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Artikel: Ferulic acid attenuates difenoconazole exposure induced liver injury in carp by modulating oxidative damage, inflammation and apoptosis.

Sun, Ying / Jin, Xiaohui / Yang, Zuwang / Hu, Zunhan / Li, Qiulu / Dong, Jingquan / Fu, Mian

Comparative biochemistry and physiology. Toxicology & pharmacology : CBP

2024 Band 280, Seite(n) 109885

Abstract: Difenoconazole (DFZ) is a widely used triazole fungicide in agricultural production. However, the presence of DFZ residue in the environment poses a significant risk to non-target organisms. Ferulic acid (FA) is a phenolic compound known for its ... ...

Abstract	Difenoconazole (DFZ) is a widely used triazole fungicide in agricultural production. However, the presence of DFZ residue in the environment poses a significant risk to non-target organisms. Ferulic acid (FA) is a phenolic compound known for its antioxidant and anti-inflammatory properties. This study aims to investigate the hepatic damage caused by DFZ in carp and explore the mechanism through which FA alleviates this damage. The findings revealed that FA enhanced the antioxidant capability of the carp's liver and reduced the accumulation of reactive oxygen species (ROS) in the liver tissue. Moreover, FA regulated the transcriptional levels of inflammation-related factors, effectively preventing the inflammatory response triggered by the NF-κB signaling pathway. Additionally, TUNEL results demonstrated that DFZ initiated apoptosis, while dietary supplementation with FA decreased the protein expression levels of Bax and Cytochrome C (Cyt c) and the transcriptional levels of bax, caspase3, caspase9, p53 genes. Furthermore, FA increased the protein expression and transcriptional levels of Bcl-2. In conclusion, FA protects against liver injury induced by DFZ exposure in carp by modulating oxidative damage, inflammation, and apoptosis.
Mesh-Begriff(e)	Animals ; Antioxidants/pharmacology ; Carps ; bcl-2-Associated X Protein ; Chemical and Drug Induced Liver Injury, Chronic ; Oxidative Stress ; Inflammation/chemically induced ; Triazoles/toxicity ; Apoptosis ; Coumaric Acids ; Dioxolanes
Chemische Substanzen	Antioxidants ; ferulic acid (AVM951ZWST) ; difenoconazole (D9612XCH4P) ; bcl-2-Associated X Protein ; Triazoles ; Coumaric Acids ; Dioxolanes
Sprache	Englisch
Erscheinungsdatum	2024-03-03
Erscheinungsland	United States
Dokumenttyp	Journal Article
ZDB-ID	189285-x
ISSN	1532-0456 ; 0306-4492 ; 0742-8413
ISSN	1532-0456 ; 0306-4492 ; 0742-8413
DOI	10.1016/j.cbpc.2024.109885
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Abamectin causes cardiac dysfunction in carp via inhibiting redox equilibrium and resulting in immune inflammatory response and programmed cell death

Zhao, Panpan / Wang, Yan / Yang, Qiankun / Yu, Guili / Ma, Fenfen / Dong, Jingquan

Environ Sci Pollut Res. 2023 Mar., v. 30, no. 11 p.29494-29509

2023

Abstract: This study aims to investigate the effects of environmentally relevant concentrations of abamectin on the cardiac function of carp and the potential mechanisms. Here, male carp were exposed to abamectin, and cardiac function-related enzymatic markers ... ...

