Helium preconditioning protects against neonatal hypoxia–ischemia via nitric oxide mediated up-regulation of antioxidases in a rat model

Li, Y.; Liu, K.; Kang, Zhiming; Sun, Xuejun; Liu, W.W.; Mao, Yanfei

doi:10.1016/j.bbr.2015.12.001

Cited by 25 publications

(15 citation statements)

References 32 publications

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“…This apparent paradox may be explained partially by the documented protective effects of helium on the endothelium. 22 Given the increased levels of these two pro-in ammatory chemokines after RDScontrolled dives, we conclude that the RDS ascent pro le caused a worsening in diver in ammation compared with the CDM ascent pro le. This ts with the chamber evidence of no advantage to deeper stops.…”

Section: Discussionmentioning

confidence: 70%

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et al. 2017

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Section: Discussionmentioning

confidence: 70%

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et al. 2017

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“…Another pathway that may affect recovery is free radical production, increases in which are associated with greater neurological injury after HI 53 . Physiological increases in free radicals such as reactive oxygen species (ROS) are also associated with increased mitochondrial function and improved cellular antioxidant status, at least in part through activation of nuclear factor (erythroid-2)-related factor 2 (Nrf2), which has been shown to be involved in the mechanism of multiple neuroprotective strategies 54 55 56 57 . While HT is generally thought to suppress production of ROS, deeper HT may increase ROS production, as well as inhibit ROS clearance due to slower enzyme kinetics 45 54 58 .…”

Section: Discussionmentioning

confidence: 99%

Treatment temperature and insult severity influence the neuroprotective effects of therapeutic hypothermia

Wood

Osredkar

Puchades

et al. 2016

Sci Rep

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Therapeutic hypothermia (HT) is standard care for moderate and severe neonatal hypoxic-ischaemic encephalopathy (HIE), the leading cause of permanent brain injury in term newborns. However, the optimal temperature for HT is still unknown, and few preclinical studies have compared multiple HT treatment temperatures. Additionally, HT may not benefit infants with severe encephalopathy. In a neonatal rat model of unilateral hypoxia-ischaemia (HI), the effect of five different HT temperatures was investigated after either moderate or severe injury. At postnatal-day seven, rat pups underwent moderate or severe HI followed by 5 h at normothermia (37 °C), or one of five HT temperatures: 33.5 °C, 32 °C, 30 °C, 26 °C, and 18 °C. One week after treatment, neuropathological analysis of hemispheric and hippocampal area loss, and CA1 hippocampal pyramidal neuron count, was performed. After moderate injury, a significant reduction in hemispheric and hippocampal loss on the injured side, and preservation of CA1 pyramidal neurons, was seen in the 33.5 °C, 32 °C, and 30 °C groups. Cooling below 33.5 °C did not provide additional neuroprotection. Regardless of treatment temperature, HT was not neuroprotective in the severe HI model. Based on these findings, and previous experience translating preclinical studies into clinical application, we propose that milder cooling should be considered for future clinical trials.

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“…The contralateral hemisphere, exposed to hypoxia, is often used for normalization of ipsilateral lesion volume (Nijboer et al, 2007; Fan et al, 2013) and not assessed for cell death (Carloni et al, 2012; Thatipamula et al, 2015; Li et al, 2016). Studies from our group (Waddell et al, 2016; Demarest et al, 2016; Xu et al, 2015) and others (Smith et al, 2016) clearly demonstrate that neuropathology occurs in the contralateral side of brain after HI.…”

Section: Discussionmentioning

confidence: 99%

Sex-dependent mitophagy and neuronal death following rat neonatal hypoxia–ischemia

et al. 2016

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Males are more susceptible than females to long-term cognitive deficits following neonatal hypoxic-ischemic encephalopathy (HIE). Mitochondrial dysfunction is implicated in the pathophysiology of cerebral hypoxia–ischemia (HI), but the influence of sex on mitochondrial quality control (MQC) after HI is unknown. Therefore, we tested the hypothesis that mitophagy is sexually dimorphic and neuroprotective 20–24 h following the Rice–Vannucci model of rat neonatal HI at postnatal day 7 (PN7). Mitochondrial and lysosomal morphology and degree of co-localization were determined by immunofluorescence in the cerebral cortex. No difference in mitochondrial abundance was detected in the cortex after HI. However, net mitochondrial fission increased in both hemispheres of female brain, but was most extensive in the ipsilateral hemisphere of male brain following HI. Basal autophagy, assessed by immunoblot for the autophagosome marker LC3BI/II, was greater in males suggesting less intrinsic reserve capacity for autophagy following HI. Autophagosome formation, lysosome size, and TOM20/LAMP2 co-localization were increased in the contralateral hemisphere following HI in female, but not male brain. An accumulation of ubiquitinated mitochondrial protein was observed in male, but not female brain following HI. Moreover, neuronal cell death with NeuN/TUNEL co-staining occurred in both hemispheres of male brain, but only in the ipsilateral hemisphere of female brain after HI. In summary, mitophagy induction and neuronal cell death are sex dependent following HI. The deficit in elimination of damaged/dysfunctional mitochondria in the male brain following HI may contribute to male vulnerability to neuronal death and long-term neurobehavioral deficits following HIE.

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Helium preconditioning protects against neonatal hypoxia–ischemia via nitric oxide mediated up-regulation of antioxidases in a rat model

Cited by 25 publications

References 32 publications

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Treatment temperature and insult severity influence the neuroprotective effects of therapeutic hypothermia

Sex-dependent mitophagy and neuronal death following rat neonatal hypoxia–ischemia

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