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Article ; Online: Polyethylene microplastics induced inflammation via the miR-21/IRAK4/NF-κB axis resulting to endoplasmic reticulum stress and apoptosis in muscle of carp.

Liu, Tian-Jing / Yang, Jie / Wu, Jia-Wei / Sun, Xiao-Ran / Gao, Xue-Jiao

2024 Volume 145, Page(s) 109375

Abstract: As a widespread environmental pollutant, microplastics pose a great threat to the tissues and organs of aquatic animals. The carp's muscles are necessary for movement and survival. However, the mechanism of injury of polyethylene microplastics (PE-MPs) ... ...

Abstract	As a widespread environmental pollutant, microplastics pose a great threat to the tissues and organs of aquatic animals. The carp's muscles are necessary for movement and survival. However, the mechanism of injury of polyethylene microplastics (PE-MPs) to carp muscle remains unclear. Therefore, in this study, PE-MPs with the diameter of 8 μm and the concentration of 1000 ng/L were used to feed carp for 21 days, and polyethylene microplastic treatment groups was established. The results showed that PE-MPs could cause structural abnormalities and disarrangement of muscle fibers, and aggravate oxidative stress in muscles. Exposure to PE-MPs reduced microRNA (miR-21) in muscle tissue, negatively regulated Interleukin-1 Receptor Associated Kinase 4 (IRAK4), activated Nuclear Factor Kappa-B (NF-κB) pathway, induced inflammation, and led to endoplasmic reticulum stress and apoptosis. The present study provides different targets for the prevention of muscle injury induced by polyethylene microplastics.
MeSH term(s)	Animals ; Polyethylene ; Microplastics ; Plastics ; Interleukin-1 Receptor-Associated Kinases ; NF-kappa B ; Carps ; Muscles ; Apoptosis ; Endoplasmic Reticulum Stress ; Inflammation ; MicroRNAs ; Oxidative Stress ; Water Pollutants, Chemical
Chemical Substances	Polyethylene (9002-88-4) ; Microplastics ; Plastics ; Interleukin-1 Receptor-Associated Kinases (EC 2.7.11.1) ; NF-kappa B ; MicroRNAs ; Water Pollutants, Chemical
Language	English
Publishing date	2024-01-11
Publishing country	England
Document type	Journal Article
ZDB-ID	1067738-0
ISSN	1095-9947 ; 1050-4648
ISSN (online)	1095-9947
ISSN	1050-4648
DOI	10.1016/j.fsi.2024.109375
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Article ; Online: The mechanism of selenium regulating the permeability of vascular endothelial cells through selenoprotein O.

Wu, Jiawei / Zhang, Yanhe / Liu, Tianjing / Yang, Jie / Sun, Xiaoran / Gao, Xue-Jiao

Redox biology

2024 Volume 70, Page(s) 103063

Abstract: Vascular diseases, a leading cause of death in human, are strongly associated with pathological damage to blood vessels. The selenoprotein (Sel) have been reported to play important roles in vascular disease. However, the role of SelO in vascular disease ...

