Luteolin-mediated phosphoproteomic changes in chicken splenic lymphocytes: unraveling the detoxification mechanisms against ammonia-induced stress DOI
Dechun Chen,

Haojinming Tang,

Jiahao Liu

et al.

Journal of Hazardous Materials, Journal Year: 2024, Volume and Issue: 485, P. 136931 - 136931

Published: Dec. 18, 2024

Language: Английский

Luteolin enhanced antioxidant capability and induced pyroptosis through NF-κB/NLRP3/Caspase-1 in splenic lymphocytes exposure to ammonia DOI
Dechun Chen, F Shen, Jiahao Liu

et al.

The Science of The Total Environment, Journal Year: 2024, Volume and Issue: 919, P. 170699 - 170699

Published: Feb. 5, 2024

Language: Английский

Citations

24

Acute exposure to polystyrene nanoplastics induced oxidative stress in Sepia esculenta Larvae DOI Creative Commons
Xiumei Liu, Zan Li, Qian Li

et al.

Aquaculture Reports, Journal Year: 2024, Volume and Issue: 35, P. 102004 - 102004

Published: Feb. 28, 2024

Nanoplastics (NPs, < 1 μm) have attracted widespread attention due to their potential threats organisms, ecosystem, and public health. However, there is limited research on the effects of NPs cephalopods. Sepia esculenta (Mollusks, Cephalopoda, Sepioidea), an economically major species Sepiidea family in world, well received by consumers for its delicious quality rich nutrition. In present study, S. larvae were treated with polystyrene nanoplastics (PS-NPs) at 50 μg/mL 4 h, then physiological biomarkers (SOD, GSTs MDA) RNA-Seq whole body performed. Research results suggested that PS-NPs exposure had induced oxidative stress larvae. addition, several key genes signaling pathways related obtained based DEGs, GO KEGG enrichment analyses, as PPI construction analysis transcriptome data. This study enriches different organisms provides insights references revealing mechanisms caused molecular level.

Language: Английский

Citations

22

Molecular mechanism of selenium against lead-induced apoptosis in chicken brainstem relating to heat shock protein, selenoproteins, and inflammatory cytokines DOI Creative Commons
Dechun Chen, Weikang Yu, Zhiyu Hao

et al.

Ecotoxicology and Environmental Safety, Journal Year: 2024, Volume and Issue: 272, P. 116028 - 116028

Published: Feb. 3, 2024

Extensive application of lead (Pb) brought about environmental pollution and toxic reactions organisms. Selenium (Se) has the effect antagonizing Pb poisoning in humans animals. However, it is still unclear how causes brainstem toxicity. In present study, we wanted to investigate whether Se can alleviate toxicity chicken brainstems by reducing apoptosis. One hundred eighty chickens were randomly divided into four groups, namely control group, Se/Pb group. Morphological examination, ultrastructural observation, relative mRNA expressions genes on heat shock proteins (HSPs); selenoproteins; inflammatory cytokines; apoptosis-related factors investigated. The results showed that exposure led tissue damage apoptosis brainstems. Furthermore, an atypical expression HSPs (HSP27, HSP40, HSP60, HSP70, HSP90); selenoprotein family glutathione peroxidase (GPx) 1, GPx2, GPx3, GPx4), thioredoxin reductases (Txnrd) (Txnrd1, Txnrd2, Txnrd3), dio famliy (diodothyronine deiodinases (Dio)1, Dio2, Dio3), as well other selenoproteins (selenoprotein (Sel)T, SelK, SelS, SelH, SelM, SelU, SelI, SelO, Selpb, n1 (Sepn1), Sepp1, Sepx1, Sepw1, 15-kDa (Sep15), selenophosphate synthetases 2 (SPS2)); cytokines (Interleukin (IL-2), IL-4, IL-6, IL-12β, IL-17, Interferon-γ (IFN-γ)); (B-cell lymphoma-2 (Bcl-2), tumor protein 53 (p53), Bcl-2 Associated X (Bax), Cytochrome c (Cyt c), Caspase-3) identified. An reaction induced after Pb. alleviated abnormal HSPs, selenoproteins, cytokines, tissues treated with indicated inflammatory, involved Se-resisted poisoning. Overall, had resistance against poisoning, be act antidote for

