Neurotoxic effects of heavy metal pollutants in the environment: Focusing on epigenetic mechanisms

Environmental Pollution, Journal Year: 2024, Volume and Issue: 345, P. 123563 - 123563

Published: Feb. 13, 2024

Language: Английский

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Male reproductive toxicity of inorganic nanoparticles in rodent models: A systematic review

Chemico-Biological Interactions, Journal Year: 2022, Volume and Issue: 363, P. 110023 - 110023

Published: June 25, 2022

Language: Английский

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Enhancement of apoptosis in HCT116 and HepG2 cells by Coix lacryma-jobi var. lacryma-jobi seed extract in combination with sorafenib

Chinese Herbal Medicines, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 1, 2025

Language: Английский

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Exploring the dermal safety of green-synthesized Ag–TiO₂ nanocomposites for topical applications

RSC Advances, Journal Year: 2025, Volume and Issue: 15(12), P. 9320 - 9334

Published: Jan. 1, 2025

We investigated Ag–TiO 2 nanocomposites (NCs) synthesized using leaf extracts of Azadirachta indica and Mangifera for topical applications.

Language: Английский

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Nanoparticles induced neurotoxicity

Nanotoxicology, Journal Year: 2025, Volume and Issue: unknown, P. 1 - 28

Published: April 16, 2025

The early development of nanotechnology has spurred major interest on the toxicity nanoparticles (NPs) due to their ability penetrate biological barriers such as BBB. This review aims at addressing how silver (AgNPs), titanium dioxide (TiO2NPs), zinc oxide (ZnONPs), iron (Fe3O4NPs), carbon NPs, Copper (Cu-NPs), silicon (SiO2 NPs) and quantum dots cause neurotoxicity. Some signaling that occur are related oxidative stress, neuroinflammation, mitochondrial dysfunction cell equilibrium, hence results in neuronal damage neurodegeneration. It is critical describe there multiple ways by NPs may be toxic based size surface, dosage, recipient's age health condition. A vitro vivo analysis provides information about potentials preventive measures including modification NP surface antioxidant treatment. underline necessity comprehensive safety assessments allow further utilization across economy.

Language: Английский

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MARCKS as a Target for Pathological Tunneling Nanotubes in Glioblastoma

Research Square (Research Square), Journal Year: 2025, Volume and Issue: unknown

Published: April 29, 2025

During glioblastoma (GBM) progression, therapeutic resistance is influenced by a heterogeneous network of tumor- and tumor-promoting cells in the tumor microenvironment. Biological attacks against (i.e. chemoradiotherapy) induce tumoral defense mechanisms bolstered sophisticated communication aberrant signaling pathways. Tunneling nanotubes (TNTs) have been well documented to mediate this process aiding metabolic rescue or facilitating recruitment reprogramming normal become tumor-supportive. GBM brain tumor-initiating (BTIC) target human astrocytes (NHA) using TNTs, therefore investigating interaction potential mediators involved critical. Myristoylated Alanine Rich C-Kinase Substrate (MARCKS) has never investigated as regulator TNTs despite several overlapping In present study, we demonstrate role for MARCKS effector domain (ED) PKC activation formation functionality between BTICs NHAs. We employ cell-penetrable peptide derived from (MED2), PKC-targeting drugs, an inducible ED U87 model elucidate TNT regulation

Language: Английский

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Protective Effects of (-)-Butaclamol Against Gentamicin-Induced Ototoxicity: In Vivo and In Vitro Approaches

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(9), P. 4201 - 4201

Published: April 28, 2025

Gentamicin-induced ototoxicity leads to irreversible sensorineural hearing loss due structural and functional damage inner ear hair cells. In this study, we identified (-)-butaclamol as a potent protective agent against gentamicin-induced cytotoxicity through high-content screening (HCS) of natural compound library. (-)-Butaclamol significantly enhanced cell viability in both HEI-OC1 cells zebrafish neuromasts, demonstrating robust protection gentamicin toxicity. Mechanistically, inhibited intrinsic apoptosis, evidenced by reduced TUNEL-positive counts the downregulation BAX caspase-3, alongside upregulation BCL-2. Moreover, activated key survival signaling pathways, including AKT/mTOR ERK, while suppressing inflammatory regulator NF-κB. Additional analyses revealed that effectively mitigated oxidative stress restored autophagic activity, confirmed CellROX LysoTracker assays. Notably, TMRE staining showed preserved mitochondrial membrane potential cells, indicating protection. Collectively, these findings suggest exerts comprehensive cytoprotective effects modulating enhancing signaling, restoring cellular homeostasis. These results highlight therapeutic provide foundation for future studies aimed at its clinical application.

Language: Английский

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KaiXinSan improves learning and memory impairment by regulating cholesterol homeostasis in mice overloaded with 27-OHC

The Journal of Steroid Biochemistry and Molecular Biology, Journal Year: 2024, Volume and Issue: 245, P. 106622 - 106622

Published: Sept. 24, 2024

Language: Английский

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Bibliometric insights into the inflammation and mitochondrial stress in ischemic stroke

Experimental Neurology, Journal Year: 2024, Volume and Issue: 378, P. 114845 - 114845

Published: June 4, 2024

Language: Английский

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HMGB1 derived from lung epithelial cells after cobalt nanoparticle exposure promotes the activation of lung fibroblasts

Nanotoxicology, Journal Year: 2024, Volume and Issue: 18(6), P. 565 - 581

Published: Aug. 17, 2024

We have previously demonstrated that exposure to cobalt nanoparticles (Nano-Co) caused extensive interstitial fibrosis and inflammatory cell infiltration in mouse lungs. However, the underlying mechanisms of Nano-Co-induced pulmonary remain unclear. In this study, we investigated role high-mobility group box 1 (HMGB1) epithelial cell-fibroblast crosstalk fibrosis. Our results showed Nano-Co remarkable production release HMGB1, as well nuclear accumulation HIF-1α human bronchial cells (BEAS-2B) a dose- time-dependent manner. Pretreatment with CAY10585, an inhibitor against HIF-1α, significantly blocked overexpression HMGB1 lysate supernatant BEAS-2B induced by exposure, indicating induces HIF-1α-dependent release. addition, treatment lung fibroblasts (MRC-5) conditioned media from Nano-Co-exposed increased RAGE expression, MAPK signaling activation, enhanced expression fibrosis-associated proteins, such fibronectin, collagen 1, α-SMA. knockdown had no effects on activation MRC-5 fibroblasts. Finally, inhibition ERK1/2, p38, JNK all abolished cells, suggesting might be key downstream signal HMGB1/RAGE promote fibroblast activation. These findings important implications for understanding pro-fibrotic potential Nano-Co.

Language: Английский

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