Biological Trace Element Research, Journal Year: 2024, Volume and Issue: unknown
Published: Oct. 31, 2024
Language: Английский
Biological Trace Element Research, Journal Year: 2025, Volume and Issue: unknown
Published: Jan. 17, 2025
Chronic fluorosis is often accompanied by neurological symptoms, leading to attention, memory and learning ability decline causing tension, anxiety, depression, other mental symptoms. In the present study, we analyzed molecular mechanisms of SIRT1-BDNF regulation PI3K-AKT, MAPK, FOXO1A in F-treated BV2 cells. The cytotoxic effect sodium fluoride (NaF) on cells was assessed using Cell Counting Kit-8 (CCK-8), crystal violet, 5-ethynyl-2'-deoxyuridine (EdU) staining. cycle progression apoptosis were evaluated through flow cytometry western blotting. Reactive oxygen species (ROS) levels, oxidative stress, inflammatory markers measured ROS staining, microplate reader assays, role SIRT1 fluoride-induced toxicity for glial determined activator SRT1720. experiments demonstrated that NaF toxic cells, inhibited their proliferative ability, halted cell progression, triggered cellular apoptosis, promoted stress (detected ROS, SOD, MDA, GSH-Px, T-AOC) associated protein NQO-1 HO-1, elevated mediator IL-1and IL-6 expression). fluoride-exposed groups had reduced SIRT1, BDNF, TrkB, PI3K, AKT, MAPK expression increased expression. SRT1720 mitigated harmful effects NaF, stimulated proliferation decreased factors, suppressed results indicate potentially harms suppressing activation, significantly damage. Furthermore, signaling pathway might regulate nerve damage caused poisoning may be a protective factor treating brain injury.
Language: Английский
Citations
1
Toxics, Journal Year: 2025, Volume and Issue: 13(2), P. 83 - 83
Published: Jan. 24, 2025
Prolonged excessive intake of fluoride (F) can result in fluorosis, leading to a range tissue oxidative damages. Therefore, mitigating the stress induced by fluorosis has become significant research concern. Consequently, how relieve caused is an urgent matter. In present study, intestinal porcine epithelial (IPEC-J2) cells were chosen explore underlying mechanism tea polyphenols (TPs) on F-induced stress. The results show that cytotoxicity IPEC-J2 F presented dose-dependent manner according cell viability. Additionally, treatment inhibited activity T-SOD, CAT, and GSH-Px as well their transcription levels, increased reactive oxygen (ROS) formation damage rates, then promoted apoptosis through TUNEL mitochondrial membrane potential detection when compared with from control group. As main antioxidant ingredient tea, TPs alleviated oxidation via blocking ROS generation LDH’s release, promoting tight junction (TJ) proteins activities enzymes cells. These provide new strategy for impairment.
Language: Английский
Citations
1
Environmental Research, Journal Year: 2025, Volume and Issue: unknown, P. 121102 - 121102
Published: Feb. 1, 2025
Language: Английский
Citations
1
Food and Chemical Toxicology, Journal Year: 2025, Volume and Issue: unknown, P. 115267 - 115267
Published: Jan. 1, 2025
Language: Английский
Citations
0
Biological Trace Element Research, Journal Year: 2025, Volume and Issue: unknown
Published: Jan. 21, 2025
Language: Английский
Citations
0
Frontiers in Toxicology, Journal Year: 2025, Volume and Issue: 7
Published: April 1, 2025
Introduction: Microplastics are ubiquitous environmental pollutants with potential neurotoxic effects that can impair learning and memory. MicroRNAs essential regulators of a number physiological pathological processes, but detailed information on the impact miRNAs microplastics is lacking. Methods: In present study, polystyrene (PS-MPs) were administered orally miR-103a-3p was injected intracerebroventricularly as treatment for PS-MPs-induced neurotoxicity. Results Discussion: Performance in novel object discrimination Y-maze Barnes maze tests indicated mitigates deleterious PS-MPs Oxidative stress, pyroptosis, apoptosis inflammation induced by modulated after miR- 103a-3p injection reducing malondialdehyde, protein carbonyl, nitrite, caspase 3, 1, TNFα, NLRP3 levels hippocampal tissue. Our results also showed reverse astrocytic reaction SIRT1 BDNF levels. MiR-103a-3p alleviated endoplasmic reticulum (ER) stress through PERK, CHOP GRP78. These findings imply exerts neuroprotective influence against cognitive deficits exposure to PS-MPs. This achieved inflammation, oxidative stress.
Language: Английский
Citations
0
Phytomedicine, Journal Year: 2025, Volume and Issue: 143, P. 156838 - 156838
Published: May 10, 2025
Language: Английский
Citations
0
Frontiers in Endocrinology, Journal Year: 2024, Volume and Issue: 15
Published: March 15, 2024
Background Patients on hemodialysis have a higher burden of cognitive impairment than individuals the same age in general population. Studies found link between cognition and skeletal muscle function. However, few studies investigated these associations underlying mechanisms patients hemodialysis. Methods A total 166 were enrolled this longitudinal study. Cognitive function was assessed by Montreal Assessment (MoCA) scores. Skeletal indicators evaluated using Inbody S10. Plasma brain-derived neurotrophic factor (BDNF) concentrations measured enzyme-linked immunosorbent assay. The primary outcome change MoCA mediation analysis performed to examine indirect effect decline through BDNF. Results Among patients, average 49.9 ± 11.2 years. Of with median follow-up 1,136 days, 133 participated We defined scores decreased ≥2 points at 3 years from baseline measurement as (CD). Compared cognitively unchanged group, CD had significantly lower fat-free mass, soft lean index (all P<0.05). After adjusting for potential confounders, protective predictors CD. significant increase plasma BDNF levels observed group. Mediation suggested that played mediating role 20-35% muscle. Conclusion is predictor undergoing dialysis. mediates relationship
Language: Английский
Citations
3
Ecotoxicology and Environmental Safety, Journal Year: 2024, Volume and Issue: 281, P. 116681 - 116681
Published: July 4, 2024
Fluoride exposure has been implicated as a potential risk factor for hypertension, but the underlying mechanisms remain unclear. This study investigated role of RhoA/ROCK signaling pathway in fluoride-induced hypertension. Male Wistar rats were divided into different groups and exposed to varying concentrations sodium fluoride (NaF) or chloride (NaCl) via drinking water. The rats' blood pressure was measured, their aortic tissue utilized high-throughput sequencing analysis. Additionally, rat A7r5 cell models established using NaF and/or Fasudil. evaluated effects on pressure, pathological changes aorta, well protein/mRNA expression levels phenotypic transformation indicators (a-SMA, calp, OPN) vascular smooth muscle cells (VSMCs), along with (RhoA, ROCK1, ROCK2, MLC/p-MLC). results demonstrated that led increased pressure. High-throughput analysis revealed differential gene associated contraction, emerging key regulator. Pathological such elastic membrane rupture collagen fiber deposition, observed following exposure. However, fasudil, ROCK inhibitor, mitigated these changes. Both vitro vivo confirmed activation VSMCs from contractile synthetic state upon Fasudil effectively inhibited activities ROCK1 ROCK2 attenuated VSMCs. In conclusion, induce hypertension through cells. These provide new insights mechanism
Language: Английский
Citations
3
Biological Trace Element Research, Journal Year: 2024, Volume and Issue: unknown
Published: May 18, 2024
Language: Английский
Citations
2