Umbelliferone ameliorates cerebral ischemia–reperfusion injury via upregulating the PPAR gamma expression and suppressing TXNIP/NLRP3 inflammasome

Wang, Xiangxiang; Li, Ruipeng; Wang, Xuan; Fu, Qiang

doi:10.1016/j.neulet.2015.06.016

Cited by 110 publications

(79 citation statements)

References 23 publications

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“…), and the whole plant of Rutaceae rue ( Ruta graveolens L .). It has been reported that Umb functions as an antioxidant and anti‐inflammatory agent in a rat model of cerebral ischemia‐reperfusion injury . This investigation studied the CUMS‐induced rat model to evaluate the antidepressive‐like effects of Umb on insulin resistance.…”

Section: Introductionmentioning

confidence: 99%

Umbelliferone attenuates unpredictable chronic mild stress induced‐insulin resistance in rats

Tao

Wang

et al. 2016

IUBMB Life

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The aim of this study was to investigate whether umbelliferone (Umb) could attenuate insulin resistance in unpredictable chronic mild stress (CUMS)-induced rats. Behavioral changes were evaluated through sucrose preference test (SPT), openfield test, forced swimming test, and tail suspension test (TST), suggesting that Umb (20 and 40 mg/kg) could effectively improve depression symptoms. Oral glucose tolerance test and serum insulin indicated that Umb attributed to the control of blood glucose levels. The phosphorylation of insulin receptor, insulin receptor substrate (IRS)21, glycogen synthase kinase-3b, PI3K, and Akt was increased in Umb (20 and 40 mg/kg) treatment according to Western blot analysis. Taken together, the current results suggested the ameliorative effect of Umb against insulin resistance in the CUMS-induced rats. V C 2016 IUBMB Life, 68(5): [403][404][405][406][407][408][409] 2016

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Section: Introductionmentioning

confidence: 99%

Umbelliferone attenuates unpredictable chronic mild stress induced‐insulin resistance in rats

Tao

Wang

et al. 2016

IUBMB Life

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“…In addition, expression of TXNIP in the vascular endothelium is regulated in a flow-dependent manner, which can serve as a mechanosensitive switch for endothelial cell inflammation (23)(24)(25). Previous studies have demonstrated the association of the TXNIP/NLRP3 inflammasome pathway in cerebral and myocardial IRI via aggravation of inflammation damage (26)(27)(28). To date, there are no reports on the role of this pathway in DCD liver transplantation.…”

mentioning

confidence: 99%

Hypothermic oxygenated perfusion (HOPE) attenuates ischemia/reperfusion injury in the liver through inhibition of the TXNIP/NLRP3 inflammasome pathway in a rat model of donation after cardiac death

Zeng

et al. 2018

FASEB j.

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Hypothermic oxygenated perfusion (HOPE) is a relatively new dynamic preservation procedure that has not been widely implemented in liver transplantation despite its advantages. Improved graft protection is one such advantage offered by HOPE and has been attributed to multiple mechanisms, one of which may be the modulation of the thioredoxin-interacting protein (TXNIP)/NOD-like receptor protein 3 (NLRP3) inflammasome pathway. The TXNIP/NLRP3 inflammasome pathway plays a critical role in sterile inflammation under oxidative stress as a result of ischemia/reperfusion injury (IRI). In the current study, we aimed to investigate the graft protection offered by HOPE and its impact on the TXNIP/NLRP3 inflammasome pathway. To simulate conditions of donation after cardiac death (DCD) liver transplantation, rat livers were exposed to 30 min of warm ischemia after cardiac arrest. Livers were then preserved under cold storage (CS) or with HOPE for 3 h. Livers were then subjected to 1 h of isolated reperfusion. Liver injuries were assessed on the isolated perfusion rat liver model system before and after reperfusion. Compared with the CS group, the HOPE group had a significant reduction in liver injury and improvement in liver function. Our findings also revealed that reperfusion injury induced liver damage and activated the TXNIP/NLRP3 inflammasome pathway in DCD rat livers. Pretreatment of DCD rat livers with HOPE inhibited the TXNIP/NLRP3 inflammasome pathway and attenuated liver IRI. Attenuation of oxidative stress as a result of HOPE led to the down-regulation of the TXNIP/NLRP3 inflammasome pathway and thus offered superior protection compared with the traditional CS method of organ preservation.-He, W., Ye, S., Zeng, C., Xue, S., Hu, X., Zhang, X., Gao, S., Xiong, Y., He, X., Vivalda, S., Li, L., Wang, Y., Ye, Q. Hypothermic oxygenated perfusion (HOPE) attenuates ischemia/reperfusion injury in the liver through inhibition of the TXNIP/NLRP3 inflammasome pathway in a rat model of donation after cardiac death.