Abstract	This study aims to investigate the effects of environmentally relevant concentrations of abamectin on the cardiac function of carp and the potential mechanisms. Here, male carp were exposed to abamectin, and cardiac function-related enzymatic markers were examined. Cardiac histopathology, redox equilibrium, inflammation, and cell death were evaluated. Abamectin exposure caused cardiac dysfunction by upregulating lactate dehydrogenase (LDH), aspartate aminotransferase (AST), creatine kinase (CK), creatine Kinase MB isoenzyme (CK-MB) and white blood cells (WBCs), and decreasing red blood cells (RBCs) and hemoglobin (Hb). DHE staining and biochemical assays revealed that abamectin caused ROS release and oxidative stress by inhibiting Nrf2-ARE pathway. Histopathological and real-time fluorescence quantitative PCR (RT-qPCR) assays revealed that abamectin caused myocardial fiber swelling and inflammatory cell infiltration, enhanced pro-inflammatory cytokines tumor necrosis factor-α (Tnf-α), interleukin-1 beta (Il-1β), and Il-6 levels and attenuated anti-inflammatory cytokines Il-10 and transforming growth factor beta 1 (Tgf-β1) through activating NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome and nuclear factor kappa-B (NF-κB) pathway. Tunel staining showed that abamectin triggered cardiac apoptosis via activating p53-mediated mitochondrial apoptosis with elevated bcl2-associated X (Bax), reduced B-cell lymphoma-2 (Bcl-2), and activated Caspase-9 and Caspase-3. Immunoblot analysis revealed that abamectin activated autophagic flow by inhibiting mammalian target of rapamycin (mTOR), resulting in the conversion of LC3B from LC3-I to LC3-II, elevation of autophagy protein 5 (Atg5), and reduction of p62. Overall, abamectin caused cardiac dysfunction in carp via inhibiting redox equilibrium and resulting in immune inflammatory response and programmed cell death.
Schlagwörter	B-lymphocytes ; abamectin ; apoptosis ; aspartate transaminase ; autophagy ; cardiac output ; carp ; caspase-3 ; caspase-9 ; creatine kinase ; fluorescence ; hemoglobin ; histopathology ; inflammasomes ; inflammation ; interleukin-10 ; interleukin-1beta ; interleukin-6 ; isozymes ; lactate dehydrogenase ; males ; mammals ; mitochondria ; necrosis ; neoplasms ; oxidative stress ; quantitative polymerase chain reaction ; rapamycin
Sprache	Englisch
Erscheinungsverlauf	2023-03
Umfang	p. 29494-29509.
Erscheinungsort	Springer Berlin Heidelberg
Dokumenttyp	Artikel ; Online
ZDB-ID	1178791-0
ISSN	1614-7499 ; 0944-1344
ISSN (online)	1614-7499
ISSN	0944-1344
DOI	10.1007/s11356-022-24004-6
Datenquelle	NAL Katalog (AGRICOLA)

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Artikel ; Online: Malvidin alleviates LPS-induced septic intestinal injury through the nuclear factor erythroid 2-related factor 2/reactive oxygen species/NLRP3 inflammasome pathway.

Wang, Guanglu / Ma, Fenfen / Zhang, Wei / Xin, Yue / Ping, Kaixin / Wang, Yan / Dong, Jingquan

Inflammopharmacology

2023 Band 32, Heft 1, Seite(n) 893–901

Abstract: Emerging evidence suggests that the gastrointestinal tract plays a crucial role in the pathophysiology of sepsis, a leading cause of mortality among patients admitted to the intensive care unit (ICU). Malvidin, belonging to the flavonoid family of ... ...

Abstract	Emerging evidence suggests that the gastrointestinal tract plays a crucial role in the pathophysiology of sepsis, a leading cause of mortality among patients admitted to the intensive care unit (ICU). Malvidin, belonging to the flavonoid family of compounds, exhibits a range of capabilities including anti-inflammatory and antioxidant properties. Studies have demonstrated that Malvidin exhibits a dose-dependent effect in mitigating sepsis-induced intestinal injury. The advantageous impact of Malvidin in safeguarding against sepsis-induced intestinal injury is associated with its capacity to counteract oxidative stress, inhibit cellular apoptosis, diminish the secretion of pro-inflammatory cytokines, and regulate the synthesis of inflammasomes. The findings indicate that Malvidin, a natural compound, exhibits protective effects on the gut by activating the nuclear factor erythroid 2-related factor 2/reactive oxygen species/NLRP3 inflammasome pathway. These results have significant implications for potential clinical applications and offer valuable insights into the treatment of sepsis-induced intestinal injury.
Mesh-Begriff(e)	Humans ; Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; Reactive Oxygen Species ; Lipopolysaccharides ; Sepsis/drug therapy ; Anthocyanins
Chemische Substanzen	Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; malvidin (10463-84-0) ; Reactive Oxygen Species ; Lipopolysaccharides ; Anthocyanins
Sprache	Englisch
Erscheinungsdatum	2023-12-15
Erscheinungsland	Switzerland
Dokumenttyp	Journal Article
ZDB-ID	1080058-x
ISSN	1568-5608 ; 0925-4692
ISSN (online)	1568-5608
ISSN	0925-4692
DOI	10.1007/s10787-023-01378-8
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Abamectin causes toxicity to the carp respiratory system by triggering oxidative stress, inflammation, and apoptosis and inhibiting autophagy.

