Endothelial Function in Dyslipidemia: Roles of LDL-Cholesterol, HDL-Cholesterol and Triglycerides

Cells, Journal Year: 2023, Volume and Issue: 12(9), P. 1293 - 1293

Published: May 1, 2023

Dyslipidemia is associated with endothelial dysfunction. Endothelial dysfunction the initial step for atherosclerosis, resulting in cardiovascular complications. It clinically important to break process of complications patients dyslipidemia. Lipid-lowering therapy enables improvement function likely that relationships components a lipid profile such as low-density lipoprotein cholesterol, high-density cholesterol and triglycerides are not simple. In this review, we focus on roles function.

Language: Английский

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A Systematic Review on Advances in Management of Oxidative Stress-Associated Cardiovascular Diseases

Antioxidants, Journal Year: 2024, Volume and Issue: 13(8), P. 923 - 923

Published: July 29, 2024

Oxidative stress plays a significant role in the pathogenesis of cardiovascular diseases, such as myocardial ischemia/reperfusion injury, atherosclerosis, heart failure, and hypertension. This systematic review aims to integrate most relevant studies on oxidative management diseases. We searched literatures PubMed database using specific keywords. put emphasis those manuscripts that were published more recently higher impact journals. reviewed total 200 articles. examined current managements including supplements like resveratrol, vitamins C E, omega-3 fatty acids, flavonoids, coenzyme-10, which have shown antioxidative properties potential benefits. In addition, we pharmacological treatments newly discovered antioxidants nanoparticles show effects targeting pathways. Lastly, biomarkers, soluble transferrin receptor, transthyretin, cystatin evaluating antioxidant status identifying risk. By addressing mechanisms, this paper emphasizes importance maintaining balance between oxidants progression is registered with International Platform Registered Systematic Review Meta-analysis Protocols (INPLASY), registration # INPLASY202470064.

Language: Английский

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Low-density lipoprotein particles in atherosclerosis

Frontiers in Physiology, Journal Year: 2022, Volume and Issue: 13

Published: Aug. 30, 2022

Among the diseases causing human death, cardiovascular disease (CVD) remains number one according to World Health Organization report in 2021. It is known that atherosclerosis pathological basis of CVD. Low-density lipoprotein (LDL) plays a pivotal role initiation and progression atherosclerotic CVD (ASCVD). LDL cholesterol (LDL-C) traditional biological marker LDL. However, large numbers patients who have achieved recommended LDL-C goals still ASCVD risk. In multiple prospective studies, particle (LDL-P) reported be more accurate predicting risk than LDL-C. LDL-Ps differ size, density chemical composition. Numerous clinical studies proved atherogenic mechanisms are determined not only by size but also modifications. Of note, small dense (sdLDL) particles possess stronger ability compared with intermediate subfractions. Besides, oxidized (ox-LDL) another factor atherosclerosis. lipid-lowering drugs, statins induce dramatic reductions LDL-P lesser extend. Recently, proprotein convertase subtilsin/kexin type 9 inhibitors (PCSK9i) been demonstrated effective lowering levels LDL-C, LDL-P, as well events. this article, we will make short review metabolism, discuss discordance between outline action focusing on sdLDL ox-LDL, summarize methods used for measurement subclasses, conclude advances LDL-lowering therapies using PCSK9i.

Language: Английский

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Nrf2/HO‐1, NF‐κB and PI3K/Akt signalling pathways decipher the therapeutic mechanism of pitavastatin in early phase liver fibrosis in rats

Journal of Cellular and Molecular Medicine, Journal Year: 2024, Volume and Issue: 28(3)

Published: Jan. 12, 2024

Liver fibrosis is a common chronic hepatic disease. This study aimed to investigate the effect of pitavastatin (Pit) against thioacetamide (TAA)-induced liver fibrosis. Rats were divided into four groups: (1) control group; (2) TAA group (100 mg/kg, i.p.) three times weekly for 2 weeks; (3 and 4) TAA/Pit-treated group, in which Pit was administered orally (0.4 0.8 mg/kg/day) weeks following injections. caused damage manifested by elevated serum transaminases, reduced albumin histological alterations. Hepatic malondialdehyde (MDA) increased, glutathione (GSH) superoxide dismutase (SOD) decreased TAA-administered rats. upregulated inflammatory markers NF-κB, NF-κB p65, TNF-α IL-6. Treatment with ameliorated prevented histopathological changes TAA-intoxicated suppressed MDA, cytokines PI3K mRNA In addition, enhanced antioxidants boosted nuclear factor erythroid 2-related (Nrf2) heme oxygenase-1 (HO-1) mRNA. Moreover, immunohistological studies supported ability reduce via suppressing p-AKT expression. conclusion, effectively prevents TAA-induced attenuating oxidative stress response. The hepatoprotective efficacy associated upregulation Nrf2/HO-1 downregulation PI3K/Akt signalling pathways.

Language: Английский

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Supplementation with aspalathin and sulforaphane protects cultured cardiac cells against dyslipidemia-associated oxidative damage

Metabolism Open, Journal Year: 2025, Volume and Issue: 25, P. 100346 - 100346

Published: Jan. 5, 2025

Dyslipidemia is a prominent pathological feature responsible for oxidative stress-induced cardiac damage. Due to their high antioxidant content, dietary compounds, such as aspalathin and sulforaphane, are increasingly explored cardioprotective effects against lipid-induced toxicity. Cultured H9c2 cardiomyoblasts, an in vitro model routinely used assess the pharmacological effect of drugs, were pretreated with (1 μM) sulforaphane (10 before exposure palmitic acid (0.25 mM) induce lipidemic-related complications. The results showed that both enhanced cellular metabolic activity improved mitochondrial respiration correlating mRNA expression genes involved function, including uncoupling protein 2, peroxisome proliferator-activated receptor, gamma coactivator 1-alpha, nuclear respiratory factor 1, ubiquinol-cytochrome c reductase complex assembly 1. Beyond attenuating lipid peroxidation, compounds also suppressed intracellular reactive oxygen species responses, erythroid 2-related 2. These envisaged benefits associated decreased apoptosis. This preclinical study supports warrants further investigation into potential these or foods rich protecting damage within myocardium.