Language: Английский

Citations

18

Plant Secondary Metabolites as Modulators of Mitochondrial Health: An Overview of Their Anti-Oxidant, Anti-Apoptotic, and Mitophagic Mechanisms DOI Open Access

Julia Anchimowicz,

Piotr Zielonka, Sławomir Jakieła

et al.

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(1), P. 380 - 380

Published: Jan. 4, 2025

Plant secondary metabolites (PSMs) are a diverse group of bioactive compounds, including flavonoids, polyphenols, saponins, and terpenoids, which have been recognised for their critical role in modulating cellular functions. This review provides comprehensive analysis the effects PSMs on mitochondrial health, with particular emphasis therapeutic potential. Emerging evidence shows that these improve function by reducing oxidative stress, promoting biogenesis, regulating key processes such as apoptosis mitophagy. Mitochondrial dysfunction, hallmark many pathologies, neurodegenerative disorders, cardiovascular diseases, metabolic syndrome, has shown to benefit from protective PSMs. Recent studies show can dynamics, stabilise membranes, enhance bioenergetics, offering significant promise prevention treatment mitochondrial-related diseases. The molecular mechanisms underlying effects, modulation signalling pathways direct interactions proteins, discussed. integration into strategies is highlighted promising avenue improving efficacy while minimising side commonly associated synthetic drugs. also highlights need future research elucidate specific roles individual synergistic within complex plant matrices, may further optimise utility. Overall, this work valuable insights health potential natural agents targeting dysfunction.

Language: Английский

Citations

3

Co-Exposure to Ammonia and Lipopolysaccharide-Induced Impaired Energy Metabolism via the miR-1599/HK2 Axis and Triggered Autophagy, ER Stress, and Apoptosis in Chicken Cardiomyocytes DOI Creative Commons

Zhiyu Hao,

Minna Qiu,

Yuhao Liu

et al.

Poultry Science, Journal Year: 2025, Volume and Issue: 104(4), P. 104965 - 104965

Published: March 1, 2025

Ammonia (NH3) and lipopolysaccharide (LPS), common pollutants in poultry farming environments, pose significant health risks by disrupting cellular processes. Although previous studies have demonstrated the individual effect of NH3 or LPS on human animal health, mechanisms underlying their combined impact chicken heart tissue remain poorly understood. In this study, we established a cardiotoxicity model to investigate effects and/or exposure energy metabolism, autophagy, endoplasmic reticulum (ER) stress, apoptosis cardiomyocytes. Our findings indicated that or/and reduced ATPase activity ATP content, led downregulation HK2, PK, PDHX, SDH, upregulation AMPK, resulting impaired metabolism Additionally, found gga-miR-1599/HK2 axis as key regulator involved LPS-induced impairment. The impairment activated AMPK/mTOR pathway, which subsequently triggered evidenced Beclin, LC3-I, LC3-II. Furthermore, decreased mTOR expression induced ER markers such ATF6, GRP78, IRE1, PERK. turn, increased CHOP expression, downregulated Bcl-2 upregulated Bim, elevated levels Bax, caspase-9, caspase-3, ultimately triggering apoptosis. This study provides valuable insights into co-exposure identifies potential molecular targets for mitigating these adverse effects.

Language: Английский

Citations

1

New insights into the spleen injury by mitochondrial dysfunction of chicken under polystyrene microplastics stress DOI Creative Commons

Tiantian Guo,

Xiren Geng,

Yue Zhang

et al.