Abstract	Vascular diseases, a leading cause of death in human, are strongly associated with pathological damage to blood vessels. The selenoprotein (Sel) have been reported to play important roles in vascular disease. However, the role of SelO in vascular disease has not been conclusively investigated. The present experiment was to investigate the regulatory mechanism of the effect of SelO on the permeability of vascular endothelial. The H.E staining, FITC-Dextran staining, Dil-AC-LDL staining and FITC-WGA staining showed that vascular structure was damaged, and intercellular junctions were disrupted with selenium (Se)-deficient. Immunohistochemistry, qPCR and Western blot revealed decreased expression of the adhesion plaque proteins vinculin, talin and paxillin, decreased expression of the vascular connectivity effector molecules connexin, claudin-1 and E-cadherin and increased expression of JAM-A and N-cadherin, as well as decreased expression of the ZO-1 signaling pathways ZO-1, Rock, rhoGEF, cingulin and MLC-2. In a screening of 24 Sel present in mice, SelO showed the most pronounced changes in vascular tissues, and a possible association between SelO and vascular intercellular junction effectors was determined using IBM SPSS Statistics 25. Silencing of SelO, vascular endothelial intercellular junction adverse effects present. The regulatory relationship between SelO and vascular endothelial intercellular junctions was determined. The results showed that Se deficiency lead to increased vascular endothelial permeability and vascular tissue damage by decreasing SelO expression, suggesting a possible role for SelO in regulating vascular endothelial permeability.
MeSH term(s)	Humans ; Animals ; Mice ; Endothelial Cells/metabolism ; Selenium/metabolism ; Vascular Diseases/pathology ; Permeability ; Selenoproteins/genetics ; Selenoproteins/metabolism
Chemical Substances	Selenium (H6241UJ22B) ; Selenoproteins
Language	English
Publishing date	2024-02-01
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2024.103063
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Article ; Online: Lithium intoxication induced pyroptosis via ROS/NF-κB/NLRP3 inflammasome regulatory networks in kidney of mice.

Jing, Hongyuan / Wang, Fuhan / Gao, Xue-Jiao

Environmental toxicology

2022 Volume 37, Issue 4, Page(s) 825–835

Abstract: Humans and animals may be exposed to increasing contaminant lithium (Li) concentrations in the environment with the use and disposal of Li-containing products. Meanwhile, Li plays a key role in the treatment of human mental disorders, while the excessive ...

Abstract	Humans and animals may be exposed to increasing contaminant lithium (Li) concentrations in the environment with the use and disposal of Li-containing products. Meanwhile, Li plays a key role in the treatment of human mental disorders, while the excessive accumulation of Li salts in the body can cause renal damage and nephrotic syndrome. In this study, the mechanism of renal inflammatory reaction induced by Li excessive intake was studied by establishing mice models in vitro and in vivo. The results of histopathology staining and TdT-mediated dUTP nick-end labeling assay showed that high Li condition (Lithium carbonate, 20 mg/kg/twice a day, i.e., for 30 consecutive days) caused inflammatory damage and apoptosis in kidney tissue cells. Western blot, qPCR, and immunohistochemical analysis were used to further study. In the vivo experiments, we found that Li reduced antioxidant enzyme capacity (glutathione peroxidase, total superoxide dismutase, total antioxidant capacity, and catalase) and induced the production of reactive oxygen species (ROS). Moreover, excessive Li activated nuclear factor kappa-B (NF-κB) signaling pathway and nucleotide-binding oligomerization domain-like receptors domains-containing protein 3 (NLRP3) inflammasome, resulting in activation of inflammatory factors tumor necrosis factor-α and IL-1β in the kidney of mice. In the vitro study, ROS as an upstream signal phosphorylated IκBα and NF-κB, up-regulated the NLRP3 inflammasome, increased caspase3, 6, 7, and 9 to exaggerate inflammation response, finally inducing pyroptosis in renal cells.
MeSH term(s)	Animals ; Inflammasomes/metabolism ; Kidney/pathology ; Lithium/toxicity ; Mice ; NF-kappa B/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Pyroptosis ; Rats ; Rats, Sprague-Dawley ; Reactive Oxygen Species/metabolism
Chemical Substances	Inflammasomes ; NF-kappa B ; NLR Family, Pyrin Domain-Containing 3 Protein ; Nlrp3 protein, mouse ; Nlrp3 protein, rat ; Reactive Oxygen Species ; Lithium (9FN79X2M3F)
Language	English
Publishing date	2022-01-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	1463449-1
ISSN	1522-7278 ; 1520-4081
ISSN (online)	1522-7278
ISSN	1520-4081
DOI	10.1002/tox.23446
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Article: Lithium intoxication induced pyroptosis via ROS/NF‐κB/NLRP3 inflammasome regulatory networks in kidney of mice

Jing, Hongyuan / Wang, Fuhan / Gao, Xue‐jiao

Environmental toxicology. 2022 Apr., v. 37, no. 4

2022

Abstract: Humans and animals may be exposed to increasing contaminant lithium (Li) concentrations in the environment with the use and disposal of Li‐containing products. Meanwhile, Li plays a key role in the treatment of human mental disorders, while the excessive ...

