Neuroprotective effect of magnesium sulfate and dexamethasone on intrauterine ischemia in the fetal rat brain: ultrastructural evaluation

Hastürk, Aşkın Esen; Harman, Ferhat; Arca, Turkan; Sargon, Mustafa F.; Kılınç, Kamer; Kaptanoğlu, Erkan

doi:10.5137/1019-5149.jtn.8541-13.1

Cited by 8 publications

(9 citation statements)

References 19 publications

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“…Coronal sections (50–150 μ m) were cut with a vibratome (UC7; Leica EM, Solms, Germany). Sections were used to observe dopaminergic neuron morphology under a transmission electron microscope (H‐7650, Hitachi, Troy, MI, USA) as previously described …”

Section: Methodsmentioning

confidence: 99%

β‐asarone and levodopa co‐administration protects against 6‐hydroxydopamine‐induced damage in parkinsonian rat mesencephalon by regulating autophagy: down‐expression Beclin‐1 and light chain 3B and up‐expression P62

Huang

Deng

et al. 2015

Clin Exp Pharma Physio

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In this study, we investigated Beclin-1, light chain (LC)3B, and p62 expression in 6-hydroxydopamine (6-OHDA)-induced parkinsonian rats after β-asarone and levodopa (l-dopa) co-administration. Unilateral 6-OHDA injection into the medial forebrain bundle was used to create the models, except in sham-operated rats. Rats were divided into eight groups: sham-operated group; 6-OHDA model group; madopar group (75 mg/kg, per os (p.o.)); l-dopa group (60 mg/kg, p.o.); β-asarone group (15 mg/kg, p.o.); β-asarone + l-dopa co-administered group (15 mg/kg + 60 mg/kg, p.o.); 3-methyladenine group (500 nmol, intraperitoneal injection); and rapamycin group (1 mg/kg, intraperitoneal injection). Then, Beclin-1, LC3B, and p62 expression in the mesencephalon were detected. The mesencephalon was also observed by transmission electron microscope. The results showed that Beclin-1 and LC3B expression decreased and that p62 expression increased significantly in the madopar, l-dopa, β-asarone, and co-administered groups when compared with the 6-OHDA model. Beclin-1 and LC3B expression in the β-asarone and co-administered groups were less than in the madopar or l-dopa groups, whereas p62 expression in the β-asarone and co-administered groups was higher than in the madopar or l-dopa groups. In addition, a significant decrease in autophagosome was exhibited in the β-asarone and co-administered groups when compared with the 6-OHDA group. Our findings indicate that Beclin-1 and LC3B expression decreased, whereas p62 expression increased after co-administration treatment. In sum, all data suggest that the co-administration of β-asarone and l-dopa may contribute to the treatment of 6-OHDA-induced damage in rats by inhibiting autophagy activity.

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Section: Methodsmentioning

confidence: 99%

β‐asarone and levodopa co‐administration protects against 6‐hydroxydopamine‐induced damage in parkinsonian rat mesencephalon by regulating autophagy: down‐expression Beclin‐1 and light chain 3B and up‐expression P62

Huang

Deng

et al. 2015

Clin Exp Pharma Physio

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“…These drugs inhibit the synthesis of almost all known cytokines and cell surface molecules required for immune function and suppress the activity of nuclear factor kappa B (NF‐κB) . Several reports have recently demonstrated that systemic corticosteroid administration might have a protective effect against I/R injury in several organs, including the liver, kidney and brain, via through the immunosuppressive functions of corticosteroid . Based on these findings, we speculate that the application of corticosteroid would protect against the development of a PU after cutaneous I/R in mice.…”

Section: Introductionmentioning

confidence: 74%

Topical betamethasone butyrate propionate exacerbates pressure ulcers after cutaneous ischemia–reperfusion injury

