The multi-level effect of chlorpyrifos during clownfish metamorphosis DOI Creative Commons
Mathieu Reynaud, Stefano Vianello,

Shu‐Hua Lee

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown

Published: Aug. 4, 2024

Abstract Chemical pollution in coastal waters, particularly from agricultural runoff organophosphates, poses a significant threat to marine ecosystems, including coral reefs. Pollutants such as chlorpyrifos (CPF) are widely used agriculture and have adverse effects on life humans. In this paper, we investigate the impact of CPF metamorphosis reef fish model, clownfish Amphiprion ocellaris , focusing disruption thyroid hormone (TH) signalling pathways. Our findings reveal that by reducing TH levels, exposure impairs formation characteristic white bands larvae, indicative progression. Interestingly, treatment can rescue these effects, establishing direct causal link between effect disruption. The body shape changes occurring during also impacted exposure, less advanced CPF-treated larvae than control conditions. Moreover, transcriptomic analysis elucidates CPF’s all components pathway. Additionally, induces systemic cholesterol vitamin D metabolism, DNA repair, immunity, highlighting its broader TH-independent impacts. often overlooked Developing enhancing models, offers more comprehensive understanding how chemical affects ecosystems. This approach provides new insights into complex mechanisms underlying toxicity metamorphosis, shedding light environmental pollutants organisms. Highlights Chlorpyrifos is an insecticide for past five decades has humans progression During lose their elongated transform miniature ovoid-shaped adults, impacts

Language: Английский

Protective effect of melatonin on imidacloprid-induced pyroptosis and ferroptosis by mediating peptidoglycan in the gut of the common carp (Cyprinus carpio) DOI

Zhiruo Miao,

Peiyu Zhao,

Qiyuan Cao

et al.

Pesticide Biochemistry and Physiology, Journal Year: 2024, Volume and Issue: 202, P. 105935 - 105935

Published: April 28, 2024

Language: Английский

Citations

5
Emerging mechanisms of non-alcoholic steatohepatitis and novel drug therapies DOI
Hao Chen, Yang Zhou, Haiping Hao

et al.

Chinese Journal of Natural Medicines, Journal Year: 2024, Volume and Issue: 22(8), P. 724 - 745

Published: Aug. 1, 2024

Language: Английский

Citations

5
Carnosic Acid Directly Targets STING C‐Terminal Tail to Improve STING‐Mediated Inflammatory Diseases DOI Creative Commons

Wenqing Mu,

Guang Xu, Ling Li

et al.

Advanced Science, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 18, 2025

Abstract cGAS (cyclic GMP‐AMP synthase)‐STING (stimulator of interferon genes) signaling plays a vital role in innate immunity, while its deregulation may lead to wide variety autoinflammatory and autoimmune diseases. It is essential identify specifically effective compounds inhibit the signaling. Herein, it shown that carnosic acid (CA), an active ingredient medicinal plant Rosmarinus officinalis L ., suppressed cGAS‐STING pathway activation subsequent inflammatory responses. Mechanistically, CA directly bound STING C‐terminal tail (CTT), impeded recruitment TANK‐binding kinase 1 (TBK1) onto signalosome, thereby blocking phosphorylation regulatory factor 3 (IRF3) nuclear translocation. Importantly, dramatically attenuated STING‐mediated responses vivo. Consistently, has salient ameliorative effect on disease model mediated by Trex1 deficiency, via inhibition Notably, study further indicates phenolic hydroxyl groups are for CA‐mediated inhibitory activity. Collectively, results thus as one crucial targets mediating CA's anti‐inflammatory activity, reveal CTT be novel promising target drug development.

Language: Английский

Citations

0
Exploring the Neuroprotective Role of Selenium: Implications and Perspectives for Central Nervous System Disorders DOI Creative Commons
Guanning Huang, Ying Liu,

X. W. Zhu

et al.

