Empagliflozin attenuates radiation-induced hematopoietic damage via NOX-4/ROS/p38 pathway DOI

Qidong Huo,

Tongpeng Yue, Wenxuan Li

et al.

Life Sciences, Journal Year: 2024, Volume and Issue: 341, P. 122486 - 122486

Published: Feb. 6, 2024

Language: Английский

Oxidative Stress in Pregnancy DOI Creative Commons
Konrad Grzeszczak, Natalia Łanocha-Arendarczyk, Witold Malinowski

et al.

Biomolecules, Journal Year: 2023, Volume and Issue: 13(12), P. 1768 - 1768

Published: Dec. 9, 2023

Recent years have seen an increased interest in the role of oxidative stress (OS) pregnancy. Pregnancy inherently heightens susceptibility to OS, a condition fueled by systemic inflammatory response that culminates elevated presence reactive oxygen species (ROS) and nitrogen (RNS) circulatory system. The amplified OS pregnancy can trigger series detrimental outcomes such as underdevelopment, abnormal placental function, host complications, including pre-eclampsia, embryonic resorption, recurrent loss, fetal developmental anomalies, intrauterine growth restriction, and, extreme instances, death. body’s mitigate uncontrolled increase RNS/ROS levels requires trace elements take part non-enzymatic enzymatic defense processes, namely, copper (Cu), zinc (Zn), manganese (Mn), selenium (Se). Determination ROS concentrations poses challenge due their short half-lives, prompting use marker proteins, malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx), reductase (GR), catalase (CAT), (GSH). These markers, indicative intensity, offer indirect assessments complications. Given limitations conducting experimental studies on pregnant women, animal models serve valuable substitutes for in-depth research. This review delves into mechanism underscores pivotal markers evaluation.

Language: Английский

Citations

44

Phenotypic switching of vascular smooth muscle cells in atherosclerosis, hypertension, and aortic dissection DOI Creative Commons
Mohamed Elmarasi, Ibrahim Elmakaty, Basel Elsayed

et al.

Journal of Cellular Physiology, Journal Year: 2024, Volume and Issue: 239(4)

Published: Jan. 30, 2024

Abstract Vascular smooth muscle cells (VSMCs) play a critical role in regulating vasotone, and their phenotypic plasticity is key contributor to the pathogenesis of various vascular diseases. Two main VSMC phenotypes have been well described: contractile synthetic. Contractile VSMCs are typically found tunica media vessel wall, responsible for tone diameter. Synthetic VSMCs, on other hand, intima adventitia, involved repair remodeling. Switching between synthetic occurs response insults stimuli, such as injury or inflammation, this allows adapt changing environmental cues regulate tone, growth, repair. Furthermore, can also switch osteoblast‐like chondrocyte‐like cell phenotypes, which may contribute calcification pathological processes like formation atherosclerotic plaques. This provides discusses mechanisms that switching its development A better understanding these essential effective diagnostic therapeutic strategies.

Language: Английский

Citations

34

Salidroside Mediated the Nrf2/GPX4 Pathway to Attenuates Ferroptosis in Parkinson’s Disease DOI Creative Commons
Jun Shen, Shasha Chen, Xin Li

et al.

Neurochemical Research, Journal Year: 2024, Volume and Issue: 49(5), P. 1291 - 1305

Published: Feb. 29, 2024

Abstract Parkinson’s Disease (PD) is characterized by the loss of dopaminergic neurons, with ferroptosis playing a significant role. Salidroside (SAL) has shown neuroprotective potential, this study aims to explore its capacity mitigate in PD, focusing on modulation Nuclear Factor E2-Related 2 (Nrf2)/ Glutathione Peroxidase 4 (GPX4) pathway. Male C57BL/6 mice were subjected 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induce PD-like symptoms, followed SAL and Nrf2 inhibitor administration. Then behavioral tests, immunohistochemical staining, transmission electron microscopy, Western blot analysis conducted assess motor functions, pathological changes, ferroptosis, related protein expressions. In vitro, SH-SY5Y cells treated erastin protective effects SAL. Additionally, A53T-α-synuclein (α-syn) was used stimulate PD model, (ML385) utilized elucidate role Nrf2/GPX4 pathway mitigating PD. vivo , significantly improved functions reduced expression α-syn, while increasing tyrosine hydroxylase (TH) mice. treatment notably enhanced levels antioxidants MDA iron content substantia nigra vitro increased TH, GPX4, expression, mitochondrial membrane potential whereas alleviated through pathway, as evidenced erastin-induced α-syn overexpressing cells. While these reversed upon inhibition. demonstrates pathology positioning promising therapeutic target. However, future studies should focus long-term SAL, pharmacokinetics, addressing multifactorial nature pathogenesis.

Language: Английский

Citations

19

Flavonoids: Potential therapeutic agents for cardiovascular disease DOI Creative Commons
Yingxue Liu, Jing Luo, Peng Lin

et al.

