Postconditioning with repeated mild hypoxia protects neonatal hypoxia-ischemic rats against brain damage and promotes rehabilitation of brain function

Deng, Qingqing; Chang, Yanqun; Cheng, Xiaomao; Luo, Xingang; Zhang, Jing; Tang, Xiaoyuan

doi:10.1016/j.brainresbull.2018.02.006

Cited by 13 publications

(9 citation statements)

References 26 publications

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“…For instance, LPS was found to reduce infarct volume following middle cerebral artery occlusion ( Sardari et al, 2020 ). Postconditioning with repeated mild hypoxia promotes brain rehabilitation and protects neonatal hypoxia-ischemic rats from brain damage ( Deng et al, 2018 ). LPS preconditioning protects against organ damage following ischemic reperfusion in cardiorenal and brain tissues ( Ha et al, 2008 ; Vartanian et al, 2011 ; He et al, 2018 ).…”

Section: Discussionmentioning

confidence: 99%

Preeclamptic programming unevenly perturbs inflammatory and renal vasodilatory outcomes of endotoxemia in rat offspring: modulation by losartan and pioglitazone

et al. 2023

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Introduction: Preeclampsia (PE) enhances the vulnerability of adult offspring to serious illnesses. The current study investigated whether preeclamptic fetal programming impacts hemodynamic and renal vasodilatory disturbances in endotoxic adult offspring and whether these interactions are influenced by antenatal therapy with pioglitazone and/or losartan.Methods: PE was induced by oral administration of L-NAME (50 mg/kg/day) for the last 7 days of pregnancy. Adult offspring was treated with lipopolysaccharides (LPS, 5 mg/kg) followed 4-h later by hemodynamic and renovascular studies.Results: Tail-cuff measurements showed that LPS decreased systolic blood pressure (SBP) in male, but not female, offspring of PE dams. Moreover, PE or LPS reduced vasodilations elicited by acetylcholine (ACh, 0.01–7.29 nmol) or N-ethylcarboxamidoadenosine (NECA, 1.6–100 nmol) in perfused kidneys of male rats only. The latter effects disappeared in LPS/PE preparations, suggesting a postconditioning action for LPS against renal manifestation of PE. Likewise, elevations caused by LPS in serum creatinine and inflammatory cytokines (TNFα and IL-1β) as well as in renal protein expression of monocyte chemoattractant protein-1 (MCP-1) and AT1 receptors were attenuated by the dual PE/LPS challenge. Gestational pioglitazone or losartan reversed the attenuated ACh/NECA vasodilations in male rats but failed to modify LPS hypotension or inflammation. The combined gestational pioglitazone/losartan therapy improved ACh/NECA vasodilations and eliminated the rises in serum IL-1β and renal MCP-1 and AT1 receptor expressions.Conclusion: Preeclamptic fetal programming of endotoxic hemodynamic and renal manifestations in adult offspring depends on animal sex and specific biological activity and are reprogrammed by antenatal pioglitazone/losartan therapy.

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Section: Discussionmentioning

confidence: 99%

Preeclamptic programming unevenly perturbs inflammatory and renal vasodilatory outcomes of endotoxemia in rat offspring: modulation by losartan and pioglitazone

et al. 2023

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“…Since recent studies indicated that hypoxia stimulates astrocytes to secrete HIF‐1α, exerts a neuroprotective effect and promotes neural functional recovery, 31 for which VEGF is a downstream target gene that stimulates angiogenesis, maintains blood supply, and participates in neuroplasticity and brain neurological functional recovery, 32 we further investigated whether zinc mediated the HIF‐1α/VEGF pathway during ischemic repair in vivo and in vitro. Our cellular experiment found that the expression of HIF‐1α is increased in astrocytes after OGD treatments.…”

Section: Discussionmentioning

confidence: 99%

Zinc improves neurological recovery by promoting angiogenesis via the astrocyte‐mediated HIF‐1α/VEGF signaling pathway in experimental stroke