Poultry Science, Journal Year: 2024, Volume and Issue: 103(6), P. 103674 - 103674

Published: March 16, 2024

Microplastics biological toxicity, environmental persistence and chemicals have been paid widespread attention. exposed to chicken spleen injury of the specific mechanism is unclear. Thus, we randomly assigned chickens 4 groups: C (normal diet), L-MPs (1 mg/L), M-MPs (10 H-MPs (100 assessed damage after 42 d exposure. Morphologically, boundary between red white pulp was blurred, along with expansion pulp. It further speculated that microplastics induced mitochondrial dynamic homeostasis (Drp1 upgraded, Mfn1, Mfn2, OPA1 reduced), provoked apoptotic pathway (Bcl-2/Bax decreased, cytc, caspase3, caspase9 raised), resulting in redox imbalance lipid peroxide accumulation (MDA increased, CAT, GSH, T-AOC plummeted), stimulated ferroptosis (FTH1, GPX4, SLC7A11 decreased). Here explored impact polystyrene on spleen, as well programmed death (apoptosis ferroptosis) involved, regulative role mitochondria this process. This could be significant importance bridging gap laboratory research microplastics-induced chicken.

Language: Английский

Citations

7

Golgi apparatus regulated pyroptosis through the miR-32-5p/Golga7/NLRP3 axis in chicken splenic lymphocytes exposure to ammonia DOI

Jiahao Liu,

Haifeng Liu,

Haojinming Tang

et al.

Environmental Pollution, Journal Year: 2024, Volume and Issue: unknown, P. 124923 - 124923

Published: Sept. 1, 2024

Language: Английский

Citations

4

Pre-clinical evidence for mitochondria as a therapeutic target for luteolin: a mechanistic view DOI
Marcos Roberto de Oliveira

Chemico-Biological Interactions, Journal Year: 2025, Volume and Issue: unknown, P. 111492 - 111492

Published: March 1, 2025

Language: Английский

Citations

0

Inhalation of ammonia promotes apoptosis and induces autophagy in hepatocytes via Bax/BCl-2 and m-TOR/ATG5/LC-3bII axes DOI
Bohan Chen, Xiaoqing Liu, Shouyan Wu

et al.

The Science of The Total Environment, Journal Year: 2023, Volume and Issue: 912, P. 169036 - 169036

Published: Dec. 5, 2023

Language: Английский

Citations

10

Mitochondrial miR-12294-5p-Regulated Copper Exposure-Caused Mitochondrial-Dependent Ferroptosis by Targeted Inhibition of CISD1 in Chicken Hepatocytes DOI

Gaolong Zhong,

Mengran Wang,

Bingxia Sun

et al.

Journal of Agricultural and Food Chemistry, Journal Year: 2024, Volume and Issue: 72(28), P. 15948 - 15958

Published: July 5, 2024

Copper (Cu) is a common trace element additive in animal and human foods, excessive intake of Cu has been shown to cause hepatotoxicity, but the underlying mechanism remains unclear. Our previous research found that exposure dramatically upregulated mitochondrial miR-12294-5p expression confirmed its targeted inhibition CISD1 chicken hepatocytes. Thus, we aimed explore potential role mitomiR-12294-5p/CISD1 axis exposure-resulted hepatotoxicity. Here, observed resulted accumulation pathological injury livers. Moreover, caused mitochondrial-dependent ferroptosis hepatocytes, which were prominent on increased Fe2+ lipid peroxidation, inhibited levels CISD1, GPX4, DHODH, IDH2, also enhanced level PTGS2. Notably, identified mitomiR-2954 effectively mitigated Cu-exposure-resulted peroxidation prevented development ferroptosis. However, increasing mitomiR-12294-5p considerably aggravated influence these indicators. Meanwhile, overexpression alleviated Cu-caused ferroptosis, while silent eliminated therapeutic inhibitor. Overall, our findings indicated played critical function hepatotoxicity chickens by regulating

Language: Английский

Citations

3