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“…In the brain, umbelliferone, a coumarin derivative with antioxidant properties, reduces Txnip expression and mitigates cerebral ischemia/reperfusion injury by suppressing NLRP3 inflammasome activation. 8 Collectively, these data suggest a crucial role of inflammasomes in the pathophysiology of ischemia/reperfusion injury in which Txnip acts as a molecular switch that links redox balance with inflammatory response.…”

Section: Thioredoxin-interacting Protein Links Oxidative Stress With mentioning

confidence: 95%

“…1–8 Thioredoxin-interacting protein, also known as Vitamin D3–upregulated protein 1 or thioredoxin-binding protein 2, belongs to a group of proteins called α-arrestins. Thioredoxin-interacting protein, which is widely expressed in multiple cellular compartments, 9 has been shown to regulate a variety of biological processes ranging from oxidative metabolism to programmed cell death.…”

Section: Introductionmentioning

confidence: 99%

The Emerging Role of Thioredoxin-Interacting Protein in Myocardial Ischemia/Reperfusion Injury

Wang

Yoshioka

2016

J Cardiovasc Pharmacol Ther

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Myocardial ischemia/reperfusion injury represents a major threat to human health and contributes to adverse cardiovascular outcomes worldwide. Despite the identification of numerous molecular mechanisms, understanding of the complex pathophysiology of this clinical syndrome remains incomplete. Thioredoxin-interacting protein (Txnip) has been of great interest in the past decade since it has been reported to be a critical regulator in human diseases with several important cellular functions. Thioredoxin-interacting protein binds to and inhibits thioredoxin, a redox protein that neutralizes reactive oxygen species (ROS), and through its interaction with thioredoxin, Txnip sensitizes cardiomyocytes to ROS-induced apoptosis. Interestingly, evidence from recent studies also suggests that some of the effects of Txnip may be unrelated to changes in thioredoxin activity. These pleiotropic effects of Txnip are mediated by interactions with other signaling molecules, such as nod-like receptor pyrin domain-containing 3 inflammasome and glucose transporter 1. Indeed, Txnip has been implicated in the regulation of inflammatory response and glucose homeostasis during myocardial ischemia/reperfusion injury. This review attempts to make the case that in addition to interacting with thioredoxin, Txnip contributes to some of the pathological consequences of myocardial ischemia and infarction through endogenous signals in multiple molecular mechanisms.

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Umbelliferone ameliorates cerebral ischemia–reperfusion injury via upregulating the PPAR gamma expression and suppressing TXNIP/NLRP3 inflammasome

Cited by 110 publications

References 23 publications

Umbelliferone attenuates unpredictable chronic mild stress induced‐insulin resistance in rats

Umbelliferone attenuates unpredictable chronic mild stress induced‐insulin resistance in rats

Hypothermic oxygenated perfusion (HOPE) attenuates ischemia/reperfusion injury in the liver through inhibition of the TXNIP/NLRP3 inflammasome pathway in a rat model of donation after cardiac death

The Emerging Role of Thioredoxin-Interacting Protein in Myocardial Ischemia/Reperfusion Injury

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