scholarly journals MicroRNA-9 Mediated the Protective Effect of Ferulic Acid on Hypoxic-Ischemic Brain Injury in Neonatal Rats

2020 ◽  
Author(s):  
Keli Yao ◽  
Qin Yang ◽  
Yajuan Li ◽  
Ting Lan ◽  
Hong Yu ◽  
...  
Keyword(s):  
Ferulic Acid ◽  
Neuronal Damage ◽  
Cerebral Atrophy ◽  
Rat Hippocampus ◽  
Protective Effects ◽  
Neonatal Rats ◽  
Adult Rats ◽  
Ischemic Brain ◽  
Morris Water Maze Task ◽  
Neuronal Pc12 Cells

AbstractNeonatal hypoxic-ischemic brain damage (NHIBD) leads to cognitive and memory impairments, and there is no effective clinical treatment. Ferulic acid (FA) is found within members of the genus Angelica, reportedly shows protective effects on neuronal damage; however, the mechanism of the protective effects of FA on rats following NHIBD remains unclear. Using the Morris water maze task, we herein found that the impairment of spatial memory formation in adult rats exposed to NHIBD was significantly reversed by FA treatment and the administration of LNA-miR-9. RT-PCR analyses revealed that miRNA-9 was significantly increased in the hippocampus of neonatal rats and neuronal PC12 cells following NHIBD and that FA and LNA-miR-9 both inhibited the expression of miRNA-9, suggesting that the therapeutic effect of FA was mainly attributed to the inhibition of miRNA-9 expression. Indeed, the silencing of miR-9 by LNA-miR-9 or FA similarly attenuated neuronal damage and cerebral atrophy in the rat hippocampus after NHIBD, which was consistent with the restored expression levels of brain-derived neurotrophic factor (BDNF). Therefore, FA treatment may protect against neuronal death through the inhibition of miRNA-9 induction in the rat hippocampus following hypoxic-ischemic damage.

scholarly journals Hydrogen Gas Attenuates Hypoxic-Ischemic Brain Injury via Regulation of the MAPK/HO-1/PGC-1a Pathway in Neonatal Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-16 ◽  
Author(s):  
Peipei Wang ◽  
Mingyi Zhao ◽  
Zhiheng Chen ◽  
Guojiao Wu ◽  
Masayuki Fujino ◽  
...  
Keyword(s):  
Brain Injury ◽  
Protein Kinase ◽  
Pc12 Cells ◽  
Heme Oxygenase 1 ◽  
Ischemic Brain Injury ◽  
Protective Effects ◽  
Neonatal Rats ◽  
Ischemic Brain ◽  
Differentiated Pc12 Cells ◽  
Hypoxic Ischemic Brain Injury

Neonatal hypoxic-ischemic encephalopathy (HIE) is a leading cause of death in neonates with no effective treatments. Recent advancements in hydrogen (H2) gas offer a promising therapeutic approach for ischemia reperfusion injury; however, the impact of this approach for HIE remains a subject of debate. We assessed the therapeutic effects of H2 gas on HIE and the underlying molecular mechanisms in a rat model of neonatal hypoxic-ischemic brain injury (HIBI). H2 inhalation significantly attenuated neuronal injury and effectively improved early neurological outcomes in neonatal HIBI rats as well as learning and memory in adults. This protective effect was associated with initiation time and duration of sustained H2 inhalation. Furthermore, H2 inhalation reduced the expression of Bcl-2-associated X protein (BAX) and caspase-3 while promoting the expression of Bcl-2, nuclear factor erythroid-2-related factor 2, and heme oxygenase-1 (HO-1). H2 activated extracellular signal-regulated kinase and c-Jun N-terminal protein kinase and dephosphorylated p38 mitogen-activated protein kinase (MAPK) in oxygen-glucose deprivation/reperfusion (OGD/R) nerve growth factor-differentiated PC12 cells. Inhibitors of MAPKs blocked H2-induced HO-1 expression. HO-1 small interfering RNA decreased the expression of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and sirtuin 1 (SIRT1) and reversed the protectivity of H2 against OGD/R-induced cell death. These findings suggest that H2 augments cellular antioxidant defense capacity through activation of MAPK signaling pathways, leading to HO-1 expression and subsequent upregulation of PGC-1α and SIRT-1 expression. Thus, upregulation protects NGF-differentiated PC12 cells from OGD/R-induced oxidative cytotoxicity. In conclusion, H2 inhalation exerted protective effects on neonatal rats with HIBI. Early initiation and prolonged H2 inhalation had better protective effects on HIBI. These effects of H2 may be related to antioxidant, antiapoptotic, and anti-inflammatory responses. HO-1 plays an important role in H2-mediated protection through the MAPK/HO-1/PGC-1α pathway. Our results support further assessment of H2 as a potential therapeutic for neurological conditions in which oxidative stress and apoptosis are implicated.