Exploration, Journal Year: 2025, Volume and Issue: unknown

Published: April 1, 2025

ABSTRACT Selenium (Se) is a crucial element in selenoproteins, key biomolecules for physiological function vivo. As selenium‐rich organ, the central nervous system can express all 25 kinds of which protect neurons by reducing oxidative stress and inflammatory response. However, decreased Se levels are prevalent variety neurological disorders, not conducive to treatment prognosis patients. Thus, biological study has emerged as focal point investigating pivotal role trace elements neuroprotection. This paper presents comprehensive review pathogenic mechanism diseases, protective Se, selenoproteins. Additionally, application neuroprotective agent disorder therapy, including ischemic stroke, Alzheimer's, Parkinson's, other summarized. The present aims offer novel insights methodologies prevention disorders with providing scientific basis development innovative Se‐based neuroprotectants promote their clinical against diseases.

Language: Английский

Citations

0
The multi-level effect of chlorpyrifos during clownfish metamorphosis DOI Creative Commons
Mathieu Reynaud, Stefano Vianello,

Shu‐Hua Lee

et al.

Molecular and Cellular Endocrinology, Journal Year: 2025, Volume and Issue: 603, P. 112535 - 112535

Published: April 6, 2025

Language: Английский

Citations

0
Smaller-Sized Silica Nanoparticles Exacerbated Cardiomyocyte Pyroptosis by Impairing Mitophagy to Activate mtDNA-cGAS-STING Signaling DOI
Dong‐Xu Han, Tong Xu,

Xuan Lyu

et al.

Journal of Agricultural and Food Chemistry, Journal Year: 2025, Volume and Issue: unknown

Published: April 8, 2025

Silica nanoparticles (SiNPs) are a nanometer powder widely used in various consumer products, engineering, the food industry, and medical applications. Environmental SiNPs have attracted attention owing to their exposure cardiovascular adverse events. Here, we exposed C57/BL6 mouse HL-1 cells with different-sized (50, 300 nm, 1 μm) investigate underlying mechanism of its toxicity. Mice three-sized showed significant weight loss after 21 days treatment. Heart tibia length ratio histopathology staining indicated increased heart volume cross-sectional area myocardial fibers mice SiNPs. In vivo vitro experiments results that causes size-dependent mitochondrial damage initiates mitophagy. Notably, compared caused by nm μm exposure, 50 blocked autophagy flux, leading excessive accumulation DNA (mtDNA) cytoplasm, ultimately exacerbating downstream cGAS-STING pathway-mediated pyroptosis. This study revealed potential health risks helped understand differences cytotoxicity different sizes.

Language: Английский

Citations

0
Xiezhuo Tiaozhi formula inhibits macrophage pyroptosis in the non-alcoholic fatty liver disease by targeting the SIRT1 pathway DOI Creative Commons
Lulu Tian,

Jing Chen,

Meiqi Yang

et al.

Phytomedicine, Journal Year: 2024, Volume and Issue: 131, P. 155776 - 155776

Published: May 24, 2024

Non-alcoholic fatty liver disease (NAFLD) is a challenging to interfere with and represents potential long-term risk factor for hepatic fibrosis cancer. The Xiezhuo Tiaozhi (XZTZ) formula, water extract from crude herbs, has been widely used as an anti-NAFLD agent through clinical observation. However, the underlying pharmacological mechanisms of XZTZ formula its impact on pathways against NAFLD have not elucidated. Our study aims investigate effects regulatory treat NAFLD. possible active components were identified using ultra-performance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF/MS) molecular docking. To further explore mechanisms, forty-eight 6-week-old male C57BL/6J mice given individual attention high-fat high-sugar diet (HFHSD) or relevant control (Ctrl) diets 16 weeks successfully construct mouse model. Subsequently, levels serum biochemicals, pathological changes in liver, pyroptosis assessed therapeutic formula. Further, LPS-induced RAW264.7 cells Immortalized Mouse Kupffer (ImKC) verify vitro. We 7 chemical compounds 2 targets plausible points treatment Subsequent histopathological analysis revealed marked steatosis lipid accumulation HFHSD while conditions effectively ameliorated by administration Additionally, our work demonstrated that could attenuate M1 polarization, promote M2 suppress via SIRT1 pathway tissue samples. Moreover, validation performed ImKC showing silencing weaken relative affirmed role was associated macrophage. These findings suggest alleviated mice. ameliorations are involving attenuation promotion anti-pyroptosis pathway.

