Preconditioning with recombinant high-mobility group box 1 protein protects the kidney against ischemia–reperfusion injury in mice

Wu, Huiling; Steenstra, Renske; Boer, Elianne C.S. de; Zhao, Cathy; Ma, Jin; Stelt, Jorieke M. van der; Chadban, Steven J.

doi:10.1038/ki.2013.475

Cited by 52 publications

(47 citation statements)

References 26 publications

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“…24) HMGB1 initiates a signaling cascade leading to activation of NF-κB and upregulation of downstream proinflammatory genes in a mouse model of renal I/R injury, and administration of a neutralizing antibody to HMGB1 provided significant renoprotection. 25,26) In agreement with these results, we found that isoflurane preconditioning not only reduced the elevated circulating and renal HMGB1 levels, but also suppressed NF-κB, downstream IL-1β, and TNF-α expression 24 h after reperfusion. Therefore, renoprotection may be mediated by inhibiting NF-κB activation and the production of the proinflammatory cytokines.…”

Section: Discussionsupporting

confidence: 78%

Isoflurane Preconditioning Ameliorates Renal Ischemia-Reperfusion Injury through Antiinflammatory and Antiapoptotic Actions in Rats

Liang

et al. 2014

Biological & Pharmaceutical Bulletin

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Renal ischemia-reperfusion (I/R) injury is a major cause of acute kidney injury via inflammation and cell apoptosis. Volatile anesthetics have been shown to exert organ-protective effects against kidney damage in vivo and in vitro. In the present study, we investigated the effects of isoflurane, a commonly used volatile anesthetic, on renal I/R injury and the underlying mechanisms. Rats subjected to renal I/R displayed higher serum creatinine and blood urea nitrogen levels than sham rats as well as severe histopathological damage. Renal I/R also resulted in a nuclear factor-κB (NF-κB)-mediated inflammatory response and dysfunction of the p53-Bax-caspase-3 apoptotic pathway. Rats preconditioned with 1.5% isoflurane for 2 h had better renal function and less tubular apoptosis 24 h after I/R injury than control rats. Pretreatment with isoflurane suppressed renal NF-κB activation, leading to a reduction in proinflammatory molecules (high-mobility group box 1, interleukin-1β, and tumor necrosis factor-α) both in the kidneys and circulation. In addition, rats subjected to isoflurane preconditioning had a higher Bcl-2/Bax ratio and less cleaved caspase-3. Our findings suggest that preconditioning with a clinically relevant concentration of isoflurane attenuates renal I/R injury, based at least in part on its ability to modulate renal inflammation and apoptosis.Key words acute kidney injury; ischemia-reperfusion; volatile anesthetic; inflammation; apoptosis Renal ischemic-reperfusion (I/R) injury is a major cause of acute kidney injury (AKI), which occurs in many clinical settings including shock, renal transplantation, and renal artery angioplasty.1) Renal I/R injury always implies a poor prognosis and no effective therapy is currently available. Although the underlying mechanisms for renal I/R injury have been extensively studied, the pathophysiologic process involving inflammation and cell apoptosis and its relationship to subsequent renal injury remain to be fully elucidated.Nuclear factor-κB (NF-κB) is one of the most critical transcription factors involved in many inflammatory conditions, including renal I/R injury. Activation of NF-κB is a critical step in the systemic and renal inflammatory response, which leads to the release of proinflammatory cytokines including high-mobility group box 1 (HMGB1), 2) interleukin-1β (IL-1β), 3) and tumor necrosis factor-α (TNF-α).4) It has also been observed that the p53-Bax-caspase-3 apoptotic pathway is involved in renal I/R injury. 4,5) P53 can induce the downregulation of anti-apoptotic Bcl-2 and the upregulation of pro-apoptotic Bax. A decrease in the Bcl-2/Bax ratio triggers cytochrome c release from mitochondria, which results in the activation of caspase-3 and a chain reaction leading to apoptosis.6,7) Therefore, inhibiting the coexisting processes of inflammation and apoptosis provides a potential approach to the prevention and treatment of renal I/R injury.Isoflurane is a volatile anesthetic commonly used in clinical surgical settings. Previous studies have indicated ...

