Argon protects hypoxia-, cisplatin- and gentamycin-exposed hair cells in the newborn rat’s organ of Corti

Yarin, Yury M.; Amarjargal, Nyamaa; Fuchs, Julia; Haupt, H.; Mazurek, Birgit; Morozova, Svetlana V.; Gross, Johann

doi:10.1016/j.heares.2004.09.015

Cited by 39 publications

(38 citation statements)

References 53 publications

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“…Similar results have been reported in some animal studies [12,13]. These studies support the idea of a dose-dependent pattern of cisplatin-mediated damage [2,11,12].…”

Section: Introductionsupporting

confidence: 91%

Low, but Not High, Doses of Cisplatin Damage Cochlear Hair Cells in C57 Mouse Organotypic Cultures

Zeng

Xianlin²,

Chen³

et al. 2016

ORL

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Aims: The purpose of this study was to investigate the characteristics of cisplatin-induced C57 mouse cochlear hair cell damage in vitro. Methods: Forty-seven cochleae harvested from 2- to 4-day-old C57 mice were used. Forty specimens were treated with different concentrations of cisplatin (10, 25, 50, 100, 400, and 1,000 μmol/l) for 48 h. The remaining seven specimens were used as a control group. Results: The rate of hair cell loss increased from 14.5 to 78.4% over cisplatin concentrations of 10 to 100 μmol/l, whereas hair cell loss decreased to 48.8 and 8.77% at concentrations of 400 and 1,000 μmol/l, respectively. Apoptosis was detected by DAPI staining in the areas of hair cell damage. Hair cell loss rates differed significantly among the cisplatin-treated groups. Linear regression analysis of cisplatin dose versus hair cell number showed a significant negative correlation for cisplatin doses up to 100 μmol/l and a positive correlation with further increases up to 1,000 μmol/l. Conclusions: We conclude that cisplatin-induced hair cell damage was concentration dependent only up to a certain dose and that injury resistance may occur in cochlear cells treated with higher doses of cisplatin.

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“…Similar results have been reported in some animal studies [12,13]. These studies support the idea of a dose-dependent pattern of cisplatin-mediated damage [2,11,12].…”

Section: Introductionsupporting

confidence: 91%

Low, but Not High, Doses of Cisplatin Damage Cochlear Hair Cells in C57 Mouse Organotypic Cultures

Zeng

Xianlin²,

Chen³

et al. 2016

ORL

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“…It was reported that argon was protective against hypoxia-induced injury in cultured neurons 21,22 . In an in vivo model of acute focal cerebral ischaemia in adult rats, exposure to 50% argon significantly reduced infarct volumes and neurological deficits after the occlusion 23 .…”

Section: Discussionmentioning

confidence: 99%

Heme Oxygenase-1 Mediates Neuroprotection Conferred by Argon in Combination with Hypothermia in Neonatal Hypoxia–Ischemia Brain Injury

et al. 2016

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Background Hypoxic–ischemic encephalopathy is a major cause of mortality and disability in the newborn. The authors investigated the protective effects of argon combined with hypothermia on neonatal rat hypoxic–ischemic brain injury. Methods In in vitro studies, rat cortical neuronal cell cultures were challenged by oxygen and glucose deprivation for 90 min and exposed to 70% Ar or N2 with 5% CO2 balanced with O2, at 33°C for 2 h. Neuronal phospho-Akt, heme oxygenase-1 and phospho-glycogen synthase kinase-3β expression, and cell death were assessed. In in vivo studies, neonatal rats were subjected to unilateral common carotid artery ligation followed by hypoxia (8% O2 balanced with N2 and CO2) for 90 min. They were exposed to 70% Ar or N2 balanced with oxygen at 33°, 35°, and 37°C for 2 h. Brain injury was assessed at 24 h or 4 weeks after treatment. Results In in vitro studies, argon–hypothermia treatment increased phospho-Akt and heme oxygenase-1 expression and significantly reduced the phospho-glycogen synthase kinase-3β Tyr-216 expression, cytochrome C release, and cell death in oxygen–glucose deprivation–exposed cortical neurons. In in vivo studies, argon–hypothermia treatment decreased hypoxia/ischemia-induced brain infarct size (n = 10) and both caspase-3 and nuclear factor-κB activation in the cortex and hippocampus. It also reduced hippocampal astrocyte activation and proliferation. Inhibition of phosphoinositide-3-kinase (PI3K)/Akt pathway through LY294002 attenuated cerebral protection conferred by argon–hypothermia treatment (n = 8). Conclusion Argon combined with hypothermia provides neuroprotection against cerebral hypoxia–ischemia damage in neonatal rats, which could serve as a new therapeutic strategy against hypoxic–ischemic encephalopathy.