Language: Английский

Citations

3
Hippo-YAP/TAZ-ROS signaling axis regulates metaflammation induced by SelenoM deficiency in high-fat diet-derived obesity DOI Creative Commons
Jingzeng Cai, Jiaqiang Huang, Di Li

et al.

Journal of Advanced Research, Journal Year: 2024, Volume and Issue: unknown

Published: June 1, 2024

Metabolic inflammation (metaflammation) in obesity is primarily initiated by proinflammatory macrophage infiltration into adipose tissue. SelenoM contributes to the modulation of antioxidative stress and multiple pathological processes; however, its roles metaflammation (M1)-like state tissue have not been determined. We hypothesize that could effectively regulate via Hippo-YAP/TAZ-ROS signaling axis derived from a high-fat diet. Morphological changes were examined hematoxylin-eosin (H&E) staining fluorescence microscopy. The glucose tolerance test (GTT) insulin (ITT) used evaluate impact deficiency on blood levels. RNA-Seq analysis, LC-MS Mass spectrometry analysis western blotting performed detect levels genes proteins related glycolipid metabolism Herein, we evaluated inflammatory features metabolic microenvironment mice with SelenoM-deficient tissues multi-omics analyses. deletion resulted disturbances resistance, thereby accelerating weight gain, adiposity, hyperglycemia. Mice lacking white adipocytes developed severe adipocyte hypertrophy impaired lipolysis. aggravated generation ROS reducing equivalents (NADPH glutathione) adipocytes, promoting cytokine production M1-proinflammatory reaction, which was change nuclear factor kappa-B (NF-κB) macrophages. Mechanistically, promoted Hippo-YAP/TAZ-ROS-mediated transcriptional regulation targeting large tumor suppressor 2 (LATS2). Moreover, supplementation N-acetyl cysteine (NAC) reduce excessive oxidative partially rescued responses M1 activation. Our data indicate ameliorates mainly obesity. identification as key regulator presents opportunities for development novel therapeutic interventions dysfunction

Language: Английский

Citations

3
Selenoprotein W modulates tau homeostasis in an Alzheimer’s disease mouse model DOI Creative Commons
Bingyu Ren,

Jiaxin Situ,

Xuelian Huang

et al.

Communications Biology, Journal Year: 2024, Volume and Issue: 7(1)

Published: July 17, 2024

Abstract Lower selenium levels are observed in Alzheimer’s disease (AD) brains, while supplementation shows multiple benefits. Selenoprotein W (SELENOW) is sensitive to changes and binds tau, reducing tau accumulation. However, whether restoration of SELENOW has any protective effect AD models its underlying mechanism remain unknown. Here, we confirm the association between downregulation pathology, revealing SELENOW’s role promoting degradation through ubiquitin‒proteasome system. competes with Hsp70 interact ubiquitination inhibiting acetylation at K281. deficiency leads synaptic defects, dysregulation impaired long-term potentiation, resulting memory deficits mice. Conversely, overexpression triple transgenic mice ameliorates impairment tau-related pathologies, featuring decreased 4-repeat isoform, phosphorylation Ser396 Ser404, neurofibrillary tangles neuroinflammation. Thus, contributes regulation homeostasis maintenance, implicating potential AD.

Language: Английский

Citations

3
Lutein protects senescent ciliary muscle against oxidative stress through the Keap1/Nrf2/ARE pathway DOI
Ning Gao, Xiang Gao,

Miaomiao Du

et al.

Phytomedicine, Journal Year: 2024, Volume and Issue: 134, P. 155982 - 155982

Published: Aug. 30, 2024

Language: Английский

Citations

3