Zhu

et al. 2022

CNS Neurosci Ther

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“…Stroke is a leading cause of disability in adults, resulting in social and economic burdens worldwide [81,82]. Numerous attempts [1,2,13,[83][84][85][86][87][88][89][90][91][92][93][94] have been made to reveal the pathological mechanisms underlying cerebral ischemia and to design new drugs [2,[95][96][97][98][99] that reduce the effects of complications due to stroke [100][101][102]. Because all of the pharmacological interventions that have been tested to date have failed, new targets for novel therapies are needed.…”

Section: Discussionmentioning

confidence: 99%

Roles Played by the Na+/Ca2+ Exchanger and Hypothermia in the Prevention of Ischemia-Induced Carrier-Mediated Efflux of Catecholamines into the Extracellular Space: Implications for Stroke Therapy

et al. 2019

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The release of [ 3 H]dopamine ([ 3 H]DA) and [ 3 H]noradrenaline ([ 3 H]NA) in acutely perfused rat striatal and cortical slice preparations was measured at 37 °C and 17 °C under ischemic conditions. The ischemia was simulated by the removal of oxygen and glucose from the Krebs solution. At 37 °C, resting release rates in response to ischemia were increased; in contrast, at 17 °C, resting release rates were significantly reduced, or resting release was completely prevented. The removal of extracellular Ca 2+ further increased the release rates of [ 3 H]DA and [ 3 H]NA induced by ischemic conditions. This finding indicated that the Na + /Ca 2+ exchanger (NCX), working in reverse in the absence of extracellular Ca 2+ , fails to trigger the influx of Ca 2+ in exchange for Na + and fails to counteract ischemia by further increasing the intracellular Na + concentration ([Na + ] i ). KB-R7943, an inhibitor of NCX, significantly reduced the cytoplasmic resting release rate of catecholamines under ischemic conditions and under conditions where Ca 2+ was removed. Hypothermia inhibited the excessive release of [ 3 H] DA in response to ischemia, even in the absence of Ca 2+ . These findings further indicate that the NCX plays an important role in maintaining a high [Na + ] i , a condition that may lead to the reversal of monoamine transporter functions; this effect consequently leads to the excessive cytoplasmic tonic release of monoamines and the reversal of the NCX. Using HPLC combined with scintillation spectrometry, hypothermia, which enhances the stimulation-evoked release of DA, was found to inhibit the efflux of toxic DA metabolites, such as 3,4-dihydroxyphenylacetaldehyde (DOPAL). In slices prepared from human cortical brain tissue removed during elective neurosurgery, the uptake and release values for [ 3 H]NA did not differ from those measured at 37 °C in slices that were previously maintained under hypoxic conditions at 8 °C for 20 h. This result indicates that hypothermia preserves the functions of the transport and release mechanisms, even under hypoxic conditions. Oxidative stress (H 2 O 2 ), a mediator of ischemic brain injury enhanced the striatal resting release of [ 3 H]DA and its toxic metabolites (DOPAL, quinone). The study supports our earlier findings that during ischemia transmitters are released from the cytoplasm. In addition, the major findings of this study that hypothermia of brain slice preparations prevents the extracellular calcium concentration ([Ca 2+ ] o )-independent non-vesicular transmitter release induced by ischemic insults, inhibiting Na + /Cl − -dependent membrane transport of monoamines and their toxic metabolites into the extracellular space, where they can exert toxic effects.

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Postconditioning with repeated mild hypoxia protects neonatal hypoxia-ischemic rats against brain damage and promotes rehabilitation of brain function

Cited by 13 publications

References 26 publications

Preeclamptic programming unevenly perturbs inflammatory and renal vasodilatory outcomes of endotoxemia in rat offspring: modulation by losartan and pioglitazone

Preeclamptic programming unevenly perturbs inflammatory and renal vasodilatory outcomes of endotoxemia in rat offspring: modulation by losartan and pioglitazone

Zinc improves neurological recovery by promoting angiogenesis via the astrocyte‐mediated HIF‐1α/VEGF signaling pathway in experimental stroke

Roles Played by the Na+/Ca2+ Exchanger and Hypothermia in the Prevention of Ischemia-Induced Carrier-Mediated Efflux of Catecholamines into the Extracellular Space: Implications for Stroke Therapy

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