Feng, Huimiao / Zhou, Ping / Liu, Feixue / Zhang, Wei / Yang, Haitao / Li, Xueqing / Dong, Jingquan

Environmental science and pollution research international

2023 Band 30, Heft 19, Seite(n) 55200–55213

Abstract: Abamectin is a commonly used pesticide in agriculture and fisheries and poses a risk to aquatic species. However, the mechanism of its toxic effects on fish remains to be discovered. In this study, we explored the effects of abamectin exposure at ... ...

Abstract	Abamectin is a commonly used pesticide in agriculture and fisheries and poses a risk to aquatic species. However, the mechanism of its toxic effects on fish remains to be discovered. In this study, we explored the effects of abamectin exposure at different concentrations on the respiratory system of carp. Carp were divided into three groups, namely the control group, low-dose abamectin treatment group, and high-dose abamectin treatment group. Gill tissue was collected after abamectin exposure for histopathological, biochemical, tunnel, mRNA, and protein expression analysis. Histopathological analysis indicated that abamectin damaged the gill structure. Biochemical analysis showed that abamectin triggered oxidative stress with lowered antioxidant enzyme activities and increased MDA content. Moreover, abamectin led to enhanced INOS levels and pro-inflammatory transcription, activating inflammation. Tunnel results demonstrated that exposure to abamectin induced gill cell apoptosis through an exogenous pathway. In addition, exposure to abamectin activated the PI3K/AKT/mTOR pathway, leading to inhibition of autophagy. Overall, abamectin caused respiratory system toxicity in carp via triggering oxidative stress, inflammation, and apoptosis and inhibiting autophagy. The study suggests that abamectin has a profound toxicity mechanism in the respiratory system of carp, contributing to a better understanding of pesticide risk assessment in aquatic systems.
Mesh-Begriff(e)	Animals ; Carps/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Oxidative Stress ; Antioxidants/metabolism ; Apoptosis ; Inflammation/chemically induced ; Respiratory System/metabolism ; Pesticides/pharmacology ; Autophagy
Chemische Substanzen	abamectin (5U8924T11H) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Antioxidants ; Pesticides
Sprache	Englisch
Erscheinungsdatum	2023-03-08
Erscheinungsland	Germany
Dokumenttyp	Journal Article
ZDB-ID	1178791-0
ISSN	1614-7499 ; 0944-1344
ISSN (online)	1614-7499
ISSN	0944-1344
DOI	10.1007/s11356-023-26166-3
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Pesticide avermectin-induced hepatotoxicity and growth inhibition in carp: Ameliorative capacity and potential mechanisms of quercetin as a dietary additive.

Xin, Yue / Li, Xueqing / Ping, Kaixin / Xiang, Yannan / Li, Mengxin / Li, Xing / Yang, Haitao / Dong, Jingquan

Aquatic toxicology (Amsterdam, Netherlands)

2024 Band 268, Seite(n) 106859

Abstract: Flavonoid quercetin (QUE) has biological activities of anti-oxidation, anti-inflammation and anti-apoptosis, however, its protective effects against avermectin (AVM) induced liver toxicity in carp remains unclear. The objective of this research is to ... ...