Abstract	Humans and animals may be exposed to increasing contaminant lithium (Li) concentrations in the environment with the use and disposal of Li‐containing products. Meanwhile, Li plays a key role in the treatment of human mental disorders, while the excessive accumulation of Li salts in the body can cause renal damage and nephrotic syndrome. In this study, the mechanism of renal inflammatory reaction induced by Li excessive intake was studied by establishing mice models in vitro and in vivo. The results of histopathology staining and TdT‐mediated dUTP nick‐end labeling assay showed that high Li condition (Lithium carbonate, 20 mg/kg/twice a day, i.e., for 30 consecutive days) caused inflammatory damage and apoptosis in kidney tissue cells. Western blot, qPCR, and immunohistochemical analysis were used to further study. In the vivo experiments, we found that Li reduced antioxidant enzyme capacity (glutathione peroxidase, total superoxide dismutase, total antioxidant capacity, and catalase) and induced the production of reactive oxygen species (ROS). Moreover, excessive Li activated nuclear factor kappa‐B (NF‐κB) signaling pathway and nucleotide‐binding oligomerization domain‐like receptors domains–containing protein 3 (NLRP3) inflammasome, resulting in activation of inflammatory factors tumor necrosis factor‐α and IL‐1β in the kidney of mice. In the vitro study, ROS as an upstream signal phosphorylated IκBα and NF‐κB, up‐regulated the NLRP3 inflammasome, increased caspase3, 6, 7, and 9 to exaggerate inflammation response, finally inducing pyroptosis in renal cells.
Keywords	Western blotting ; antioxidant activity ; antioxidant enzymes ; carbonates ; catalase ; ecotoxicology ; glutathione peroxidase ; histopathology ; humans ; immunohistochemistry ; inflammasomes ; inflammation ; kidneys ; lithium ; necrosis ; neoplasms ; nephrotic syndrome ; oligomerization ; poisoning ; pyroptosis ; reactive oxygen species ; superoxide dismutase
Language	English
Dates of publication	2022-04
Size	p. 825-835.
Publishing place	John Wiley & Sons, Inc.
Document type	Article
Note	JOURNAL ARTICLE
ZDB-ID	1463449-1
ISSN	1522-7278 ; 1520-4081
ISSN (online)	1522-7278
ISSN	1520-4081
DOI	10.1002/tox.23446
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Zinc Deficiency Induces Inflammation and Apoptosis via Oxidative Stress in the Kidneys of Mice

Xu, Yueqi / Li, Ang / Li, Xiang / Deng, Xian / Gao, Xue-jiao

Biol Trace Elem Res. 2023 Feb., v. 201, no. 2 p.739-750

2023

Abstract: Zinc (Zn) is an essential element that regulates not only cellular immunity but also antioxidant and anti-inflammatory agents. The present study investigated the effect of Zn deficiency on renal cell apoptosis and its mechanism. A Zn-deficient kidney ... ...

