ROS-mediated inflammatory response in liver damage via regulating the Nrf2/HO-1/NLRP3 pathway in mice with trichloroethylene hypersensitivity syndrome

Wang, Feng; Hong, Yiting; Jiang, Wei; Wang, Yican; Chen, Muyue; Zang, Dandan; Zhu, Qingsan

doi:10.1080/1547691x.2022.2111003

Cited by 7 publications

(3 citation statements)

References 24 publications

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“…When cells are exposed to oxidative stress, Nrf2 dissociates from the cytosolic repressor protein Kelch‐like ECH‐associated protein 1 (Keap1) 22 . Subsequently, Nrf2 is translocated into the nucleus, where it binds DNA sequences known as antioxidant response elements (ARE) to regulate the expression of various downstream genes, promoting the restoration of redox homeostasis 20,23 . Therefore, we speculated that Nrf2/HO‐1 signalling pathway activation exerts an essential role in protecting ECs from cell senescence induced by oxidative stress.…”

Section: Introductionmentioning

confidence: 99%

Gastrodin alleviates premature senescence of vascular endothelial cells by enhancing the Nrf2/HO‐1 signalling pathway

Tong,

Tian,

et al. 2023

J Cellular Molecular Medi

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Endothelial dysfunction is an independent risk factor for stroke. The dysfunction of endothelial cells (EC) is closely concerned with EC senescence. Gastrodin (GAS) is an organic compound extracted from the dried root mass of the Orchidaceae plant Gastrodiae gastrodiae. It is used clinically to treat diseases such as vertebrobasilar insufficiency, vestibular neuronitis and vertigo. In the present study, we used hydrogen peroxide (H2O2)‐induced human umbilical vein endothelial cells (HUVECs) to establish an in vitro EC senescence model and to investigate the role and mechanism of GAS in EC senescence. It's found that H2O2‐treated HUVECs increased the proportion of senescence‐associated β‐galactosidase (SA β‐gal) positive cells and the relative protein expression levels of senescence‐associated cyclin p16 and p21. In addition, GAS reduced the proportion of SA β‐gal positive cells and the relative protein expression levels of p16 and p21, and increased the proliferation and migration ability of HUVECs. Meanwhile, GAS increased the expression of the anti‐oxidative stress protein HO‐1 and its nuclear expression level of Nrf2. The anti‐senescence effect of GAS was blocked when HO‐1 expression was inhibited by SnPPIX. Furthermore, absence of HO‐1 abolished the effect of GAS on HUVEC proliferation and migration. In conclusion, GAS ameliorated H2O2‐induced cellular senescence and enhanced cell proliferation and migration by enhancing Nrf2/HO‐1 signalling in HUVECs. These findings of our study expanded the understanding of GAS pharmacology and suggested that GAS may offer a potential therapeutic agent for stroke.

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Section: Introductionmentioning

confidence: 99%

Gastrodin alleviates premature senescence of vascular endothelial cells by enhancing the Nrf2/HO‐1 signalling pathway

Tong,

Tian,

et al. 2023

J Cellular Molecular Medi

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“…Increased ROS leads to hepatic ischemia/reperfusion injury in the endotoxemia model [17]. The use of ROS scavengers can inhibit hepatic oxidative stress, thereby reducing liver injury induced by exposure to trichloroethylene [18]. Mitochondria-targeted antioxidants significantly reduced cell death and mitochondrial injury in ischemia-reperfusion rats [19].…”

Section: Introductionmentioning

confidence: 99%

IL-6 Mutation Attenuates Liver Injury Caused by Aeromonas hydrophila Infection by Reducing Oxidative Stress in Zebrafish