Protective effects of C-phycocyanin against kainic acid-induced neuronal damage in rat hippocampus

1999 ◽  
Vol 276 (2) ◽  
pp. 75-78 ◽  
Author(s):  
Victor Rimbau ◽  
Antoni Camins ◽  
Cheyla Romay ◽  
Ricardo González ◽  
Mercè Pallàs
Keyword(s):  
Kainic Acid ◽  
Neuronal Damage ◽  
Rat Hippocampus ◽  
Protective Effects

Protective Effects of Valproic Acid Against Hypoxic-Ischemic Brain Injury in Neonatal Rats

2005 ◽  
Vol 20 (7) ◽  
pp. 582-587 ◽  
Author(s):  
Nimet Kabakus ◽  
Ilknur Ay ◽  
Sabiha Aysun ◽  
Figen Söylemezoglu ◽  
Ayhan Özcan ◽  
...  
Keyword(s):  
Valproic Acid ◽  
Brain Injury ◽  
Ischemic Brain Injury ◽  
Protective Effects ◽  
Neonatal Rats ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury

scholarly journals MicroRNA-9 mediated the protective effect of ferulic acid on hypoxic-ischemic brain damage in neonatal rats

PLoS ONE ◽  
2020 ◽  
Vol 15 (5) ◽  
pp. e0228825 ◽  
Author(s):  
Keli Yao ◽  
Qin Yang ◽  
Yajuan Li ◽  
Ting Lan ◽  
Hong Yu ◽  
...  
Keyword(s):  
Protective Effect ◽  
Ferulic Acid ◽  
Brain Damage ◽  
Neonatal Rats ◽  
Ischemic Brain Damage ◽  
Ischemic Brain

scholarly journals Protective Effects of PGC-1α Activators on Ischemic Stroke in a Rat Model of Photochemically Induced Thrombosis

2021 ◽  
Vol 11 (3) ◽  
pp. 325
Author(s):  
Fatima M. Shakova ◽  
Yuliya I. Kirova ◽  
Denis N. Silachev ◽  
Galina A. Romanova ◽  
Sergey G. Morozov
Keyword(s):  
Rat Model ◽  
Nuclear Translocation ◽  
Peroxisome Proliferator ◽  
Protective Effects ◽  
Protein Markers ◽  
Peroxisome Proliferator Activated Receptor ◽  
Pharmacological Agents ◽  
Ischemic Brain ◽  
Neuroprotective Therapy ◽  
Dependent Protein

The pharmacological induction and activation of peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α), a key regulator of ischemic brain tolerance, is a promising direction in neuroprotective therapy. Pharmacological agents with known abilities to modulate cerebral PGC-1α are scarce. This study focused on the potential PGC-1α-modulating activity of Mexidol (2-ethyl-6-methyl-3-hydroxypyridine succinate) and Semax (ACTH(4–7) analog) in a rat model of photochemical-induced thrombosis (PT) in the prefrontal cortex. Mexidol (100 mg/kg) was administered intraperitoneally, and Semax (25 μg/kg) was administered intranasally, for 7 days each. The expression of PGC-1α and PGC-1α-dependent protein markers of mitochondriogenesis, angiogenesis, and synaptogenesis was measured in the penumbra via immunoblotting at Days 1, 3, 7, and 21 after PT. The nuclear content of PGC-1α was measured immunohistochemically. The suppression of PGC-1α expression was observed in the penumbra from 24 h to 21 days following PT and reflected decreases in both the number of neurons and PGC-1α expression in individual neurons. Administration of Mexidol or Semax was associated with preservation of the neuron number and neuronal expression of PGC-1α, stimulation of the nuclear translocation of PGC-1α, and increased contents of protein markers for PGC-1α activation. This study opens new prospects for the pharmacological modulation of PGC-1α in the ischemic brain.

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