Abstract	Zinc (Zn) is an essential element that regulates not only cellular immunity but also antioxidant and anti-inflammatory agents. The present study investigated the effect of Zn deficiency on renal cell apoptosis and its mechanism. A Zn-deficient kidney model in mice was created by a Zn-deficient diet. Mice were fed diets with different Zn levels for 41 days as follows: normal-Zn group (NG, 34 mg Zn/kg), low-Zn group (LG, 2 mg Zn/kg), and high-Zn group (HG, 100 mg Zn/kg). H&E staining showed that inflammatory cells and many erythrocytes exuded in the renal tissue space of the low-Zn group, and TUNEL staining indicated massive death of kidney cells in the low-Zn group. In the low-Zn group, the levels of oxygen free radicals (ROS) were significantly increased, the antioxidants were significantly decreased, and the total antioxidant capacity was decreased. Moreover, RT–qPCR and ELISA results showed that inflammatory factors (TNF-α, IL-1β, and IL-6) were significantly increased in the low-Zn group. In addition, the levels of p-IκBα, p-NF-κB p65, p-ERK, p-JNK, and p-p38 were significantly increased in the low-Zn group, indicating that zinc deficiency activates NF-κB and MAPK signalling as well as increases its expression. RT–qPCR analysis of apoptosis-related genes, including Bcl-2 Bax, Caspa8, Caspa6, and Caspa3, demonstrated that the expression levels of proapoptotic genes in mouse kidneys were significantly increased. Importantly, the in vitro results were consistent with the in vivo results. Together, these data suggested that zinc deficiency induces renal oxidative stress to activate NF-κB and MAPK signalling, thereby inducing renal cell apoptosis.
Keywords	antioxidant activity ; antioxidants ; apoptosis ; cell-mediated immunity ; death ; diet ; erythrocytes ; inflammation ; interleukin-6 ; kidneys ; mice ; models ; oxidative stress ; oxygen ; zinc
Language	English
Dates of publication	2023-02
Size	p. 739-750.
Publishing place	Springer US
Document type	Article ; Online
ZDB-ID	445336-0
ISSN	1559-0720 ; 0163-4984
ISSN (online)	1559-0720
ISSN	0163-4984
DOI	10.1007/s12011-022-03166-x
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Article ; Online: Selenium Deficiency Promotes the Expression of LncRNA-MORC3, Activating NLRP3-Caspase-1/IL-1β Signaling to Induce Inflammatory Damage and Disrupt Tight Junctions in Piglets

Xue, Yao / Wang, Honghai / Tian, Bowen / Wang, Sibi / Gao, Xue-jiao

Biol Trace Elem Res. 2023 May, v. 201, no. 5 p.2365-2376

2023

Abstract: Selenium (Se), as a trace element, is widely found in animals in the form of selenomethionine, which can provide nutrition to the body and has anti-inflammatory effects to prevent inflammatory damage in animals. In the past decade, there have been many ... ...

Abstract	Selenium (Se), as a trace element, is widely found in animals in the form of selenomethionine, which can provide nutrition to the body and has anti-inflammatory effects to prevent inflammatory damage in animals. In the past decade, there have been many studies on piglet diseases caused by selenium deficiency; however, under Se deficiency, the relationship between LncRNA-MORC3, inflammatory injury, and tight junctions in piglets has not yet been studied. We established piglet selenium deficiency models divided into three groups and obtained small intestinal tissues after 35 days of feeding. Small intestinal epithelial IPEC-J2 cells were divided into three groups, and samples were collected after 24 h of culture for qPCR and Western blot experiments. First, we found that Se deficiency led to an increase in LncRNA-MORC3 expression in piglets in vivo and in vitro. We found that the binding site of NLRP3 on LncRNA-MORC3 and the expression trends of both were the same: Se deficiency increased the secretion of NLRP3 and the expression levels of the inflammatory factors Caspase-1, ASC, IL-1β, IL-17, IL-6, IL-10, and TNF-α, which are related to the NLRP3-Caspase-1/IL-1β signaling pathway. At the same time, Se deficiency decreased the expression levels of the tight junction factors ZO-1, Z0-2, Occludin, E-cadherin, and ZEB-1. This result showed that the tight junctions were disrupted. Herein, we demonstrated that Se deficiency promotes the expression of both LncRNA-MORC3 and inflammatory factors in piglets to activate the NLRP3-Caspase-1/IL-1β signaling pathway and disrupt tight junctions. Ultimately, these factors lead to inflammatory damage in piglet small intestinal tissues.
Keywords	Western blotting ; cadherins ; caspase-1 ; epithelium ; interleukin-10 ; interleukin-17 ; interleukin-6 ; intestines ; nutrition ; occludins ; piglets ; secretion ; selenium ; selenomethionine ; tight junctions
Language	English
Dates of publication	2023-05
Size	p. 2365-2376.
Publishing place	Springer US
Document type	Article ; Online
ZDB-ID	445336-0
ISSN	1559-0720 ; 0163-4984
ISSN (online)	1559-0720
ISSN	0163-4984
DOI	10.1007/s12011-022-03341-0
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Article ; Online: Selenium Deficiency Causes Iron Death and Inflammatory Injury Through Oxidative Stress in the Mice Gastric Mucosa.