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“…Since then, different studies have demonstrated argon's protective effect on various cells and organs. This virtue has been proven for the sensory cells of the inner ear [4] and the retina [5] and for the neuronal cells of the cerebrum [6,7,8,9], as well as for individual organ functions including kidney and heart protection [10,11,12]. However, the underlying protective mechanisms are only partly understood.…”

Section: Introductionmentioning

confidence: 99%

“…To the best of our knowledge, the organ-protective effects of the noble gas argon on the liver have not yet been investigated. Based on the literature regarding argon's protective effect on various tissues [4,5,6,7,8,9,10,11,12], our a priori hypothesis was that argon inhalation 60 min prior to partial hepatectomy (70%) has a positive effect on LR in rats.…”

Section: Introductionmentioning

confidence: 99%

Argon Delays Initiation of Liver Regeneration after Partial Hepatectomy in Rats

et al. 2017

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Background: The liver can heal up to restitutio ad integrum following damage resulting from various causes. Different studies have demonstrated the protective effect of argon on various cells and organs. To the best of our knowledge, the organ-protective effects of the noble gas argon on the liver have not yet been investigated, although argon appears to influence signal paths that are well-known mediators of liver regeneration. We hypothesized that argon inhalation prior to partial hepatectomy (70%) has a positive effect on the initiation of liver regeneration in rats. Methods: Partial hepatectomy (70%) with or without inhaled argon (50 vol%) was performed for 1 h. Liver tissue was harvested after 3, 36, and 96 h to analyze the mRNA and protein expression of hepatocyte growth factor (HGF), interleukin-6 (IL-6), tumor necrosis factor-α, and extracellular signal-regulated kinase 1/2. Histological tissue samples were prepared for immunohistochemistry (bromodeoxyuridine [BrdU], Ki-67, and TUNEL) and blood was analyzed regarding the effects of argon on liver function. Statistical analyses were performed using 1-way ANOVA followed by the post hoc Tukey-Kramer test. Results: After 3 h, the primary outcome parameter of hepatocyte proliferation was significantly reduced with argon 50 vol% inhalation in comparison to nitrogen inhalation (BrdU: 15.7 ± 9.7 vs. 7.7 ± 3.1 positive cells/1,000 hepatocytes, p = 0.013; Ki-67: 17.6 ± 13.3 vs. 4.7 ± 5.4 positive cells/1,000 hepatocytes, p = 0.006). This was most likely mediated by significant downregulation of HGF (after 3 h: 5.2 ± 3.2 vs. 2.3 ± 1.0 fold, p = 0.032; after 96 h: 2.1 ± 0.5 vs. 1.3 ± 0.3 fold, p = 0.029) and IL-6 (after 3 h: 43.7 ± 39.6 vs. 8.5 ± 9.2 fold, p = 0.032). Nevertheless, we could detect no significant effect on the weight of the residual liver, liver-body weight ratio, or liver blood test results after argon inhalation. Conclusion: Impairment of liver regeneration was apparent after argon 50 vol% inhalation that was most probably mediated by downregulation of HGF and IL-6 in the initial phase. However, the present study was not adequately powered to prove that argon has detrimental effects on the liver. Further studies are needed to evaluate the effects of argon on livers with preexisting conditions as well as on ischemia-reperfusion models.

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Argon protects hypoxia-, cisplatin- and gentamycin-exposed hair cells in the newborn rat’s organ of Corti

Cited by 39 publications

References 53 publications

Low, but Not High, Doses of Cisplatin Damage Cochlear Hair Cells in C57 Mouse Organotypic Cultures

Low, but Not High, Doses of Cisplatin Damage Cochlear Hair Cells in C57 Mouse Organotypic Cultures

Heme Oxygenase-1 Mediates Neuroprotection Conferred by Argon in Combination with Hypothermia in Neonatal Hypoxia–Ischemia Brain Injury

Argon Delays Initiation of Liver Regeneration after Partial Hepatectomy in Rats

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