Zhai,

Wang,

et al. 2023

IJMS

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Interleukin-6 (IL-6), a pleiotropic cytokine, plays a crucial role in acute stress induced by bacterial infection and is strongly associated with reactive oxygen species (ROS) production. However, the role of IL-6 in the liver of fish after Aeromonas hydrophila infection remains unclear. Therefore, this study constructed a zebrafish (Danio rerio) il-6 knockout line by CRISPR/Cas9 to investigate the function of IL-6 in the liver post bacterial infection. After infection with A. hydrophila, pathological observation showed that il-6−/− zebrafish exhibited milder liver damage than wild-type (WT) zebrafish. Moreover, liver transcriptome sequencing revealed that 2432 genes were significantly up-regulated and 1706 genes were significantly down-regulated in il-6−/− fish compared with WT fish after A. hydrophila infection. Further, gene ontology (GO) analysis showed that differentially expressed genes (DEGs) were significantly enriched in redox-related terms, including oxidoreductase activity, copper ion transport, etc. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that DEGs were significantly enriched in pathways such as the PPAR signaling pathway, suggesting that il-6 mutation has a significant effect on redox processes in the liver after A. hydrophila infection. Additionally, il-6−/− zebrafish exhibited lower malondialdehyde (MDA) levels and higher superoxide dismutase (SOD) activities in the liver compared with WT zebrafish following A. hydrophila infection, indicating that IL-6 deficiency mitigates oxidative stress induced by A. hydrophila infection in the liver. These findings provide a basis for further studies on the role of IL-6 in regulating oxidative stress in response to bacterial infections.

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“…TCE exposure without appropriate occupational protection is associated with TCE hypersensitivity syndrome (THS), which is also termed occupational medicamentosa-like dermatitis (OMDT) in China. In addition to widespread skin lesions, OMDT is often accompanied with multiple organ damage, especially hepatitis and kidney injury (Wang et al, 2022;Wang et al, 2021). TCE sensitization-induced kidney injury is an unsolved health problem which, to a large extent, has increased the burden of disease.…”

Section: Introductionmentioning

confidence: 99%

Viral mimic polyinosine-polycytidylic acid promotes renal endothelial cell injury via HMGB1 acetylation in trichloroethylene-sensitized mice

Wang

Hong

Zang

et al. 2023

Preprint

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Viral infection or reactivation seems to be critical in trichloroethylene hypersensitivity syndrome (THS), which is also called occupational medicamentosa-like dermatitis (OMDT) in China. Our previous studies reported that polyinosinic-polycytidylic acid (poly I:C) amplified hepatitis in TCE-sensitized mice. However, whether poly I:C plays a role in TCE-induced renal damage remains to be clarified. To this end, a TCE-sensitized mouse model was established. Renal damage, especially renal endothelial cell dysfunction, was assessed. The activation of high mobility group box protein 1 (HMGB1) was further detected to elucidate the possible role of poly I:C in TCE sensitization-induced renal damage. Our results showed that poly I:C pretreatment aggravated the renal histological changes and dysfunction in TCE-sensitized mice. Renal endothelial cell injuries might be a key driver of kidney damage, in which poly I:C pretreatment acted as an amplifier in TCE sensitization. In addition, poly I:C, combined with Toll-like receptor (TLR) 3, promotes the acetylation and release of HMGB1 from renal endothelial cells. Taken together, our findings highlighted a novel role of poly I:C pretreatment in TCE sensitization-induced renal endothelial cell injuries.

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ROS-mediated inflammatory response in liver damage via regulating the Nrf2/HO-1/NLRP3 pathway in mice with trichloroethylene hypersensitivity syndrome

Cited by 7 publications

References 24 publications

Gastrodin alleviates premature senescence of vascular endothelial cells by enhancing the Nrf2/HO‐1 signalling pathway

Gastrodin alleviates premature senescence of vascular endothelial cells by enhancing the Nrf2/HO‐1 signalling pathway

IL-6 Mutation Attenuates Liver Injury Caused by Aeromonas hydrophila Infection by Reducing Oxidative Stress in Zebrafish

Viral mimic polyinosine-polycytidylic acid promotes renal endothelial cell injury via HMGB1 acetylation in trichloroethylene-sensitized mice

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