Uchiyama

Yamada

Perera

et al. 2016

Experimental Dermatology

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Ischaemia-reperfusion (I/R) is involved in the development of various organ diseases. There has been increasing evidence that cutaneous I/R injury is associated with the pathogenesis of pressure ulcers (PUs), especially at the early stage presenting as non-blanchable erythema. However, there is no evidence-based treatment for early-stage PUs. Our objective was to assess the effects of topical steroid on the development of PUs after cutaneous I/R injury in mice. Cutaneous I/R was performed by trapping the dorsal skin between two magnetic plates for 12 h, followed by plate removal. Topical application of betamethasone butyrate propionate (BBP) in I/R areas significantly increased the size of PUs after I/R. The number of thromboses was increased, and CD31(+) vessels were decreased in the I/R area treated with topical BBP. The number of oxidative stress-associated DNA-damaged cells and apoptotic cells in the I/R area was increased by topical BBP treatment. In addition, the mRNA level of NADPH oxidase 4 (Nox4), the essential enzyme that produces reactive oxygen species, was significantly increased and that of NF-E2-related factor 2 (Nrf2), a transcription factor that regulates the expression of antioxidant proteins, was inhibited in the I/R area treated by BBP. The number of CD68(+) macrophages and the level of transforming growth factor-beta in lesional skin were also decreased by BBP. These results suggest that a topical steroid might accelerate the formation of PUs induced by cutaneous I/R injury by aggravating oxidative stress-induced tissue damage. Topical steroids might not be recommended for the treatment of acute-phase decubitus ulcers.

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“…Prevented ↑ lipid peroxidation induced by ischemia 30 min after reperfusion. (continued on next page) reduced lipid peroxidation and mitochondrial damage induced by transient occlusion of utero-ovarian arteries 60 min after reperfusion (Hasturk et al, 2013). Overall, such studies suggest that maternal MgSO4 treatment may act through distinct mechanisms, especially by inhibiting oxidative stress, and could also be used to prevent HI damage in addition to being an efficient prophylactic therapy for infants at risk of prematurity.…”

Section: Male and Femalementioning

confidence: 93%

“…MgSO 4 , used as a preventive treatment, has anti‐oxidant properties in a model of maternal hypoxia by reducing free radicals overproduction in term fetuses brains of guinea pigs (Maulik et al, 1999), and decreases lipid peroxidation 30 min after reperfusion following bilateral occlusion of utero‐ovarian arteries in rats (Solaroglu et al, 2011). In a similar model, maternal MgSO 4 treatment associated to dexamethasone reduced lipid peroxidation and mitochondrial damage induced by transient occlusion of utero‐ovarian arteries 60 min after reperfusion (Hasturk et al, 2013). Overall, such studies suggest that maternal MgSO4 treatment may act through distinct mechanisms, especially by inhibiting oxidative stress, and could also be used to prevent HI damage in addition to being an efficient prophylactic therapy for infants at risk of prematurity.…”

Section: Pharmacological Agentsmentioning

confidence: 99%

Pregnancy as a valuable period for preventing hypoxia‐ischemia brain damage

Netto

Sanches

Odorcyk

et al. 2018

Intl J of Devlp Neuroscience

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Neonatal brain Hypoxia-Ischemia (HI) is one of the major causes of infant mortality and lifelong neurological disabilities. The knowledge about the physiopathological mechanisms involved in HI lesion have increased in recent years, however these findings have not been translated into clinical practice. Current therapeutic approaches remain limited; hypothermia, used only in term or near-term infants, is the golden standard. Epidemiological evidence shows a link between adverse prenatal conditions and increased risk for diseases, health problems, and psychological outcomes later in life, what makes pregnancy a relevant period for preventing future brain injury. Here, we review experimental literature regarding preventive interventions used during pregnancy, i.e., previous to the HI injury, encompassing pharmacological, nutritional and/or behavioral strategies. Literature review used PubMed database. A total of forty one studies reported protective properties of maternal treatments preventing perinatal hypoxia-ischemia injury in rodents. Pharmacological agents and dietary supplementation showed mainly anti-excitotoxicity, anti-oxidant or anti-apoptotic properties. Interestingly, maternal preconditioning, physical exercise and environmental enrichment seem to engage the same referred mechanisms in order to protect neonatal brain against injury. This construct must be challenged by further studies to clearly define the main mechanisms responsible for neuroprotection to be explored in experimental context, as well as to test their potential in clinical settings.

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Neuroprotective effect of magnesium sulfate and dexamethasone on intrauterine ischemia in the fetal rat brain: ultrastructural evaluation

Cited by 8 publications

References 19 publications

β‐asarone and levodopa co‐administration protects against 6‐hydroxydopamine‐induced damage in parkinsonian rat mesencephalon by regulating autophagy: down‐expression Beclin‐1 and light chain 3B and up‐expression P62

β‐asarone and levodopa co‐administration protects against 6‐hydroxydopamine‐induced damage in parkinsonian rat mesencephalon by regulating autophagy: down‐expression Beclin‐1 and light chain 3B and up‐expression P62

Topical betamethasone butyrate propionate exacerbates pressure ulcers after cutaneous ischemia–reperfusion injury

Pregnancy as a valuable period for preventing hypoxia‐ischemia brain damage

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