Abstract	Flavonoid quercetin (QUE) has biological activities of anti-oxidation, anti-inflammation and anti-apoptosis, however, its protective effects against avermectin (AVM) induced liver toxicity in carp remains unclear. The objective of this research is to explore the biologically potent effects of QUE in AVM-induced hepatotoxicity in carp and its underlying mechanism. Therefore, we established a liver injury model in carp induced by AVM to evaluate QUE against AVM induced liver toxicity in carp. In this investigation, AVM dosage was determined as 2.404 μg/L for both groups, and an experimentation of 30 days duration was carried out. Various methods including hematoxylin and eosin (H&E) staining, biochemical kits, real-time quantitative PCR (qRT-PCR), western blotting, TUNEL, reactive oxygen species (ROS) staining, immunofluorescence (Hoseinifar, et al.,), and oil red O staining were used in this study. Results showed that the growth inhibition of carp was relieved in the QUE treatment group comparing to the AVM group. In the QUE treatment group, there was a significant decrease in the levels of ALT and AST in carp liver tissue. Additionally, the histopathological damage and lipid accumulation were alleviated compared to the AVM group. Moreover, QUE prevented AVM induced decrease in the activities of antioxidant enzymes of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), glutathione (GSH), catalase (CAT) and the accumulation of reactive oxygen species (ROS), but reduced accumulation of malondialdehyde (MDA). In addition, the mRNA levels of liver pro-inflammatory factors of tumor necrosis factor-α (TNF-α), interleukin-1β (iL-1β), interleukin-6 (iL-6), interleukin-10 (iL-10) and the protein levels of NOD-like receptor protein 3 (NLRP3) inflammasome were significantly down-regulated in the QUE treatment group in comparison to the AVM group. We also found that QUE could affect the expression of Bcl2-associated x (Bax), B-cell lymphoma-2 (Bcl-2), cleaved-cysteinyl aspartate specific proteinase (CCaspase3) key apoptotic proteins and TUNEL-labeled apoptotic hepatocytes by regulating SIRT1/FOXO3a signal pathway. In summary, QUE alleviated the growth inhibition, liver oxidative damage, lipid accumulation, inflammatory response, and apoptosis of carp induced by AVM. QUE is a potential protective agent against liver injury induced by AVM in carp.
Mesh-Begriff(e)	Animals ; Quercetin/pharmacology ; Reactive Oxygen Species/metabolism ; Carps/metabolism ; Water Pollutants, Chemical/toxicity ; Antioxidants/pharmacology ; Antioxidants/metabolism ; Oxidative Stress ; Glutathione/metabolism ; Apoptosis ; Chemical and Drug Induced Liver Injury/prevention & control ; Lipids ; Ivermectin/analogs & derivatives
Chemische Substanzen	Quercetin (9IKM0I5T1E) ; Reactive Oxygen Species ; avermectin (73989-17-0) ; Water Pollutants, Chemical ; Antioxidants ; Glutathione (GAN16C9B8O) ; Lipids ; Ivermectin (70288-86-7)
Sprache	Englisch
Erscheinungsdatum	2024-02-05
Erscheinungsland	Netherlands
Dokumenttyp	Journal Article
ZDB-ID	782699-0
ISSN	1879-1514 ; 0166-445X
ISSN (online)	1879-1514
ISSN	0166-445X
DOI	10.1016/j.aquatox.2024.106859
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Gypenoside XLIX Activates the Sirt1/Nrf2 Signaling Pathway to Inhibit NLRP3 Inflammasome Activation to Alleviate Septic Acute Lung Injury.

Ping, Kaixin / Yang, Rongrong / Chen, Huizhen / Xie, Shaocheng / Xiang, Yannan / Li, Mengxin / Lu, Yingzhi / Dong, Jingquan

Inflammation

2024

Abstract: Currently, treatment options for acute lung injury (ALI) are limited. Gypenoside XLIX (Gyp-XLIX) is known for its anti-inflammatory properties, but there is a lack of extensive research on its effects against ALI. This study induced ALI in mice through ... ...

