Diacerein protects against glycerol-induced acute kidney injury: Modulating oxidative stress, inflammation, apoptosis and necroptosis

Abdellatif, Rania; Hegab, Islam Ibrahim; Atef, Marwa Mohamed; Sadek, Mona Tayssir; Hafez, Yasser Mostafa

doi:10.1016/j.cbi.2019.04.008

Cited by 47 publications

(43 citation statements)

References 36 publications

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“…Consistent with previous studies, our results revealed marked increases in muscle damage markers (serum creatine kinase and LDH) in the glycerol-injected group compared to the control group. 1 , 3 , 5 The released products have been reported to undergo glomerular filtration causing intratubular obstruction, renal vasoconstriction, inflammatory response, and production of reactive oxygen species leading to AKI. 3 , 4 Renal impairment was evident in the AKI group as witnessed by prominent elevations in serum urea and creatinine levels associated with elevated relative kidney weight as previously reported.…”

Section: Discussionmentioning

confidence: 99%

Using Green Biosynthesized Lycopene-Coated Selenium Nanoparticles to Rescue Renal Damage in Glycerol-Induced Acute Kidney Injury in Rats

Albrakati

Alsharif

Alzahrani

et al. 2021

IJN

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Purpose Selenium nanoparticles (SeNPs) have recently gained much attention in nanomedicine applications owing to their unique biological properties. Biosynthesis of SeNPs using nutraceuticals as lycopene (LYC) maximizes their stability and bioactivities. In this context, this study aimed to elucidate the renoprotective activity of SeNPs coated with LYC (LYC-SeNPs) in the acute kidney injury (AKI) model. Methods Rats were divided into six groups: control, AKI (glycerol-treated), AKI+sodium selenite (Na 2 SeO 3 ; 0.5 mg/kg), AKI+LYC (10 mg/kg), AKI+LYC-SeNPs (0.5 mg/kg) and treated for 14 days. Results Glycerol treatment evoked significant increases in rhabdomyolysis-related markers (creatine kinase and LDH). Furthermore, relative kidney weight, Kim-1, neutrophil gelatinase-associated lipocalin (NGAL), serum urea, and creatinine in the AKI group were elevated. Glycerol-injected rats displayed declines in reduced glutathione level, and superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase activities, paralleled with downregulations in Nfe2l2 and Hmox-1 expressions and high renal MDA and NO contents. Glycerol-induced renal inflammation was evident by rises in TNF-α, IL-1β, IL-6, and upregulated Nos2 expression. Also, apoptotic (elevated caspase-3, Bax, and cytochrome-c with lowered Bcl-2) and necroptotic (elevated Pipk3 expression) changes were reported in damaged renal tissue. Co-treatment with Na 2 SeO 3 , LYC, or LYC-SeNPs restored the biochemical, molecular, and histological alterations in AKI. In comparison with Na 2 SeO 3 or LYC treatment, LYC-SeNPs had the best nephroprotective profile. Conclusion Our findings authentically revealed that LYC-SeNPs co-administration could be a prospective candidate against AKI-mediated renal damage via antioxidant, anti-inflammatory, anti-apoptotic and anti-necroptotic activities.

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Section: Discussionmentioning

confidence: 99%

Using Green Biosynthesized Lycopene-Coated Selenium Nanoparticles to Rescue Renal Damage in Glycerol-Induced Acute Kidney Injury in Rats

Albrakati

Alsharif

Alzahrani

et al. 2021

IJN

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“…28,30,41,44 Recently, other pharmacological agents that interfere with RIPK3 have been identified such as diacerein, ponatinib, sorafenib and phenhydan. [66][67][68][69][70] Intriguingly, specific RIPK3 inhibitors such as GSK'840, GSK'843, and GSK'872 at high concentrations, despite their ability to inhibit necroptosis, favour the assembly of RIPK1/FADD/ caspase-8/FLIP L (complex IIb) leading to caspase activation and apoptosis. 71,72 In a rodent model of catalytically inactive RIPK3 D161N, mice could not survive through the embryonic period because of lethal caspase-8-mediated apoptosis.…”

Section: Other Potential Interventions Against Necroptosis and Ripkmentioning

confidence: 99%

“…Various studies have been carried out and demonstrated the cardioprotective effects of RIPK3 knockdown in the model of cardiac I/R injury 28,30,41,44 . Recently, other pharmacological agents that interfere with RIPK3 have been identified such as diacerein, ponatinib, sorafenib and phenhydan 66‐70 . Intriguingly, specific RIPK3 inhibitors such as GSK'840, GSK'843, and GSK'872 at high concentrations, despite their ability to inhibit necroptosis, favour the assembly of RIPK1/FADD/caspase‐8/FLIP L (complex IIb) leading to caspase activation and apoptosis 71,72 .…”