Heliyon, Journal Year: 2024, Volume and Issue: 10(12), P. e32563 - e32563

Published: June 1, 2024

Flavonoids are found in the roots, stems, leaves, and fruits of many plant taxa. They related to growth development, pigment formation, protection against environmental stress. function as antioxidants exert anti-inflammatory effects cardiovascular system by modulating classical inflammatory response pathways, such TLR4-NF-ĸB, PI3K-AKT, Nrf2/HO-1 signalling pathways. There is increasing evidence for therapeutic flavonoids on hypertension, atherosclerosis, other diseases. The potential clinical value diseases has been widely explored. For example, studies have evaluated roles regulation blood pressure via endothelium-dependent non-endothelium-dependent pathways myocardial systolic diastolic functions influencing calcium homeostasis smooth muscle-related protein expression. also hypoglycaemic, hypolipidemic, anti-platelet, autophagy, antibacterial effects. In this paper, role mechanism were reviewed order provide reference application future.

Language: Английский

Citations

18

The potential effect of natural antioxidants on endothelial dysfunction associated with arterial hypertension DOI Creative Commons
Rosamaria Caminiti, Cristina Carresi, Rocco Mollace

et al.

Frontiers in Cardiovascular Medicine, Journal Year: 2024, Volume and Issue: 11

Published: Feb. 2, 2024

Arterial hypertension represents a leading cause of cardiovascular morbidity and mortality worldwide, the identification effective solutions for treating early stages elevated blood pressure (BP) is still relevant issue risk prevention. The pathophysiological basis occurrence BP onset arterial have been widely studied in recent years. In addition, consistent progress development novel, powerful, antihypertensive drugs their appropriate applications controlling increased our potential successfully managing disease states characterized by abnormal pressure. However, mechanisms responsible disruption endogenous contributing to maintenance within normal range are yet be fully clarified. Recently, evidence has shown that several natural antioxidants containing active ingredients originating from plant extracts, used alone or combination, may represent valid solution counteracting hypertension. particular, there show enhance viability endothelial cells undergoing oxidative damage, an effect could play crucial role events accompanying present review aims reassess stress on dysfunction progression covering unmet needs treatment such diseases.

Language: Английский

Citations

10

Synergistic Neuroprotection Through Epigenetic Modulation by Combined Curcumin-Enriched Turmeric Extract and L-Ascorbic Acid in Oxidative Stress-Induced SH-SY5Y Cell Damage DOI Creative Commons
Jurairat Khongrum, Nootchanat Mairuae, Tongjit Thanchomnang

et al.

Foods, Journal Year: 2025, Volume and Issue: 14(5), P. 892 - 892

Published: March 5, 2025

Epigenetic modulation plays a crucial role in neuroprotection by regulating cellular responses to stress, inflammation, and oxidative damage, particularly neurodegenerative diseases. Recognizing the therapeutic potential of epigenetic regulators, this study investigated synergistic neuroprotective effects curcumin-enriched turmeric extract combined with L-ascorbic acid, focusing on its pathways stress-induced neuronal damage. SH-SY5Y cells were treated combination at 20 40 µg/mL, subsequently exposed 200 µM hydrogen peroxide (H2O2) induce stress. Cell viability was assessed using MTT assay, while mechanisms evaluated analyzing markers modulation, apoptosis. The significantly enhanced cell viability, upregulated sirtuin-1 (SIRT1), reduced DNA methyltransferase 1 (DNMT1) expression, indicating effective modulation. Enhanced antioxidant defenses observed, as evidenced increased activities superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), along decreased malondialdehyde (MDA) reactive oxygen species (ROS) levels, alleviating Additionally, it suppressed nuclear factor kappa B (NF-κB) activity downstream mediator interleukin-6 (IL-6), thereby mitigating inflammation. treatment also anti-apoptotic Bcl-2 expression reducing pro-apoptotic markers, including caspase-3 caspase-9, suggesting inhibition intrinsic apoptotic pathway. These findings highlight novel combination, demonstrating ability modulate suppressing preventing undesired Its multifaceted properties make promising functional ingredient foods for disease intervention. However, further investigations, animal studies clinical trials, are essential evaluate safety potential.

Language: Английский

Citations

1

C‐peptide in diabetes: A player in a dual hormone disorder? DOI

Ali Dakroub,

Ali Dbouk, Aref Asfour

et al.

Journal of Cellular Physiology, Journal Year: 2024, Volume and Issue: 239(5)