Abstract	Currently, treatment options for acute lung injury (ALI) are limited. Gypenoside XLIX (Gyp-XLIX) is known for its anti-inflammatory properties, but there is a lack of extensive research on its effects against ALI. This study induced ALI in mice through cecal ligation and puncture surgery and investigated the biological activity and potential mechanisms of Gypenoside XLIX (40 mg/kg) by intraperitoneal injection. The in vitro ALI model was established using mouse lung epithelial (MLE-12) cells stimulated with lipopolysaccharide (LPS) and adenosine triphosphate (ATP). Various methods, including Hematoxylin and Eosin (H&E) staining, biochemical assay kits, Quantitative Polymerase Chain Reaction (qPCR) analysis, Western blotting, Terminal deoxynucleotidyl transferase dUTP Nick End Labeling (TUNEL) assay, immunofluorescence, and flow cytometry, were employed for this research. The results indicated that pretreatment with Gypenoside XLIX significantly alleviated pathological damage in mouse lung tissues and reduced the expression levels of inflammatory factors. Additionally, Gypenoside XLIX inhibited ROS levels and NLRP3 inflammasome, possibly mediated by the Sirt1/Nrf2 signaling pathway. Moreover, Gypenoside XLIX significantly inhibited sepsis-induced lung cell apoptosis and excessive autophagy of mitochondria. Specifically, it suppressed mitochondrial pathway apoptosis and the Pink1/Parkin pathway of mitochondrial autophagy. These findings reveal the multifaceted effects of Gypenoside XLIX in anti-inflammatory, antioxidative, and inhibition of cell apoptosis and autophagy. This provides strong support for its therapeutic potential in sepsis-related lung injuries.
Sprache	Englisch
Erscheinungsdatum	2024-05-08
Erscheinungsland	United States
Dokumenttyp	Journal Article
ZDB-ID	434408-x
ISSN	1573-2576 ; 0360-3997
ISSN (online)	1573-2576
ISSN	0360-3997
DOI	10.1007/s10753-024-02041-2
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Immunoprotective effect of silybin through blocking p53-driven caspase-9-Apaf-1-Cyt c complex formation and immune dysfunction after difenoconazole exposure in carp spleen.

Pan, Enzhuang / Xin, Yue / Li, Xueqing / Ping, Kaixin / Li, Xing / Sun, Ying / Xu, Xuhui / Dong, Jingquan

Environmental science and pollution research international

2024 Band 31, Heft 13, Seite(n) 19396–19408

Abstract: As a broad-spectrum and efficient triazole fungicide, difenoconazole is widely used, which not only pollutes the environment but also exerts toxic effects on non-target organisms. The spleen plays an important role in immune protection as an important ... ...

Abstract	As a broad-spectrum and efficient triazole fungicide, difenoconazole is widely used, which not only pollutes the environment but also exerts toxic effects on non-target organisms. The spleen plays an important role in immune protection as an important secondary lymphoid organ in carp. In this study, we assessed the protective impact of silybin as a dietary additive on spleen tissues of carp during exposure to difenoconazole. Sixty carp were separated into four groups for this investigation including control group, difenoconazole group, silybin group, and silybin and difenoconazole group. By hematoxylin-eosin staining, dihydroethidium staining, immunohistochemical staining, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay, quantitative real-time PCR assay, Western blot analysis, biochemical assays, and immune function indicator assays, we found that silybin could prevent difenoconazole-induced spleen tissue damage, oxidative stress, and immune dysfunction, and inhibited apoptosis of carp spleen tissue cells by suppressing the formation of p53-driven caspase-9-apoptotic protease activating factor-1-cytochrome C complex. The results suggested that silybin as a dietary additive could improve spleen tissue damage and immune dysfunction induced by difenoconazole in aquaculture carp.
Mesh-Begriff(e)	Animals ; Spleen/metabolism ; Caspase 9/pharmacology ; Tumor Suppressor Protein p53 ; Silybin/pharmacology ; Carps/metabolism ; Cytochromes c/metabolism ; Apoptosis ; Triazoles/pharmacology ; Dioxolanes
Chemische Substanzen	Caspase 9 (EC 3.4.22.-) ; Tumor Suppressor Protein p53 ; difenoconazole (D9612XCH4P) ; Silybin (4RKY41TBTF) ; Cytochromes c (9007-43-6) ; Triazoles ; Dioxolanes
Sprache	Englisch
Erscheinungsdatum	2024-02-15
Erscheinungsland	Germany
Dokumenttyp	Journal Article
ZDB-ID	1178791-0
ISSN	1614-7499 ; 0944-1344
ISSN (online)	1614-7499
ISSN	0944-1344
DOI	10.1007/s11356-024-32392-0
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Gypenoside XLIX alleviates intestinal injury by inhibiting sepsis-induced inflammation, oxidative stress, apoptosis, and autophagy.

