The Effect of Zeolite Zinc on Memory Performance and Hippocampal Cell Death in a Rat Model of Alzheimer’s-like Disease Induced by Aβ1–42 DOI

Maryam Zaman Fashami,

Aida Bajelan,

H.R. Shakur

et al.

Biological Trace Element Research, Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 7, 2024

Language: Английский

Zinc Toxicity: Understanding the Limits DOI Creative Commons

Hannah Schoofs,

Joyce Schmit,

Lothar Rink

et al.

Molecules, Journal Year: 2024, Volume and Issue: 29(13), P. 3130 - 3130

Published: July 1, 2024

Zinc, a vital trace element, holds significant importance in numerous physiological processes within the body. It participates over 300 enzymatic reactions, metabolic functions, regulation of gene expression, apoptosis and immune modulation, thereby demonstrating its essential role maintaining overall health well-being. While zinc deficiency is associated with risks, an excess this element can also lead to harmful effects. According World Health Organization (WHO), 6.7 15 mg per day are referred be dietary reference value. An recommended daily intake may result symptoms such as anemia, neutropenia zinc-induced copper deficiency. The European Food Safety Authority (EFSA) defines tolerable upper level (UL) 25 day, whereas Drug Administration (FDA) allows 40 day. This review will summarize current knowledge regarding calculation UL other risks zinc. For example, not limited oral consumption; routes, inhalation or topical application, pose intoxication.

Language: Английский

Citations

49

Potential Role of Natural Antioxidants in Countering Reperfusion Injury in Acute Myocardial Infarction and Ischemic Stroke DOI Creative Commons
Sofía Orellana-Urzúa, Camilo Briones-Valdivieso, Silvia Chichiarelli

et al.

Antioxidants, Journal Year: 2023, Volume and Issue: 12(9), P. 1760 - 1760

Published: Sept. 13, 2023

Stroke and acute myocardial infarction are leading causes of mortality worldwide. The latter accounts for approximately 9 million deaths annually. In turn, ischemic stroke is a significant contributor to adult physical disability globally. While reperfusion crucial tissue recovery, it can paradoxically exacerbate damage through oxidative stress (OS), inflammation, cell death. Therefore, imperative explore diverse approaches aimed at minimizing ischemia/reperfusion injury enhance clinical outcomes. OS primarily arises from an excessive generation reactive oxygen species (ROS) and/or decreased endogenous antioxidant potential. Natural compounds counteract the mechanisms linked ROS. promising preclinical results, based on monotherapies, account protective effects against by ROS, translating these models into human applications has yielded controversial evidence. However, since wide spectrum antioxidants having chemical characteristics offers varied biological actions signaling pathways, multitherapy emerged as valuable therapeutic resource. Moreover, combination in holds potential synergistic effects. This study was designed with aim providing updated overview natural suitable preventing cerebral injuries.

Language: Английский

Citations

24

Bridging the gap between theory and treatment: Transition metal complexes as successful candidates in medicine DOI

Sara Abdolmaleki,

Alireza Aliabadi, Samad Khaksar

et al.

Coordination Chemistry Reviews, Journal Year: 2025, Volume and Issue: 531, P. 216477 - 216477

Published: Feb. 8, 2025

Language: Английский

Citations

1

Endogenous Zinc‐Ion‐Triggered In Situ Gelation Enables Zn Capture to Reprogram Benign Hyperplastic Prostate Microenvironment and Shrink Prostate DOI

Jianchao Ge,

Chao Fang,

Haisong Tan

et al.

Advanced Materials, Journal Year: 2023, Volume and Issue: 36(11)

Published: Dec. 14, 2023

Abstract Benign prostatic hyperplasia (BPH) as the leading cause of urination disorder is still a refractory disease, and there have no satisfied drugs or treatment protocols yet. With identifying excessive Zn 2+ , inflammation, oxidative stress etiology aberrant hyperplasia, an injectable sodium alginate (SA) glycyrrhizic acid (GA)‐interconnected hydrogels (SAGA) featuring ‐triggered in situ gelation are developed to load lonidamine for reprogramming prostate microenvironment treating BPH. Herein, SAGA can crosslink with BPH via coordination chelation switch free bound ones, consequently alleviating ‐arisen inflammation glycolysis. Beyond capturing GA intrinsic immunoregulatory property also alleviate local scavenge reactive oxygen species (ROS). Intriguingly, chelation‐bridged interconnection enhances its mechanical regulates degradation rate enable continuous release, favoring hyperplastic acini apoptosis further inhibiting These multiple actions cooperatively reprogram characteristic symptoms shrink prostate. RNA sequencing reveals that chemotaxis, glycolysis, tumor necrosis factor (TNF) inflammation‐related pathways associated M1‐like phenotype polarization discerned action rationales such endogenous hydrogels, providing candidate avenue treat

Language: Английский

Citations

19

Protective effect of zinc gluconate on intestinal mucosal barrier injury in antibiotics and LPS-induced mice DOI Creative Commons

Wang Yong-cai,

Juan Xiao,

Sumei Wei

et al.

