance.

ClC-3 chloride channel/antiporter defect contributes to inflammatory bowel disease in humans and mice.

Background: ClC-3 channel/antiporter plays a critical role in a variety of cellular activities. ClC-3 has been detected in the ileum and colon.

Objective: To determine the functions of ClC-3 in the gastrointestinal tract.

Essential role of microRNA-155 in regulating endothelium-dependent vasorelaxation by targeting endothelial nitric oxide synthase.

Nitric oxide generated by endothelial nitric oxide synthase (eNOS) plays an important role in maintaining cardiovascular homeostasis. Under various pathological conditions, abnormal expression of eNOS contributes to endothelial dysfunction and the development of cardiovascular diseases. A variety of pathological stimuli has been reported to decrease eNOS expression mainly through decreasing eNOS mRNA stability by regulating the binding of several cytosolic proteins to the cis-acting sequences within eNOS mRNA 3' untranslated regions.