Ping, Kaixin / Yang, Rongrong / Chen, Huizhen / Xie, Shaocheng / Li, Mengxin / Xiang, Yannan / Lu, Yingzhi / Dong, Jingquan

Chemico-biological interactions

2024 Band 397, Seite(n) 111077

Abstract: Intestinal barrier dysfunction is a significant complication induced by sepsis, yet therapeutic strategies targeting such dysfunction remain inadequate. This study investigates the protective effects of Gypenoside XLIX (Gyp XLIX) against intestinal ... ...

Abstract	Intestinal barrier dysfunction is a significant complication induced by sepsis, yet therapeutic strategies targeting such dysfunction remain inadequate. This study investigates the protective effects of Gypenoside XLIX (Gyp XLIX) against intestinal damage induced by sepsis. Septic intestinal injury in mice was induced by cecum ligation and puncture (CLP) surgery. The biological activity and potential mechanisms of Gyp XLIX were explored through intraperitoneal injection of Gyp XLIX (40 mg/kg). The study demonstrates that Gyp XLIX improves the pathological structural damage of the intestine and increases tight junction protein expression as well as the number of cup cells. Through activation of the nuclear factor erythroid 2-related factor 2 - Kelch-like ECH-associated protein 1 (Nrf2-Keap1) pathway, Gyp XLIX enhances antioxidant enzyme levels while reducing the excessive accumulation of reactive oxygen species (ROS). In addition, Gyp XLIX effectively alleviates sepsis-induced intestinal inflammation by inhibiting the nuclear factor kappa B (NF-κB) pathway and activation of the NLRP3 inflammasome. Moreover, Gyp XLIX inhibits cell death through modifying phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway, further enhancing its ability to shield the intestinal barrier. The combined action of these molecular mechanisms promotes the restoration of immune balance and reduces excessive autophagy activity induced under septic conditions. In summary, Gyp XLIX exhibits a significant preventive action against intestinal damage brought on by sepsis, with its mechanisms involving the improvement of intestinal barrier function, antioxidative stress, inhibition of inflammatory response, and cell apoptosis. This research offers a potential strategy for addressing intestinal barrier impairment brought on by sepsis.
Sprache	Englisch
Erscheinungsdatum	2024-05-28
Erscheinungsland	Ireland
Dokumenttyp	Journal Article
ZDB-ID	218799-1
ISSN	1872-7786 ; 0009-2797
ISSN (online)	1872-7786
ISSN	0009-2797
DOI	10.1016/j.cbi.2024.111077
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Protective effect of feed additive Ferulic Acid on respiratory depression and oxidation imbalance of carp induced by pesticide Difenoconazole via ROS/NF-κB/NLRP3 axis.

Xiang, Yannan / Li, Mengxin / Pan, Enzhuang / Li, Ying / Yan, Weiping / Li, Yuanyuan / Ji, Guangquan / Dong, Jingquan

Fish & shellfish immunology

2024 , Seite(n) 109659

Abstract: Difenoconazole (DFZ), classified as a "low-toxicity pesticide," has seen widespread application in recent years. Nevertheless, the non-target toxicity of the substance, particularly towards aquatic creatures, has generated considerable apprehension. The ... ...