Frontiers in Microbiology, Journal Year: 2024, Volume and Issue: 15

Published: May 23, 2024

Objective The aim of the study is to investigate function and mechanism Zinc Gluconate (ZG) on intestinal mucosal barrier damage in antibiotics Lipopolysaccharide (LPS)-induced mice. Methods We established a composite mouse model by inducing using LPS. animals were divided into five groups: Control (normal model) experimental (low, medium, high-dose ZG treatments). evaluated various methods, including monitoring body weight fecal changes, assessing pathological ultrastructure ileum, analyzing expression levels tight junction (TJ)-related proteins genes, confirming TLR4/NF-κB signaling pathway, examining structure flora. Results In mice, dual induction LPS led loss, abnormalities, disruption ileocecal structure, increased permeability, disorganization microbiota structure. restored weight, alleviated diarrheal symptoms damage, maintained structural integrity epithelial cells (IECs). Additionally, reduced permeability upregulating TJ-associated (ZO-1, Occludin, Claudin-1, JAM-A) downregulating MLCK, thereby repairing induced Moreover, suppressed demonstrating anti-inflammatory properties preserving integrity. Furthermore, gut diversity richness, evidenced Shannon Observed features indices, decreased Simpson’s index. also modulated relative abundance beneficial human bacteria ( Bacteroidetes , Firmicutes Verrucomicrobia Parabacteroides Lactobacillus Akkermansia ) harmful Proteobacteria Enterobacter ), administration Conclusion attenuates LPS-induced protects

Language: Английский

Citations

8

Contribution of zinc accumulation to ischemic brain injury and its mechanisms about oxidative stress, inflammation, and autophagy: an update DOI

Xueqi Yang,

Wei Li, Mao Ding

et al.

Metallomics, Journal Year: 2024, Volume and Issue: 16(3)

Published: Feb. 28, 2024

Abstract Ischemic stroke is a leading cause of death and disability worldwide, presently, there no effective neuroprotective therapy. Zinc an essential trace element that plays important physiological roles in the central nervous system. Free zinc concentration tightly regulated by zinc-related proteins brain under normal conditions. Disruption homeostasis, however, has been found to play role mechanism injury following ischemic stroke. A large free releases from storage sites after cerebral ischemia, which affects functions survival nerve cells, including neurons, astrocytes, microglia, resulting cell death. Ischemia-triggered intracellular accumulation also disrupts function blood–brain barrier via increasing its permeability, impairing endothelial function, altering tight junction levels. Oxidative stress neuroinflammation have reported be as major pathological mechanisms ischemia/reperfusion injury. Studies showed could impair mitochondrial result oxidative stress, form positive feedback loop between reactive oxygen species production, leads series harmful reactions. Meanwhile, elevated neuroinflammation. Recent studies autophagy one toxicity Interrupting will reduce ischemia improve neurological outcomes. This review summarizes cellular tissue damage focusing on about inflammation, autophagy.

Language: Английский

Citations

6

TPEN loaded poly (lactide-co-glycolide) nanoparticles promotes neuroprotection and optic nerve regeneration DOI Creative Commons

Caiqing Wu,

Haitao Zhang, Yuze Chen

et al.

Materials Today Bio, Journal Year: 2025, Volume and Issue: unknown, P. 101670 - 101670

Published: March 1, 2025

Development of novel therapeutics for retinal ganglion cells (RGCs) protection and axon regeneration in neurodegenerative diseases, example, glaucoma, are critical challenges clinical treatment. Utilization N, N', N'-tetrakis-(2-Pyridylmethyl) ethylenediamine (TPEN), a specific chelator Zn2+, revealed positive medical potentials. However, its therapeutic effect promoting RGCs survival is restricted due to the inefficient drug delivery limited absorption. To address this, this work developed nanoparticles (NPs)-based system with sustained release TPEN, using oil-in-water (O/W) single-emulsion solvent evaporation method various surfaces coatings. Optic nerve crush (ONC) acute ocular hypertension (AOH) animal models were carried out investigate neuroprotective regenerative effects TPEN-loaded NPs. was systematically assessed through whole-mount retina immunostaining hematoxylin eosin staining histological changes. Electroretinography used evaluating visual function Axon evaluated by SMI32 stain intravitreal administration cholera Toxin Subunit B (CTB), respectively. In vivo, NPs achieved comparable on neuroprotection after ONC, reduced frequency vitreous injection half TPEN dosage compared solution. meantime, also more effectively preserved Additionally, AOH significantly enhanced treating The show promise pre-clinical testing neuro-regenerative therapies glaucoma other diseases.

Language: Английский

Citations

0

Mechanism of LCN2 in cerebral ischemia-reperfusion injury DOI Creative Commons

Luo-yang Cai,

Ying Yuan, Hai Huang

et al.

Frontiers in Neuroscience, Journal Year: 2025, Volume and Issue: 19

Published: March 20, 2025

Cerebral ischemia-reperfusion injury (CIRI) is a complex pathophysiological process faced by brain tissues after ischemic stroke treatment, which involves mechanisms of inflammatory response, oxidative stress and apoptosis, severely affects treatment outcome. Lipocalin-2 (LCN2), an acute-phase protein, significantly up-regulated CIRI promotes neural repair enhancing astrocyte phagocytosis, but its over-activation may also trigger secondary inflammation demyelination injury. LCN2 plays key role in neuroinflammation regulation regulating the polarization state astrocytes release factors, affect integrity blood–brain barrier variety pathologic processes. In view important CIRI, this article reviews mechanism LCN2, aiming to provide new ideas methods for stroke.

Language: Английский

Citations

0

The role of metal ions in stroke: current evidence and future perspectives DOI
Shaoshuai Wang,

Mengzhe Qin,

Xiaochong Fan

et al.

Ageing Research Reviews, Journal Year: 2024, Volume and Issue: 101, P. 102498 - 102498

Published: Sept. 6, 2024

Language: Английский

Citations

3

Tafluprost promotes axon regeneration after optic nerve crush via Zn2+-mTOR pathway DOI

Siting Wu,

Canying Liu, J. Tang

et al.

Neuropharmacology, Journal Year: 2023, Volume and Issue: 242, P. 109746 - 109746

Published: Oct. 12, 2023

Language: Английский

Citations

5