G protein-coupled receptor 30 activation protects hepatic ischemia-reperfusion injury of liver tissue through inhibiting NLRP3 in the rat model

Qin, Yong; Wang, Chaojun; Xu, Shengqian; Wu, Chwan-Hwa; Wang, Shi; Pan, Debiao; Ye, GuanXiong

doi:10.1080/01478885.2020.1826175

Cited by 9 publications

(6 citation statements)

References 34 publications

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“…Metformin regulates intestinal epithelial cell pyroptosis via TXNIP/NLRP3/GSDMD pathway, thereby alleviating intestinal I/R injury, 32 revealing the importance of NLRP3‐mediated pyroptosis in intestinal I/R injury. Coincidentally, GPR30 was demonstrated to inactivate NLRP3 inflammasome in hepatic I/R injury 9 . Here, we also found that GPR30 greatly blocked the activation of NLRP3 inflammasome in intestinal I/R injury.…”

Section: Discussionsupporting

confidence: 68%

“…Activation of GPR30 has been reported to reduce the inflammatory response of macrophages, suggesting that GPR30 may be a therapeutic target for inflammatory diseases 7 . Emerging evidence reveals that GPR30 is involved in regulating the pathological process of I/R injury of various types of tissue, such as liver tissues and myocardial tissues, and activation of GPR30 exerts a protective role in these I/R injuries 8,9 . Nevertheless, whether GPR30 also has involvement in intestinal I/R injury remains obscure.…”

Section: Introductionmentioning

confidence: 99%

“… 7 Emerging evidence reveals that GPR30 is involved in regulating the pathological process of I/R injury of various types of tissue, such as liver tissues and myocardial tissues, and activation of GPR30 exerts a protective role in these I/R injuries. 8 , 9 Nevertheless, whether GPR30 also has involvement in intestinal I/R injury remains obscure. Of note, the expression level of GPR30 was observed to be abnormally low in patients with inflammatory bowel disease, and GPR30‐specific inhibitor G15 impaired the protective effects of dehydroepiandrosterone on the intestinal barrier and inflammatory response in mice with colitis, reflecting that GPR30 played a key role in intestinal injury.…”

Section: Introductionmentioning

confidence: 99%

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Transcription factor Krüppel‐like factor 4 upregulated G protein‐coupled receptor 30 alleviates intestinal inflammation and apoptosis, and protects intestinal integrity from intestinal ischemia–reperfusion injury

Yin

Xie

Yao

et al. 2023

Immunity Inflam & Disease

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Introduction Intestinal ischemia/reperfusion (I/R) injury is a common clinical event occurring during multiple clinical pathological processes. Here, we designed this paper to discuss the role of G protein‐coupled receptor 30 (GPR30) playing in intestinal I/R injury. Methods An oxygen‐glucose deprivation/reoxygenation (OGD/R) cell model was established to simulate the pathological process of I/R injury. With the application of enzyme‐linked immunosorbent assay, TUNEL, and transepithelial electrical resistance (TEER) assays, the levels of inflammatory cytokines, cell apoptosis, and intestinal integrity were estimated. The corresponding proteins were estimated by applying western blot. Immunofluorescence was conducted to examine N‐terminal Gasdermin D (GSDMD‐N) expression. The interplay between KLF4 and GPR30 was demonstrated by dual‐luciferase reporter assay and chromatin immunoprecipitation. Results The results showed that GPR30 was downregulated in Caco‐2 cells exposed to OGD/R. GPR30 overexpression reduced the production of TNF‐α, IL‐6, IL‐1β, and IL‐18, the TUNEL‐positive cells, as well as the contents of p‐p65, Cox‐2, Inos, Bax, and cleaved‐PARP, but elevated the expression of Bcl‐2 in OGD/R‐induced Caco‐2 cells. In addition, OGD/R‐induced the reduction of TEER value and reduced expression of tight junction proteins in Caco‐2 cells, which was partially restored by GPR30 overexpression. Furthermore, GPR30 suppressed nod‐like receptor pyrin 3 inflammasome and GSDMD‐N expression. It was evidenced that Krüppel‐like factor 4 (KLF4) could directly bind to GPR30 promoter and positively regulate GPR30 expression. The regulation of GPR30 overexpression above was weakened by KLF4 knockdown. Conclusion Collectively, our findings suggested that KLF4 could transcriptionally upregulate GPR30, and GPR30 prevented intestine I/R injury by inhibiting inflammation and apoptosis, and maintaining intestinal integrity that provides potential targets for mitigating the I/R injury.