Abstract	Difenoconazole (DFZ), classified as a "low-toxicity pesticide," has seen widespread application in recent years. Nevertheless, the non-target toxicity of the substance, particularly towards aquatic creatures, has generated considerable apprehension. The anti-inflammatory and antioxidant effects of Ferulic Acid (FA) have attracted considerable study in this particular setting. This study established a chronic exposure model to DFZ and investigated the protective effects of FA on chronic respiratory inhibition leading to gill damage in freshwater carp. Histological analyses via HE staining indicated that FA effectively alleviated gill tissue damage induced by chronic DFZ exposure. The qRT-PCR results showed that the addition of FA reduced the expression of IL-1β, IL-6 and TNF-α while boosting the expression of IL-10 and TGF-β1. Biochemical analyses and DHE staining revealed that FA reduced MDA levels and increased CAT and GSH activities, along with T-AOC, decreased ROS accumulation in response to chronic DFZ exposure. The results obtained from Western blotting analysis demonstrated that the addition of FA effectively suppressed the activation of the NF-κB signalling pathway and the NLRP3 inflammasome pathway in the gills subjected to prolonged exposure to DFZ. In summary, FA ameliorated gill tissue inflammation and blocked ROS accumulation in carp exposed to chronic DFZ, mitigating tissue inflammation and restoring redox homeostasis through the NF-κB-NLRP3 signaling pathway. Hence, the application of FA has been found to be efficacious for improving respiratory inhibition and mitigating gill tissue inflammation and oxidative stress resulting from DFZ pollution in aquatic habitats.
Sprache	Englisch
Erscheinungsdatum	2024-05-24
Erscheinungsland	England
Dokumenttyp	Journal Article
ZDB-ID	1067738-0
ISSN	1095-9947 ; 1050-4648
ISSN (online)	1095-9947
ISSN	1050-4648
DOI	10.1016/j.fsi.2024.109659
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Protective effects of dietary additive Quercetin: nephrotoxicity and ferroptosis induced by Avermectin pesticide.

Xiang, Yannan / Wang, Qiao / Li, Mengxin / Li, Ying / Yan, Weiping / Li, Yuanyuan / Liu, Yi / Dong, Jingquan

Toxicon : official journal of the International Society on Toxinology

2024 , Seite(n) 107789

Abstract: In recent years, contamination of aquatic systems with Avermectin (AVM) has emerged as a significant concern. This contamination poses substantial challenges to freshwater aquaculture. Plant-derived Quercetin (QUE), known for its anti-inflammatory, ... ...

Abstract	In recent years, contamination of aquatic systems with Avermectin (AVM) has emerged as a significant concern. This contamination poses substantial challenges to freshwater aquaculture. Plant-derived Quercetin (QUE), known for its anti-inflammatory, antioxidant, and ferroptosis-inhibiting properties, is commonly employed as a supplement in animal feed. However, its protective role against chronic renal injury in freshwater carp induced by AVM remains unclear. This study assesses the influence of dietary supplementation with QUE on the consequences of chronic AVM exposure on carp renal function. The carp were subjected to a 30-day exposure to AVM and were provided with a diet containing 400 mg/kg of QUE. Pathological observations indicated that QUE alleviated renal tissue structural damage caused by AVM. RT-QPCR study revealed that QUE effectively reduced the increased expression levels of pro-inflammatory factors mRNA produced by AVM exposure, by concurrently raising the mRNA expression level of the anti-inflammatory factor. Quantitative analysis using DHE tests and biochemical analysis demonstrated that QUE effectively reduced the buildup of ROS in the renal tissues of carp, activity of antioxidant enzymes CAT, SOD, and GSH-px, which were inhibited by AVM, and increased the content of GSH, which was induced by prolonged exposure to AVM. QUE also reduced the levels of MDA, a marker of oxidative damage. Furthermore, assays for ferroptosis markers indicated that QUE increased the mRNA expression levels of gpx4 and slc7a11, which were reduced due to AVM induction, and it caused a reduction in the mRNA expression levels of ftl, ncoa4, and cox2, along with a drop in the Fe
Sprache	Englisch
Erscheinungsdatum	2024-06-04
Erscheinungsland	England
Dokumenttyp	Journal Article
ZDB-ID	204479-1
ISSN	1879-3150 ; 0041-0101
ISSN (online)	1879-3150
ISSN	0041-0101
DOI	10.1016/j.toxicon.2024.107789
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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