Published: Feb. 3, 2024

Abstract C‐peptide, a byproduct of insulin synthesis believed to be biologically inert, is emerging as multifunctional molecule. C‐peptide serves an anti‐inflammatory and anti‐atherogenic role in type 1 diabetes mellitus (T1DM) early T2DM. protects endothelial cells by activating AMP‐activated protein kinase α, thus suppressing the activity NAD(P)H oxidase reducing reactive oxygen species (ROS) generation. It also prevents apoptosis regulating hyperglycemia‐induced p53 upregulation mitochondrial adaptor p66shc overactivation, well caspase‐3 promoting expression B‐cell lymphoma‐2. Additionally, suppresses platelet‐derived growth factor (PDGF)‐beta receptor p44/p42 mitogen‐activated (MAP) phosphorylation inhibit vascular smooth muscle (VSMC) proliferation. diminishes leukocyte adhesion virtue its capacity abolish nuclear kappa B (NF‐kB) signaling, major pro‐inflammatory cascade. Consequently, it envisaged that supplementation T1DM might ameliorate or even prevent end‐organ damage. In marked contrast, increases monocyte recruitment migration through phosphoinositide 3‐kinase (PI‐3 kinase)‐mediated pathways, induces lipid accumulation via peroxisome proliferator‐activated γ upregulation, stimulates VSMC proliferation CD4 + lymphocyte Src‐kinase PI‐3K dependent pathways. Thus, promotes atherosclerosis microvascular damage late Indeed, now contemplated potential biomarker for resistance T2DM linked increased coronary artery disease risk. This shift understanding pathophysiology from being single hormone deficiency dual disorder warrants careful consideration unique molecule with promising diagnostic, prognostic, therapeutic applications.

Language: Английский

Citations

7

The pharmaco-epigenetics of hypertension: a focus on microRNA DOI Creative Commons

Serge Yaacoub,

Ammar Boudaka,

Ali Alkhatib

et al.

Molecular and Cellular Biochemistry, Journal Year: 2024, Volume and Issue: 479(12), P. 3255 - 3271

Published: Feb. 29, 2024

Hypertension is a major harbinger of cardiovascular morbidity and mortality. It predisposes to higher rates myocardial infarction, chronic kidney failure, stroke, heart failure than most other risk factors. By 2025, the prevalence hypertension projected reach 1.5 billion people. The pathophysiology this disease multifaceted, as it involves nitric oxide endothelin dysregulation, reactive oxygen species, vascular smooth muscle proliferation, vessel wall calcification, among others. With advent new biomolecular techniques, various studies have elucidated gaping hole in etiology mechanisms hypertension. Indeed, epigenetics, DNA methylation, histone modification, microRNA-mediated translational silencing appear play crucial roles altering molecular phenotype into hypertensive profile. Here, we critically review experimentally determined associations between microRNA (miRNA) molecules pharmacotherapy. Particular attention given epigenetic underlying physiological responses antihypertensive drugs like candesartan, relevant clopidogrel, aspirin, statins Furthermore, how miRNA affects pharmaco-epigenetics especially highlighted.

Language: Английский

Citations

7

Hollow manganese dioxide-chitosan hydrogel for the treatment of atopic dermatitis through inflammation-suppression and ROS scavenging DOI Creative Commons

Yaguang Wu,

Zihao Zhou, Min Zhang

et al.

Journal of Nanobiotechnology, Journal Year: 2023, Volume and Issue: 21(1)

Published: Nov. 17, 2023

Abstract Atopic dermatitis (AD) is a chronic inflammatory disease associated with immune dysfunction. High levels of reactive oxygen species (ROS) can lead to oxidative stress, release pro-inflammatory cytokines, and T-cell differentiation, thereby promoting the onset worsening AD. In this study, we innovatively used quaternary ammonium chitosan (QCS) tannic acid (TA) as raw materials design prepare therapeutic hydrogel(H-MnO 2 -Gel) loaded hollow manganese dioxide nanoparticles (H-MnO NPs). system, hydrogel mainly cross-linked by dynamic ion hydrogen bonding between QCS TA, resulting in excellent moisture retention properties. Moreover, due inherent antioxidant properties QCS/TA, well outstanding H O scavenging ability H-MnO NPs, exhibits significant ROS capability. vitro experiments have shown that -Gel good cellular biocompatibility. Importantly, an AD-induced mouse model, significantly enhanced effects reducing epidermal thickness, mast cell number, IgE antibodies. These findings suggest -Gel, effectively clearing regulating microenvironment, provides promising approach for treatment

Language: Английский

Citations

15

Dietary Salt Can Be Crucial for Food-Induced Vascular Inflammation DOI Creative Commons
Syed Masudur Rahman Dewan, Sara Shahid Meem, Amrin Yeasin Proma

et al.

Clinical Pathology, Journal Year: 2024, Volume and Issue: 17

Published: Jan. 1, 2024

Salt enhances the taste as well nutritional value of food. Besides, several reports are available on incidence and epidemiology various illnesses in relation to salt intake. Excessive consumption has been found be linked with high blood pressure, renal disease, other cardiovascular disorders due result vascular inflammation. Nevertheless, studies aimed at elucidating molecular processes that produce inflammation have yet reach their conclusions. This article emphasizes significance investigating mechanisms underlying both acute chronic induced by salt. It also explores logical inferences behind cellular oxidative stress role endothelial dysfunction potential initiator inflammatory segments remain poorly understood. is therefore hypothesized one causes such atherosclerosis. The hypothesis’s secrets, when revealed, can help assure health proactive efforts development appropriate preventative measures, combination medication, dietary lifestyle adjustments.

Language: Английский

Citations

4