Xu, Shuang / Kang, Zibo / Li, Kan / Li, Xueying / Zhang, Yanhe / Gao, Xue-Jiao

Biological trace element research

2023 Volume 202, Issue 3, Page(s) 1150–1163

Abstract: Selenium (Se) is a trace element essential for the maintenance of normal physiological functions in living organisms. Oxidative stress is a state in which there is an imbalance between oxidative and antioxidant effects in the body. A deficiency of Se can ...

Abstract	Selenium (Se) is a trace element essential for the maintenance of normal physiological functions in living organisms. Oxidative stress is a state in which there is an imbalance between oxidative and antioxidant effects in the body. A deficiency of Se can make the body more inclined to oxidation, which can induce related diseases. The aim of this experimental study was to investigate the mechanisms by which Se deficiency affects the digestive system through oxidation. The results showed that Se deficiency treatment led to a decrease in the levels of GPX4 and antioxidant enzymes and an increase in the levels of ROS, MDA, and lipid peroxide (LPO) in the gastric mucosa. Oxidative stress was activated. Triple stimulation of ROS, Fe
MeSH term(s)	Animals ; Mice ; Selenium/pharmacology ; Reactive Oxygen Species/metabolism ; NF-kappa B/metabolism ; Iron/pharmacology ; Toll-Like Receptor 4/genetics ; Toll-Like Receptor 4/metabolism ; Oxidative Stress ; Antioxidants/metabolism ; Apoptosis ; Necrosis ; Malnutrition
Chemical Substances	Selenium (H6241UJ22B) ; Reactive Oxygen Species ; NF-kappa B ; Iron (E1UOL152H7) ; Toll-Like Receptor 4 ; Antioxidants
Language	English
Publishing date	2023-07-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	445336-0
ISSN	1559-0720 ; 0163-4984
ISSN (online)	1559-0720
ISSN	0163-4984
DOI	10.1007/s12011-023-03754-5
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Article ; Online: Green tea polyphenols inhibit TBBPA-induced lung injury

Lv, Hongli / Wang, Jingjing / Geng, Yuan / Xu, Tianchao / Han, Fuxin / Gao, Xue-Jiao / Guo, Meng-Yao

Food & function

2024 Volume 15, Issue 7, Page(s) 3411–3419

Abstract: Tetrabromobisphenol A (TBBPA) is a global pollutant. When TBBPA is absorbed by the body through various routes, it can have a wide range of harmful effects on the body. Green tea polyphenols (GTPs) can act as antioxidants, resisting the toxic effects of ... ...

Abstract	Tetrabromobisphenol A (TBBPA) is a global pollutant. When TBBPA is absorbed by the body through various routes, it can have a wide range of harmful effects on the body. Green tea polyphenols (GTPs) can act as antioxidants, resisting the toxic effects of TBBPA on animals. The effects and mechanisms of GTP and TBBPA on oxidative stress, inflammation and apoptosis in the mouse lung are unknown. Therefore, we established
MeSH term(s)	Mice ; Animals ; NF-kappa B/genetics ; NF-kappa B/metabolism ; Antioxidants/pharmacology ; Antioxidants/metabolism ; Reactive Oxygen Species/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; Lung Injury/chemically induced ; Lung Injury/drug therapy ; Oxidative Stress ; Apoptosis ; Inflammation/drug therapy ; Inflammation/metabolism ; Polyphenols/pharmacology ; Tea ; Guanosine Triphosphate/metabolism ; Guanosine Triphosphate/pharmacology ; Polybrominated Biphenyls
Chemical Substances	NF-kappa B ; Antioxidants ; tetrabromobisphenol A (FQI02RFC3A) ; Reactive Oxygen Species ; Tumor Necrosis Factor-alpha ; Polyphenols ; Tea ; Guanosine Triphosphate (86-01-1) ; Polybrominated Biphenyls
Language	English
Publishing date	2024-04-02
Publishing country	England
Document type	Journal Article
ZDB-ID	2612033-1
ISSN	2042-650X ; 2042-6496
ISSN (online)	2042-650X
ISSN	2042-6496
DOI	10.1039/d4fo00480a
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Article ; Online: Rosmarinic acid alleviates intestinal inflammatory damage and inhibits endoplasmic reticulum stress and smooth muscle contraction abnormalities in intestinal tissues by regulating gut microbiota.

