N-acetylcysteine reduces the renal oxidative stress and apoptosis induced by hemorrhagic shock

Moreira, Miriam Aparecida; Irigoyen, Maria Cláudia; Saad, Karen Ruggeri; Saad, Paulo Fernandes; Koike, Márcia Kiyomi; Montero, Edna Frasson de Souza; Martins, José Luiz

doi:10.1016/j.jss.2016.02.020

Cited by 22 publications

(23 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Thus, it is expected that NAC may reduce excessive oxidative damage produced in the kidneys by both BPA and IR through scavenging the free radicals and replenishing the depleted cellular antioxidants. Consistent with the current study, NAC has been reported to be effective at attenuating or minimizing oxidative stress as well as enhancing the overall redox status inside the cell under various oxidant‐derived disorders, including ischemia and reperfusion . The role of NAC in reducing cognitive dysfunction after exposure to BPA by its antioxidant capacity has also been demonstrated …”

Section: Resultssupporting

confidence: 88%

“…*p < .05 between groups well as enhancing the overall redox status inside the cell under various oxidant-derived disorders, including ischemia and reperfusion. 12,28 The role of NAC in reducing cognitive dysfunction after exposure to BPA by its antioxidant capacity has also been demonstrated. 14 At this point, it is most likely that antioxidant properties of NAC are one of the main mechanisms by which it exerts protective effects in the current study.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Bisphenol A aggravates renal ischemia–reperfusion injury by disrupting mitochondrial homeostasis and N‐acetylcysteine mitigates the injurious outcomes

et al. 2019

View full text Add to dashboard Cite

Exposure to bisphenol A (BPA), a chemical generally used in consumer products, becomes a global public health concern, as humans are increasingly exposed through their daily consuming activities. Renal ischemia–reperfusion (RIR) is the major cause of acute kidney injury with high prevalence and increased long‐term risks for multiple comorbidities and mortality. As the kidney is susceptible to these conditions, we explored whether the outcomes following the RIR episode could be influenced by BPA exposure, and investigated the therapeutic possibility by N‐acetylcysteine (NAC) including the mechanisms involved. Three groups of male Wistar rats were fed with vehicle, BPA 5, and 50 mg/kg, respectively, for five consecutive weeks then underwent the sham operation. Three other groups with identical treatment underwent bilateral renal IR induction (45‐min ischemia followed by 24‐hr reperfusion). An additional RIR group was treated with BPA 50 plus NAC 100 mg/kg. BPA‐exposed rats that encountered RIR episode showed dose‐dependent worsening of RIR injury as evidenced by augmentations of renal dysfunction and histopathological abnormalities, oxidative stress, apoptosis, mitochondrial functional impairment, mitochondrial dynamic, and mitophagy disproportion compared with the vehicle‐exposed RIR group. The NAC therapy considerably attenuated the exacerbated effects of BPA, which was associated with increased AMP‐activated protein kinase (AMPK), PGC‐1α, silent information regulator 3 or sirtuin 3 (SIRT3), and mitofusin 2 (MFN2) expressions but decreased Phosphorylated dynamin‐related protein 1 (p‐DRP1)/Dynamin‐related protein 1 (DRP1), PTEN‐induced putative kinase (PINK), and PARKIN expressions. These findings reveal the detrimental effect of repeated BPA exposure on the renal outcomes following the IR episode, and further demonstrate the protective efficacy of NAC by maintaining mitochondrial homeostasis, which is, partly, mediated through the AMPK‐PGC‐1α‐SIRT3 axis.

show abstract

Section: Resultssupporting

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Bisphenol A aggravates renal ischemia–reperfusion injury by disrupting mitochondrial homeostasis and N‐acetylcysteine mitigates the injurious outcomes

et al. 2019

View full text Add to dashboard Cite

show abstract

“…N-acetylcysteine (NAC) is a widely used antioxidant drug whose metabolism results in an increase in intracellular glutathione that produces sulfhydryl groups directly eliminating ROS [35, 36]. Our results showed that in contrast with the decrease in ROS expression and the reduction in MDA concentration, the decreased activity of SOD was restored by NAC in SCIR injury (Figures 1(a), 1(b), and 1(c)).…”