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Section: Discussionsupporting

confidence: 68%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Transcription factor Krüppel‐like factor 4 upregulated G protein‐coupled receptor 30 alleviates intestinal inflammation and apoptosis, and protects intestinal integrity from intestinal ischemia–reperfusion injury

Yin

Xie

Yao

et al. 2023

Immunity Inflam & Disease

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“…A hepatic vessel-interrupted mice model can be effectively used to evaluate potential therapeutic drugs for hepatic IRI. 37 In this study, we employed the liver vessel interruptioninduced ischemia/reperfusion injury murine model to comprehensively evaluate the protective effects of 3 against hepatic IRI. 10 To evaluate the severity of hepatic injury, we measured the levels of three essential enzymes: alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH), which served as reliable indicators of liver damage.…”

mentioning

confidence: 99%

“…A hepatic vessel-interrupted mice model can be effectively used to evaluate potential therapeutic drugs for hepatic IRI . In this study, we employed the liver vessel interruption-induced ischemia/reperfusion injury murine model to comprehensively evaluate the protective effects of 3 against hepatic IRI .…”

mentioning

confidence: 99%

Bioactive Indole Alkaloid from Aspergillus amoenus TJ507 That Ameliorates Hepatic Ischemia/Reperfusion Injury

et al. 2023

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Hepatic ischemia/reperfusion injury (IRI) is a major factor contributing to the failure of hepatic resection and liver transplantation. As part of our ongoing investigation into bioactive compounds derived from fungi, we isolated eight indole alkaloids (1–8) from the endophytic fungus Aspergillus amoenus TJ507. Among these alkaloids, one previously undescribed compound, amoenamide D (1), was identified. The planar structure of 1 was elucidated by extensive spectroscopic analysis, including HRESIMS and NMR spectra. The absolute configuration of 1 was elucidated by using electronic circular dichroism calculations. Notably, in the CoCl2-induced hepatocyte damage model, notoamide Q (3) exhibited significant anti-hypoxia injury activity. Furthermore, in a murine hepatic ischemia/reperfusion injury model, treatment with 3 prevents IRI-induced liver damage and hepatocellular apoptosis. Consequently, 3 might serve as a potential lead compound to prevent hepatic ischemia/reperfusion injury.

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Neural Stem Cell Extracellular Vesicles Carrying YBX1 Inhibited Neuronal Pyroptosis Through Increasing m6A-modified GPR30 Stability and Expression in Ischemic Stroke

Peng,

He,

Lin

et al. 2023

Transl. Stroke Res.

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G protein-coupled receptor 30 activation protects hepatic ischemia-reperfusion injury of liver tissue through inhibiting NLRP3 in the rat model

Cited by 9 publications

References 34 publications

Transcription factor Krüppel‐like factor 4 upregulated G protein‐coupled receptor 30 alleviates intestinal inflammation and apoptosis, and protects intestinal integrity from intestinal ischemia–reperfusion injury

Transcription factor Krüppel‐like factor 4 upregulated G protein‐coupled receptor 30 alleviates intestinal inflammation and apoptosis, and protects intestinal integrity from intestinal ischemia–reperfusion injury

Bioactive Indole Alkaloid from Aspergillus amoenus TJ507 That Ameliorates Hepatic Ischemia/Reperfusion Injury

Neural Stem Cell Extracellular Vesicles Carrying YBX1 Inhibited Neuronal Pyroptosis Through Increasing m6A-modified GPR30 Stability and Expression in Ischemic Stroke

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