Section: Introductionmentioning

confidence: 99%

The role of RIPK3‐regulated cell death pathways and necroptosis in the pathogenesis of cardiac ischaemia‐reperfusion injury

2020

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Despite advancements in management of acute myocardial infarction, this disease remains one of the leading causes of death. Timely reestablishment of epicardial coronary blood flow is the cornerstone of therapy; however, substantial amount of damage can occur as a consequence of cardiac ischaemia/reperfusion (I/R) injury. It has been previously proposed that the pathway leading to major cell death, apoptosis, is responsible for cardiac I/R injury. Nevertheless, there is compelling evidence to suggest that necroptosis, a programmed necrosis, contributes remarkably to both myocardial injury and microcirculatory dysfunction following cardiac I/R injury. Receptor‐interacting protein kinase 1 (RIPK1), RIPK3, and mixed‐lineage kinase domain‐like pseudokinase (MLKL) are shown as the major mediators of necroptosis. In addition to the traditional perception that RIPK1/RIPK3/MLKL‐dependent plasma membrane rupture is fundamental to this process, several RIPK3‐related pathways such as endoplasmic reticulum stress and mitochondrial fragmentation have also been implicated in cardiac I/R injury. In this review, reports from both in vitro and in vivo studies regarding the roles of necroptosis and RIPK3‐regulated necrosis in cardiac I/R injury have been collectively summarized and discussed. Furthermore, reports on potential interventions targeting these processes to attenuate cardiac I/R insults to the heart have been presented in this review. Future investigations adding to the knowledge obtained from these previous studies are needed in the pursuit of discovering the most effective pharmacological agent to improve cardiac I/R outcomes.

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“…On the other hand, various inhibitors of the HSP90 have been documented to downregulate necroptosis (Kongensin A 172 , G-TPP 173 , geldanamycin 174 , gamitrinib 10 , DHQ3 175 and 17-demethoxy-reblastatin 175 ). Cyclosporine A 176 , Diacerein 177 (Used in Europe and Asia to treat joint diseases), immunosuppressive and antiproliferative Rapamycin 178 and traditional Chinese medicine such as patchouli alcohol 179 have been also documented to reduce the expression of principal necroptotic mediators. Ex-527 180 (which completed a phase II clinical trial in Huntington disease) regulates necroptosis through the inhibition of Sirt1 deacetylase.…”

Section: Drugs To Regulate Necroptosis Intensitymentioning

confidence: 99%

Current translational potential and underlying molecular mechanisms of necroptosis

et al. 2019

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Cell death has a fundamental impact on the evolution of degenerative disorders, autoimmune processes, inflammatory diseases, tumor formation and immune surveillance. Over the past couple of decades extensive studies have uncovered novel cell death pathways, which are independent of apoptosis. Among these is necroptosis, a tightly regulated, inflammatory form of cell death. Necroptosis contribute to the pathogenesis of many diseases and in this review, we will focus exclusively on necroptosis in humans. Necroptosis is considered a backup mechanism of apoptosis, but the in vivo appearance of necroptosis indicates that both caspase-mediated and caspase-independent mechanisms control necroptosis. Necroptosis is regulated on multiple levels, from the transcription, to the stability and posttranslational modifications of the necrosome components, to the availability of molecular interaction partners and the localization of receptor-interacting serine/threonine-protein kinase 1 (RIPK1), receptor-interacting serine/threonineprotein kinase 3 (RIPK3) and mixed lineage kinase domain-like protein (MLKL). Accordingly, we classified the role of more than seventy molecules in necroptotic signaling based on consistent in vitro or in vivo evidence to understand the molecular background of necroptosis and to find opportunities where regulating the intensity and the modality of cell death could be exploited in clinical interventions. Necroptosis specific inhibitors are under development, but >20 drugs, already used in the treatment of various diseases, have the potential to regulate necroptosis. By listing necroptosis-modulated human diseases and cataloging the currently available drug-repertoire to modify necroptosis intensity, we hope to kick-start approaches with immediate translational potential. We also indicate where necroptosis regulating capacity should be considered in the current applications of these drugs. Facts • Necroptosis is closely associated with the pathogenesis of many human diseases. How effective can the off-label use of already approved drugs in necroptosis-driven diseases be?

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Diacerein protects against glycerol-induced acute kidney injury: Modulating oxidative stress, inflammation, apoptosis and necroptosis

Cited by 47 publications

References 36 publications

Using Green Biosynthesized Lycopene-Coated Selenium Nanoparticles to Rescue Renal Damage in Glycerol-Induced Acute Kidney Injury in Rats

Using Green Biosynthesized Lycopene-Coated Selenium Nanoparticles to Rescue Renal Damage in Glycerol-Induced Acute Kidney Injury in Rats

The role of RIPK3‐regulated cell death pathways and necroptosis in the pathogenesis of cardiac ischaemia‐reperfusion injury

Current translational potential and underlying molecular mechanisms of necroptosis

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