Section: Resultsmentioning

confidence: 74%

Hydrogen Sulfide Inhibits Autophagic Neuronal Cell Death by Reducing Oxidative Stress in Spinal Cord Ischemia Reperfusion Injury

Xie

Yang

et al. 2017

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Autophagy is upregulated in spinal cord ischemia reperfusion (SCIR) injury; however, its expression mechanism is largely unknown; moreover, whether autophagy plays a neuroprotective or neurodegenerative role in SCIR injury remains controversial. To explore these issues, we created an SCIR injury rat model via aortic arch occlusion. Compared with normal controls, autophagic cell death was upregulated in neurons after SCIR injury. We found that autophagy promoted neuronal cell death during SCIR, shown by a significant number of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling- (TUNEL-) positive cells colabeled with the autophagy marker microtubule-associated protein 1 light chain 3, while the autophagy inhibitor 3-methyladenine reduced the number of TUNEL-positive cells and restored neurological and motor function. Additionally, we showed that oxidative stress was the main trigger of autophagic neuronal cell death after SCIR injury and N-acetylcysteine inhibited autophagic cell death and restored neurological and motor function in SCIR injury. Finally, we found that hydrogen sulfide (H2S) inhibited autophagic cell death significantly by reducing oxidative stress in SCIR injury via the AKT-the mammalian target of rapamycin (mTOR) pathway. These findings reveal that oxidative stress induces autophagic cell death and that H2S plays a neuroprotective role by reducing oxidative stress in SCIR.

show abstract

“…Given the specificity in structure and function of the kidney, renal IRI commonly occurs and is associated with many complex clinical conditions, such as hemorrhagic shock [2], renal transplantation [3], and acute renal failure [4]. Pathogenic studies have shown that apoptosis plays a vital role in renal IRI and is reduced by an imbalance in scavenging and generation of reactive oxygen species (ROS) [5, 6], but the related mechanism is poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Curcumin-carrying nanoparticles prevent ischemia-reperfusion injury in human renal cells

Jiang

et al. 2016

Oncotarget

View full text Add to dashboard Cite

Renal ischemia-reperfusion injury (IRI) is a major complication in clinical practice. However, despite its frequency, effective preventive/treatment strategies for this condition are scarce. Curcumin possesses antioxidant properties and is a promising potential protective agent against renal IRI, but its poor water solubility restricts its application. In this study, we constructed curcumin-carrying distearoylphosphatidylethanolamine-polyethylene glycol nanoparticles (Cur-NPs), and their effect on HK-2 cells exposed to IRI was examined in vitro. Curcumin encapsulated in NPs demonstrated improved water solubility and slowed release. Compared with the IRI and Curcumin groups, Cur-NP groups displayed significantly improved cell viability, downregulated protein expression levels of caspase-3 and Bax, upregulated expression of Bcl-2 protein, increased antioxidant superoxide dismutase level, and reduced apoptotic rate, reactive oxygen species level, and malondialdehyde content. Results clearly showed that Cur-NPs demonstrated good water solubility and slow release, as well as exerted protective effects against oxidative stress in cultured HK-2 cells exposed to IRI.

show abstract

N-acetylcysteine reduces the renal oxidative stress and apoptosis induced by hemorrhagic shock

Cited by 22 publications

References 33 publications

Bisphenol A aggravates renal ischemia–reperfusion injury by disrupting mitochondrial homeostasis and N‐acetylcysteine mitigates the injurious outcomes

Bisphenol A aggravates renal ischemia–reperfusion injury by disrupting mitochondrial homeostasis and N‐acetylcysteine mitigates the injurious outcomes

Hydrogen Sulfide Inhibits Autophagic Neuronal Cell Death by Reducing Oxidative Stress in Spinal Cord Ischemia Reperfusion Injury

Curcumin-carrying nanoparticles prevent ischemia-reperfusion injury in human renal cells

Contact Info

Product

Resources

About