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Section: Discussionsupporting

confidence: 78%

Isoflurane Preconditioning Ameliorates Renal Ischemia-Reperfusion Injury through Antiinflammatory and Antiapoptotic Actions in Rats

Liang

et al. 2014

Biological & Pharmaceutical Bulletin

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“…89,100,147 HMGB1 also can facilitate ischemic preconditioning, which implies that HMGB1 exposure protects from subsequent postischemic AKI. 148 This TLR2-mediated process involves the upregulation of Siglec as one of many counterregulatory mediators that limit DAMP-related immunity just like endotoxin tolerance. 149 In addition, NLRP3-deficient mice were protected from postischemic AKI.…”

Section: Tubular Necrosismentioning

confidence: 99%

Beyond Tissue Injury—Damage-Associated Molecular Patterns, Toll-Like Receptors, and Inflammasomes Also Drive Regeneration and Fibrosis

Anders

Schaefer

2014

Journal of the American Society of Nephrology

259

231

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Tissue injury initiates an inflammatory response through the actions of immunostimulatory molecules referred to as damage-associated molecular patterns (DAMPs). DAMPs encompass a group of heterogenous molecules, including intracellular molecules released during cell necrosis and molecules involved in extracellular matrix remodeling such as hyaluronan, biglycan, and fibronectin. Kidney-specific DAMPs include crystals and uromodulin released by renal tubular damage. DAMPs trigger innate immunity by activating Toll-like receptors, purinergic receptors, or the NLRP3 inflammasome. However, recent evidence revealed that DAMPs also trigger reepithelialization upon kidney injury and contribute to epithelial-mesenchymal transition and, potentially, to myofibroblast differentiation and proliferation. Thus, these discoveries suggest that DAMPs drive not only immune injury but also kidney regeneration and renal scarring. Here, we review the data from these studies and discuss the increasingly complex connection between DAMPs and kidney diseases.

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“…Nuclear factor (NF)-κB, a key downstream factor of the Toll-like receptor (TLR/NF-κB signaling pathway, mediates essential functions by regulating inflammatory factors, cell proliferation and differentiation (4). As a result, systemic inhibition of NF-κB may reduce inflammation and have damaging consequences (5).…”

Section: Introductionmentioning

confidence: 99%

Pterostilbene protects against acute renal ischemia reperfusion injury and inhibits oxidative stress, inducible nitric oxide synthase expression and inflammation in rats via the Toll‑like receptor 4/nuclear factor‑κB signaling pathway

et al. 2017

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Abstract. Previous studies have demonstrated that pterostilbene (Pter) prevents oxidative stress, suppresses cell growth and exhibits anti-fungal and anti-inflammatory effects. Pter is used to treat a number of clinical diseases, including Alzheimer's disease, various malignancies and hypercholesteremia. The aim of the present study was to investigate whether Pter protects against acute renal ischemia reperfusion injury (IRI) and inhibits oxidative stress, inducible nitric oxide synthase (iNOS) expression and inflammation in rats. A total of 40 adult male Sprague Dawley rats were divided into the following 5 groups at random: Control group, where rats were not subjected to renal IRI; IRI group, where rats were subjected to renal IRI; Pter 10 group, where rats underwent renal IRI and were treated with 10 mg/kg Pter; Pter 20 group, where rats underwent renal IRI and were treated with 20 mg/kg Pter; Pter 30 group, where rats underwent renal IRI and were treated with 30 mg/kg Pter. The results demonstrated that Pter treatment improved renal function following acute renal IRI. Compared with the untreated renal IRI group, myeloperoxidase, iNOS, interleukin (IL)-1β, IL-6 and tumor necrosis factor-α expression levels were significantly decreased (P<0.01), whereas IL-10 expression levels were significantly increased (P<0.01) following treatment with Pter in acute renal IRI rats. In addition, Pter significantly attenuated caspase-3 activity and the Toll-like receptor 4 (TLR4)/nuclear factor (NF)-κB signaling pathway induced by acute renal IRI (P<0.01). These results provide evidence to suggest that administration of Pter may protect against acute renal IRI and inhibit oxidative stress, iNOS expression and inflammation in rats via the TLR4/NF-κB signaling pathway.

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Preconditioning with recombinant high-mobility group box 1 protein protects the kidney against ischemia–reperfusion injury in mice

Cited by 52 publications

References 26 publications

Isoflurane Preconditioning Ameliorates Renal Ischemia-Reperfusion Injury through Antiinflammatory and Antiapoptotic Actions in Rats

Isoflurane Preconditioning Ameliorates Renal Ischemia-Reperfusion Injury through Antiinflammatory and Antiapoptotic Actions in Rats

Beyond Tissue Injury—Damage-Associated Molecular Patterns, Toll-Like Receptors, and Inflammasomes Also Drive Regeneration and Fibrosis

Pterostilbene protects against acute renal ischemia reperfusion injury and inhibits oxidative stress, inducible nitric oxide synthase expression and inflammation in rats via the Toll‑like receptor 4/nuclear factor‑κB signaling pathway

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