trans-Resveratrol downregulates Txnip overexpression occurring during liver ischemia-reperfusion

Nivet-Antoine, Valérie; Cottart, Charles‐Henry; Lemaréchal, Hervé; Vamy, Michel; Margaill, Isabelle; Beaudeux, Jean-Louis; Bonnefont‐Rousselot, Dominique; Borderie, Didier

doi:10.1016/j.biochi.2010.07.018

Cited by 36 publications

(33 citation statements)

References 27 publications

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“…Several studies have demonstrated that RES exerts protective effects against I/R injury in the kidneys [31], as well as the liver and brain injury by reducing oxidative stress and due to inhibition of TXNIP expression [32, 33]. In the present study, we found that TXNIP protein expression was significantly reduced after siRNA transfection in cultured HK-2 cells.…”

Section: Discussionsupporting

confidence: 68%

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Thioredoxin‐Interacting Protein Mediates NLRP3 Inflammasome Activation Involved in the Susceptibility to Ischemic Acute Kidney Injury in Diabetes

Xiao

Huang

Wang

et al. 2016

Oxidative Medicine and Cellular Longevity

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Kidney in diabetic state is more sensitive to ischemic acute kidney injury (AKI). However, the underlying mechanisms remain unclear. Herein, we examined the impact of diabetes mellitus on thioredoxin-interacting protein (TXNIP) expression and whether mediated NLRP3 activation was associated with renal ischemia/reperfusion- (I/R-) induced AKI. In an in vivo model, streptozotocin-induced diabetic rats showed higher susceptibility to I/R injury with increased TXNIP expression, which was significantly attenuated by resveratrol (RES) treatment (10 mg/kg intraperitoneal daily injection for 7 consecutive days prior to I/R induction). RES treatment significantly inhibited TXNIP binding to NLRP3 in diabetic rats subjected to renal I/R injury. Furthermore, RES treatment significantly reduced cleaved caspase-1 expression and production of IL-1β and IL-18. In an in vitro study using cultured human kidney proximal tubular cell (HK-2 cells) in high glucose condition (HG, 30 mM) subjected to hypoxia/reoxygenation (H/R), HG combined H/R (HH/R) stimulated TXNIP expression which was accompanied by increased NLRP3 expression, ROS generation, caspase-1 activity and IL-1β levels, and aggravated HK-2 cells apoptosis. All these changes were significantly attenuated by TXNIP RNAi and RES treatment. In conclusion, our results demonstrate that TXNIP-mediated NLRP3 activation through oxidative stress is a key signaling mechanism in the susceptibility to AKI in diabetic models.

show abstract

Section: Discussionsupporting

confidence: 68%

“…RES treatment can ameliorate hyperglycemia-mediated renal dysfunction or DN [30]. Several studies have demonstrated that RES exerts protective effects against I/R injury in the kidneys [31], as well as the liver and brain ischemia injury by reducing oxidative stress and downregulating TXNIP expression [32, 33]. …”

Section: Introductionmentioning

confidence: 99%

Thioredoxin‐Interacting Protein Mediates NLRP3 Inflammasome Activation Involved in the Susceptibility to Ischemic Acute Kidney Injury in Diabetes

Xiao

Huang

Wang

et al. 2016

Oxidative Medicine and Cellular Longevity

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“…Liver cells that overexpress TXNIP are primed for oxidative injury (35). This study found that TXNIP upregulation correlated with ROS overproduction in fructose-fed rat livers and fructose-exposed primary rat hepatocytes, RHPCs, HLO2, and HepG2 cells.…”

Section: Figmentioning

confidence: 58%

Reactive Oxygen Species-Induced TXNIP Drives Fructose-Mediated Hepatic Inflammation and Lipid Accumulation Through NLRP3 Inflammasome Activation

Zhang

Chen

et al. 2015

Antioxidants & Redox Signaling

202

144

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Aims: Increased fructose consumption predisposes the liver to nonalcoholic fatty liver disease (NAFLD), but the mechanisms are elusive. Thioredoxin-interacting protein (TXNIP) links oxidative stress to NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome activation and this signaling axis may be involved in fructose-induced NAFLD. Here, we explore the role of reactive oxygen species (ROS)-induced TXNIP overexpression in fructose-mediated hepatic NLRP3 inflammasome activation, inflammation, and lipid accumulation. Results: Rats were fed a 10% fructose diet for 8 weeks and treated with allopurinol and quercetin during the last 4 weeks. Five millimolars of fructose-exposed hepatocytes (primary rat hepatocytes, rat hepatic parenchymal cells [RHPCs], HLO2, HepG2) were co-incubated with antioxidants or caspase-1 inhibitor or subjected to TXNIP or NLRP3 siRNA interference. Fructose induced NLRP3 inflammasome activation and proinflammatory cytokine secretion, janus-activated kinase 2/signal transducers and activators of transcription 3-mediated inflammatory signaling, and expression alteration of lipid metabolism-related genes in cultured hepatocytes and rat livers. NLRP3 silencing and caspase-1 suppression blocked these effects in primary rat hepatocytes and RHPCs, confirming that inflammasome activation alters hepatocyte lipid metabolism. Hepatocellular ROS and TXNIP were increased in animal and cell models. TXNIP silencing blocked NLRP3 inflammasome activation, inflammation, and lipid metabolism perturbations but not ROS induction in fructoseexposed hepatocytes, whereas antioxidants addition abrogated TXNIP induction and diminished the detrimental effects in fructose-exposed hepatocytes and rat livers. Innovation and Conclusions: This study provides a novel mechanism for fructose-induced NAFLD pathogenesis by which the ROS-TXNIP pathway mediates hepatocellular NLRP3 inflammasome activation, inflammation and lipid accumulation. Antioxidant-based interventions can inhibit the ROS-TXNIP pathway. Antioxid. Redox Signal. 22, 848-870.

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“…TXNIP has been found to be a promising therapeutic target in hepatic ischemia/reperfusion injury [39] and hyperglycemia [40]. Interestingly, a recent study has found that TXNIP links the oxidative stress to inflammasome activation [26].…”

Section: Accepted Manuscriptmentioning

confidence: 99%

Effect of betaine on hepatic insulin resistance through FOXO1-induced NLRP3 inflammasome

Kim

Lee

et al. 2017

The Journal of Nutritional Biochemistry

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trans-Resveratrol downregulates Txnip overexpression occurring during liver ischemia-reperfusion

Cited by 36 publications

References 27 publications

Thioredoxin‐Interacting Protein Mediates NLRP3 Inflammasome Activation Involved in the Susceptibility to Ischemic Acute Kidney Injury in Diabetes

Thioredoxin‐Interacting Protein Mediates NLRP3 Inflammasome Activation Involved in the Susceptibility to Ischemic Acute Kidney Injury in Diabetes

Reactive Oxygen Species-Induced TXNIP Drives Fructose-Mediated Hepatic Inflammation and Lipid Accumulation Through NLRP3 Inflammasome Activation

Effect of betaine on hepatic insulin resistance through FOXO1-induced NLRP3 inflammasome

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