Language: Английский

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The Anticonvulsant Effect of Nonsteroidal Anti‐Inflammatory Drug, Fenoprofen, in Pentylenetetrazole‐Induced Epileptic Rats: Behavioral, Histological, and Biochemical Evidence

Pharmacology Research & Perspectives, Journal Year: 2025, Volume and Issue: 13(1)

Published: Feb. 1, 2025

ABSTRACT This study aimed to evaluate the anticonvulsant properties of fenoprofen on experimental model pentylenetetrazole (PTZ)‐induced epilepsy. Male Wistar rats were randomly grouped into five, and kindling was induced by intraperitoneal injection PTZ 35 (mg/kg) every other day for 1 month. Aside from control groups, three groups received injections at doses 10, 20, 40 before each injection. Rats challenged with 70 week after development. Then subjected deep anesthesia, serum brain samples prepared. Oxidative stress (OS) markers (malondialdehyde, superoxide dismutase, glutathione peroxidase) measured in samples. Hippocampal tissue used investigate relative expression OS‐related genes ( nuclear factor [ erythroid‐derived 2 ]‐ like Nrf2 )/ heme oxygenase Hmox1 )) histological studies. Seizure behavior assessed based Lüttjohann's score. In treated number myoclonic jerks generalized tonic–clonic seizure (GTCS) duration decreased significantly, while GTCS latency increased compared group. The biochemical evaluation revealed antioxidative effects fenoprofen. / HO‐1 group reversed administration. results obtained Nissl staining hippocampal also confirmed protective effect seem be through inhibition markers, induction tissue, activation Nrf2/HO‐1 signaling pathway.

Language: Английский

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Investigating the Interplay Between the Nrf2/Keap1/HO-1/SIRT-1 Pathway and the p75NTR/PI3K/Akt/MAPK Cascade in Neurological Disorders: Mechanistic Insights and Therapeutic Innovations

Molecular Neurobiology, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 7, 2025

Language: Английский

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Modulation of AMPK by esomeprazole and canagliflozin mitigates methotrexate-induced hepatotoxicity: involvement of MAPK/JNK/ERK, JAK1/STAT3, and PI3K/Akt signaling pathways

Naunyn-Schmiedeberg s Archives of Pharmacology, Journal Year: 2025, Volume and Issue: unknown

Published: March 7, 2025

Abstract This research investigated the hepatoprotective effects of esomeprazole (ESOM) and canagliflozin (CANA) against methotrexate-induced liver toxicity, focusing on AMPK modulation its regulation MAPK/JNK/ERK, JAK1/STAT3, PI3K/Akt pathways. Fifty male Wistar rats were divided into five groups: control, MTX, three pretreatment groups receiving ESOM (30 mg/kg), CANA or their combination. administered for 8 days before 1 day after a single MTX injection (20 mg/kg, intraperitoneally) 9 to induce hepatotoxicity. Liver injury, oxidative stress, inflammation, apoptosis assessed using biochemical, histopathological, immunohistochemical, qRT-PCR, western blot analyses. Data analyzed by one-way analysis variance (ANOVA) Tukey’s post hoc test, with significance at p < 0.05. Results presented as mean ± standard error (SE). Rats that received showed significant damage, marked elevated ALT, AST, MDA, MPO, iNOS, TNF-α, IL-6, IL-1β levels ( 0.01) decreased antioxidant enzymes (HO-1, Nrf2, GSH). Immunohistochemistry revealed increased NF-kB p65 caspase-9 expression 0.01), correlating histopathological changes. Pretreatment reduced enzyme levels, improved histology, restored balance, inhibited inflammatory pathways via p38MAPK/NF-kB JAK1/STAT3 0.01). Moreover, preserved activity prevented caspase-dependent Additionally, combination treatment synergistic effects, demonstrated improvements in all measured parameters. These findings suggested had potential therapeutic agents alleviating MTX-induced hepatotoxicity warranted further investigation future research.

Language: Английский

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Molecular Mechanisms of Neuroprotection: The Interplay of Klotho, SIRT-1, Nrf2, and HO-1 in Neurological Health

Behavioural Brain Research, Journal Year: 2025, Volume and Issue: unknown, P. 115545 - 115545

Published: March 1, 2025

Language: Английский

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Regulation of the Nrf2/HO-1 axis by mesenchymal stem cells-derived extracellular vesicles: implications for disease treatment

Frontiers in Cell and Developmental Biology, Journal Year: 2024, Volume and Issue: 12

Published: June 10, 2024

This comprehensive review inspects the therapeutic potential of mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) across multiple organ systems. Examining their impact on integumentary, respiratory, cardiovascular, urinary, and skeletal systems, study highlights versatility MSC-EVs in addressing diverse medical conditions. Key pathways, such as Nrf2/HO-1, consistently emerge central mediators antioxidative anti-inflammatory effects. From expediting diabetic wound healing to mitigating oxidative stress-induced skin injuries, alleviating acute lung even offering solutions for conditions like myocardial infarction renal ischemia-reperfusion injury, demonstrate promising efficacy. Their adaptability different administration routes identifying specific factors opens avenues innovative regenerative strategies. positions candidates future clinical applications, providing a overview medicine.

Language: Английский

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