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Kaliman, P A; Strel'chenko, E. V.; Nikitchenko, Irina V.; Филимоненко, В. П.

doi:10.1023/a:1023485626795

Cited by 3 publications

(3 citation statements)

References 7 publications

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“…This is consistent with the finding in mice that are exposed to endotoxin, a TLR-4 ligand, which also leads to an increase HO-1 expression in the S1 tubules as well is in response to cisplatin-induced and HgCl 2 nephrotoxicity [43], [44]. It has also been shown that mitochondrial targeted HO-1 decreases oxidant stress in renal epithelial cell and prevents excessive heme accumulation and ROS generation in vitro [45].…”

Section: Discussionsupporting

confidence: 89%

Staphylococcus aureus Sepsis Induces Early Renal Mitochondrial DNA Repair and Mitochondrial Biogenesis in Mice

Bartz

Suliman

et al. 2014

PLoS ONE

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Acute kidney injury (AKI) contributes to the high morbidity and mortality of multi-system organ failure in sepsis. However, recovery of renal function after sepsis-induced AKI suggests active repair of energy-producing pathways. Here, we tested the hypothesis in mice that Staphyloccocus aureus sepsis damages mitochondrial DNA (mtDNA) in the kidney and activates mtDNA repair and mitochondrial biogenesis. Sepsis was induced in wild-type C57Bl/6J and Cox-8 Gfp-tagged mitochondrial-reporter mice via intraperitoneal fibrin clots embedded with S. aureus. Kidneys from surviving mice were harvested at time zero (control), 24, or 48 hours after infection and evaluated for renal inflammation, oxidative stress markers, mtDNA content, and mitochondrial biogenesis markers, and OGG1 and UDG mitochondrial DNA repair enzymes. We examined the kidneys of the mitochondrial reporter mice for changes in staining density and distribution. S. aureus sepsis induced sharp amplification of renal Tnf, Il-10, and Ngal mRNAs with decreased renal mtDNA content and increased tubular and glomerular cell death and accumulation of protein carbonyls and 8-OHdG. Subsequently, mtDNA repair and mitochondrial biogenesis was evidenced by elevated OGG1 levels and significant increases in NRF-1, NRF-2, and mtTFA expression. Overall, renal mitochondrial mass, tracked by citrate synthase mRNA and protein, increased in parallel with changes in mitochondrial GFP-fluorescence especially in proximal tubules in the renal cortex and medulla. Sub-lethal S. aureus sepsis thus induces widespread renal mitochondrial damage that triggers the induction of the renal mtDNA repair protein, OGG1, and mitochondrial biogenesis as a conspicuous resolution mechanism after systemic bacterial infection.

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Section: Discussionsupporting

confidence: 89%

Staphylococcus aureus Sepsis Induces Early Renal Mitochondrial DNA Repair and Mitochondrial Biogenesis in Mice

Bartz

Suliman

et al. 2014

PLoS ONE

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“…However, interestingly enough, GSH levels, functioning through glutathione and a marker of antioxidant defence, did not significantly change in the MAKI group. Kaliman et al ( 27 ) reported that in the kidney, the GSH levels were significantly reduced 2 hours after glycerol injection in the MAKI group compared to the control group. However, this increase was not significant at hours 6 and 24.…”

Section: Discussionmentioning

confidence: 99%

The Effects of Baicalin on Myoglobinuric Acute Renal Failure in Rats

Yavuz¹,

Aydoğdu²,

Taştekin³

et al. 2018

Balkan Med J

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Background:Myoglobinuric acute kidney injury is a uremic syndrome that develops due to damage of skeletal muscle. Free radicals and nitric oxide play an important role in the pathogenesis of myoglobinuric acute kidney injury. Baicalin has multiple bioactivities, including antimicrobial, anti-inflammatory and antioxidant properties and is a potent free radical scavenger.Aims:To investigate the nephroprotective mechanism of baicalin on myoglobinuric acute kidney injury.Study Design:Animal experimentation.Methods:In our study, male Sprague Dawley rats were divided into 4 groups. Control (n=8), Baicalin (n=8), myoglobinuric acute kidney injury (n=10) and myoglobinuric acute kidney injury + baicalin (n=10). The rats were deprived of water for 24 hours before receiving intramuscular injection. The control and baicalin groups were injected intramuscularly with saline (8 ml/kg), and the myoglobinuric acute kidney injury and myoglobinuric acute kidney injury + baicalin groups were given 50% glycerol 8 ml/kg. One hour later, the control and myoglobinuric acute kidney injury groups received saline intraperitoneally, and the baicalin and myoglobinuric acute kidney injury + baicalin groups were given 200 mg/kg baicalin. Twenty-four hours after the glycerol injection, urine and blood samples were taken, and the kidneys of the rats were harvested under intraperitoneally injections of anaesthesia.Results:We found that the levels of creatinine, urea, nitric oxide, alanine transaminase, aspartate aminotransferase, creatine kinase in serum samples, malondialdehyde, nitric oxide, inducible nitric oxide synthase, and endothelial nitric oxide synthase concentrations in renal tissue were increased in the myoglobinuric acute kidney injury group compared with the control group (p<0.05). The nitric oxide and glutathione levels in the kidney were significantly decreased in the myoglobinuric acute kidney injury + baicalin group compared with the myoglobinuric acute kidney injury group (p<0.05). There were no significant differences between any other parameters.Conclusion:Our results did not show any protective effect of baicalin on myoglobinuric acute kidney injury, possibly because the different effective factors in the pathogenesis of experimental myoglobinuric acute kidney injury used in this experiment deviate from other experimental models. Moreover, detailed studies are needed to clarify the effects of baicalin in different doses and treatment durations in glycerol-induced acute kidney injury model.

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“…The first anti-inflammatory effects of HO-1 were observed in a rat model of rhabdomyolysis, and this was followed by evidence of protection in a model of lethal endotoxic shock where HO-1 expression was induced by the administration of heme [40, 41]. Similarly, low concentrations of CO were equally protective in rats and mice, mimicking HO-1 activity and ushering in the application of CO, beyond what was historically recognized as toxic [7, 42].…”

Section: Effects Of Ho-1 and Carbon Monoxide On The Innate Immune Resmentioning

confidence: 99%

The social network of carbon monoxide in medicine

Węgiel

Hanto

Otterbein

2013

Trends in Molecular Medicine

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Networking between cells is critical for proper functioning of the cellular milieu and is mediated by cascades of highly regulated and overlapping signaling molecules. The enzyme heme oxygenase-1 (HO-1) generates three separate signaling molecules through the catalysis of heme – carbon monoxide (CO), biliverdin, and iron – each of which acts via distinct molecular targets to influence cell function, both proximally and distally. This review focuses on state-of-the art developments and insights into the impact of HO-1 and CO on the innate immune response, the effects of which are responsible for an ensemble of functions that help regulate complex immunologic responses to bacterial sepsis and ischemia/reperfusion injury. HO-1 exemplifies an evolutionarily conserved system necessary for the cellular milieu to adapt appropriately, function properly, and ensure survival of the organism.

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Untitled

Cited by 3 publications

References 7 publications

Staphylococcus aureus Sepsis Induces Early Renal Mitochondrial DNA Repair and Mitochondrial Biogenesis in Mice

Staphylococcus aureus Sepsis Induces Early Renal Mitochondrial DNA Repair and Mitochondrial Biogenesis in Mice

The Effects of Baicalin on Myoglobinuric Acute Renal Failure in Rats

The social network of carbon monoxide in medicine

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