Autophagy and PPARs/NF-κB-associated inflammation are involved in hepatotoxicity induced by the synthetic phenolic antioxidant 2,4-di-tert-butylphenol in common carp (Cyprinus carpio) DOI Creative Commons
Jiaqi Xie,

Yuxiang Yin,

Bixiao Lin

et al.

Ecotoxicology and Environmental Safety, Journal Year: 2024, Volume and Issue: 284, P. 116937 - 116937

Published: Sept. 2, 2024

The synthetic phenolic antioxidant 2,4-di-tert-butylphenol (2,4-DTBP) is an emergent contaminant and can disrupt the delicate balance of aquatic ecosystems. This study aimed to investigate 2,4-DTBP-induced hepatotoxicity in common carp underlying mechanisms involved. Sixty were divided into four groups exposed 0 mg/L, 0.01 0.1 mg/L or 1 2,4-DTBP for 30 days. Here, we first demonstrated that exposure caused liver damage, manifested as hepatocyte nuclear pyknosis, inflammatory cell infiltration apoptosis. Moreover, induced hepatic reactive oxygen species (ROS) overload disrupted capacity, indicated by reduced activity enzymes superoxide dismutase (SOD), catalase (CAT) glutathione peroxidase (GSH-Px). In addition, transmission electron microscopy revealed autophagosome accumulation carp. Western blot analysis further significantly decreased protein levels mTOR increased LC3II/LC3I ratio. Furthermore, inhibited lysozyme (LZM) alkaline phosphatase (AKP) activity; immunoglobulin M (IgM), complement 3 (C3), 4 (C4) serum; mRNA proinflammatory cytokines (NF-κB, TNF-α, IL-1β IL-6); three types proliferator-activated receptors (PPARs) (α, β/δ γ). Molecular docking directly binds internal active pocket PPARs. Overall, concluded systems could induce regulating autophagy controlling responses. present provides new insights mechanism organisms furthers our understanding effects on public health ecotoxicology.

Language: Английский

Senoinflammation as the underlying mechanism of aging and its modulation by calorie restriction DOI
Sang Gyun Noh, Hyun‐Woo Kim, Seungwoo Kim

et al.

Ageing Research Reviews, Journal Year: 2024, Volume and Issue: unknown, P. 102503 - 102503

Published: Sept. 1, 2024

Language: Английский

Citations

4
Expression Profile of MicroRNAs in Breast Milk of Women With Inflammatory Bowel Disease: Correlation With Disease Activity and Medical Treatments DOI Creative Commons
Regina Golan‐Gerstl, Ami Ben Ya’acov,

Mirit Musseri

et al.

Inflammatory Bowel Diseases, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 17, 2025

Although most inflammatory bowel disease (IBD) medications are considered safe during pregnancy, their impact on microRNAs (miRNAs) in breast milk is largely unknown. MiRNAs milk, carried by milk-derived extracellular vesicles (MDEs), transmitted to the newborn's gut regulate genes. Aberrant miRNA expression profiles have been found IBD within tissue, blood, and feces, but data mother's scarce. We collected samples from 32 mothers with Crohn's (CD), 14 ulcerative colitis (UC), 44 healthy controls. analyzed through qualitative real-time polymerase chain reaction Affymetrix chips. Target genes of differentially expressed miRNAs were predicted using miRATBase. Statistical analyses conducted GraphPad Prism software Mann-Whitney tests. Milk-derived showed altered compared Specifically, miR-21 miR-320 downregulated, while Let-7a was upregulated mothers. The patterns varied between CD UC, significantly lower MiR-21 UC higher CD. Additionally, anti-tumor necrosis factor treatment pregnancy associated reduced miR-148a levels MDEs. Pathway analysis revealed that these involved immune regulation, particularly interleukin signaling pathways. This study highlights IBD, influenced its treatments. These findings emphasize maternal health composition potential implications for infant development. Understanding may guide personalized strategies promote breastfeeding among IBD.

Language: Английский

Citations

0
Immunometabolism of Tregs: mechanisms, adaptability, and therapeutic implications in diseases DOI Creative Commons
Yuming Lu, Yifan Wang, Tao Ruan

et al.

Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 16

Published: Jan. 23, 2025

Immunometabolism is an emerging field that explores the intricate interplay between immune cells and metabolism. Regulatory T (Tregs), which maintain homeostasis in immunometabolism, play crucial regulatory roles. The activation, differentiation, function of Tregs are influenced by various metabolic pathways, such as Mammalian targets rapamycin (mTOR) pathway glycolysis. Correspondingly, activated can reciprocally impact these pathways. also possess robust adaptive capabilities, thus enabling them to adapt microenvironments, including tumor microenvironment (TME). complex mechanisms diseases intriguing, particularly conditions like MASLD, where significantly upregulated contribute fibrosis, while diabetes, systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), they show downregulation reduced anti-inflammatory capacity. These phenomena suggest differentiation environment, imbalances either lead development diseases. Thus, moderate inhibitory capacity critical for maintaining system balance. Given unique immunoregulatory abilities Tregs, targeted therapeutic drugs may position novel immunotherapy. This could restoring balance, resolving dysregulation, fostering innovation progress

Language: Английский

Citations

0
Metabolic reprogram and T cell differentiation in inflammation: current evidence and future perspectives DOI Creative Commons
Yuxin Shi, Hao Zhang, Changhong Miao

et al.

Cell Death Discovery, Journal Year: 2025, Volume and Issue: 11(1)

Published: March 28, 2025

T cell metabolism and differentiation significantly shape the initiation, progression, resolution of inflammatory responses. Upon activation, cells undergo extensive metabolic shifts to meet distinct functional demands across various stages. These alterations are not only critical for defining different subsets, but also sustaining their activity in environments. Key signaling pathways-including mTOR, HIF-1α, AMPK regulate these adaptions, linking cellular energy states with fate decisions. Insights into regulation offer potential therapeutic strategies manipulate function, implications treating autoimmune diseases, chronic inflammation, cancer by targeting specific pathways.

Language: Английский

Citations

0
Regulation of immune metabolism in Th17 and Treg cells DOI Creative Commons

Zhanqing Ji,

Wei Yang, Siyao Li

et al.

Animals and zoonoses., Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 1, 2025

Language: Английский

Citations

0
Study on the Mechanism of Jieduquyuziyin prescription Improving the Condition of MRL/lpr Mice by Regulating T Cell Metabolic Reprogramming through the AMPK/mTOR Pathway DOI
Qingmiao Zhu, Yaxue Han, Xiaolong Li

et al.

Journal of Ethnopharmacology, Journal Year: 2025, Volume and Issue: 345, P. 119584 - 119584

Published: March 3, 2025

Language: Английский

Citations

0
A Comprehensive Review of Small Molecules, Targets, and Pathways in Ulcerative Colitis Treatment DOI

Xiaoxuan Cai,

Yi-Han Huang,

Yang-Chi-Dung Lin

et al.

European Journal of Medicinal Chemistry, Journal Year: 2025, Volume and Issue: 291, P. 117645 - 117645

Published: April 15, 2025

Language: Английский

Citations

0
Autophagy and PPARs/NF-κB-associated inflammation are involved in hepatotoxicity induced by the synthetic phenolic antioxidant 2,4-di-tert-butylphenol in common carp (Cyprinus carpio) DOI Creative Commons
Jiaqi Xie,

Yuxiang Yin,

Bixiao Lin

et al.

Ecotoxicology and Environmental Safety, Journal Year: 2024, Volume and Issue: 284, P. 116937 - 116937

Published: Sept. 2, 2024

The synthetic phenolic antioxidant 2,4-di-tert-butylphenol (2,4-DTBP) is an emergent contaminant and can disrupt the delicate balance of aquatic ecosystems. This study aimed to investigate 2,4-DTBP-induced hepatotoxicity in common carp underlying mechanisms involved. Sixty were divided into four groups exposed 0 mg/L, 0.01 0.1 mg/L or 1 2,4-DTBP for 30 days. Here, we first demonstrated that exposure caused liver damage, manifested as hepatocyte nuclear pyknosis, inflammatory cell infiltration apoptosis. Moreover, induced hepatic reactive oxygen species (ROS) overload disrupted capacity, indicated by reduced activity enzymes superoxide dismutase (SOD), catalase (CAT) glutathione peroxidase (GSH-Px). In addition, transmission electron microscopy revealed autophagosome accumulation carp. Western blot analysis further significantly decreased protein levels mTOR increased LC3II/LC3I ratio. Furthermore, inhibited lysozyme (LZM) alkaline phosphatase (AKP) activity; immunoglobulin M (IgM), complement 3 (C3), 4 (C4) serum; mRNA proinflammatory cytokines (NF-κB, TNF-α, IL-1β IL-6); three types proliferator-activated receptors (PPARs) (α, β/δ γ). Molecular docking directly binds internal active pocket PPARs. Overall, concluded systems could induce regulating autophagy controlling responses. present provides new insights mechanism organisms furthers our understanding effects on public health ecotoxicology.

Language: Английский

Citations

0