Li, Kan / Wu, Jiawei / Xu, Shuang / Li, Xueying / Zhang, Yanhe / Gao, Xue-Jiao

Microbiology spectrum

2023 , Page(s) e0191423

Abstract: The host-bacterial interactions play the key role in inflammatory bowel disease (IBD). Dysbiosis of the intestinal flora can lead to pathological changes in the intestine. Rosmarinic acid (RA) is a natural phenolic acid compound with antioxidant, anti- ... ...

Abstract	The host-bacterial interactions play the key role in inflammatory bowel disease (IBD). Dysbiosis of the intestinal flora can lead to pathological changes in the intestine. Rosmarinic acid (RA) is a natural phenolic acid compound with antioxidant, anti-cancer, anti-inflammatory, anti-apoptotic, anti-fibrotic, and anti-bacterial activities that has a palliative effect on acute IBD. We have established an
Language	English
Publishing date	2023-08-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	2807133-5
ISSN	2165-0497 ; 2165-0497
ISSN (online)	2165-0497
ISSN	2165-0497
DOI	10.1128/spectrum.01914-23
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Article: Selenium Deficiency Promotes Oxidative Stress-Induced Mastitis via Activating the NF-κB and MAPK Pathways in Dairy Cow

Zhang, Yanhe / Xu, Yueqi / Chen, Bowen / Zhao, Bing / Gao, Xue-jiao

Biological trace element research. 2022 June, v. 200, no. 6

2022

Abstract: Selenium (Se) is an antioxidant and immunomodulator that can participate in the control of specific endocrine pathways. Disturbance of redox homeostasis is closely related to the pathogenesis of many diseases. Se is also an important nutrient element for ...

Abstract	Selenium (Se) is an antioxidant and immunomodulator that can participate in the control of specific endocrine pathways. Disturbance of redox homeostasis is closely related to the pathogenesis of many diseases. Se is also an important nutrient element for dairy cows. First, oxidative stress (OS) induced by Se deficiency was investigated along with a possible mechanism of its induction of mammary gland inflammation. This investigation used in vivo and in vitro experiments for verification. Once the OS response was triggered, the activity of antioxidant enzymes was reduced by regulation of the concentration of Se, which led to the accumulation of ROS. TNF-α, IL-1β, and IL-6 secretion was promoted to activate the NF-κB/MAPK signaling pathway. This process further promoted the accumulation of cytokines that aggravated the inflammatory response. Herein, it was verified that Se deficiency induces OS, which leads to ROS accumulation and the secretion of inflammatory factors to activate the NF-κB/MAPK signaling pathway and promote the occurrence of mastitis.
Keywords	antioxidants ; dairy cows ; homeostasis ; immunomodulators ; inflammation ; interleukin-6 ; mammary glands ; oxidative stress ; pathogenesis ; research ; secretion ; trace elements
Language	English
Dates of publication	2022-06
Size	p. 2716-2726.
Publishing place	Springer US
Document type	Article
ZDB-ID	445336-0
ISSN	1559-0720 ; 0163-4984
ISSN (online)	1559-0720
ISSN	0163-4984
DOI	10.1007/s12011-021-02882-0
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