Neurodegeneration, Myelin Loss and Glial Response in the Three-Vessel Global Ischemia Model in Rat

Ананьина, Татьяна Викторовна; Kisel, Alena; Kudabaeva, Marina S; Чернышева, Г. А.; Smol’yakova, V. I.; Usov, K. E.; Krutenkova, Elena; Mb, Plotnikov; Khodanovich, M. Yu.

doi:10.3390/ijms21176246

Cited by 13 publications

(12 citation statements)

References 81 publications

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“…In the vehicle-treated group, Iba-1-immunoreactive microglia had hypertrophied cell body and thickened processes (activated microglia), and the phagocytic form (round cell body without processes) of microglia were also found in the stratum pyramidale of the CA1 region 4 days after ischemia/reperfusion. This result was consistent with previous studies showing that ischemia induced microglial activation and morphological changes in the hippocampus [41,42]. Treatment with purpurin reduced the phagocytic form of microglia in the stratum pyramidale, and overall Iba-1 immunoreactivity was signi cantly decreased in the hippocampal CA1 region compared to that in the vehicle-treated group.…”

Section: Discussionsupporting

confidence: 93%

Neuroprotective Effects of Purpurin Against Ischemic Damage via Anti-inflammatory and MAPK Pathway

Kim

Kwon

Jung

et al. 2021

Preprint

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Purpurin has various effects, including anti-inflammatory effects, and can efficiently cross the blood-brain barrier. In the present study, we investigated the effects of purpurin on oxidative stress in HT22 cells and ischemic damage in the hippocampal CA1 region of gerbils. Oxidative stress induced by H2O2 was significantly ameliorated by treatment with purpurin, based on changes in cell death, DNA fragmentation, formation of reactive oxygen species, and apoptosis (Bcl-2)/antiapoptosis (Bax)-related protein levels. In addition, treatment with purpurin significantly reduced the phosphorylation of c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase 1/2 (ERK), and p38 signaling in HT22 cells. Transient forebrain ischemia in gerbils led to a significant increase in locomotor activity 1 day after ischemia and significant decrease in number of surviving cells in the CA1 region 4 days after ischemia. Administration of purpurin reduced the travel distance 1 day after ischemia and increased the number of NeuN-immunoreactive neurons in the hippocampal CA1 region of the dentate gyrus 4 days after ischemia. Purpurin treatment significantly decreased microglial activation in the hippocampal CA1 region 4 days after ischemia and ameliorated the ischemia-induced increases in interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α 6 h after ischemia. In addition, purpurin significantly alleviated the ischemia-induced phosphorylation of JNK, ERK, and p38 in the hippocampus 1 day after ischemia. These results suggest that purpurin has neuroprotective potential to reduce inflammatory processes and the phosphorylation of JNK, ERK, and p38 in the hippocampus.

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Section: Discussionsupporting

confidence: 93%

Neuroprotective Effects of Purpurin Against Ischemic Damage via Anti-inflammatory and MAPK Pathway

Kim

Kwon

Jung

et al. 2021

Preprint

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“…In addition, GFAP immunoreactive astrocytes had hypertrophied and punctuated cytoplasm (reactive astrocytes) in the hippocampal CA1 region, which has functions as phagocytes after transient ischemia injury [45]. This result was consistent with previous studies showing that ischemia-induced activation of microglia and astrocytes and their morphological changes in the hippocampus [46][47][48][49]. Treatment with purpurin reduced the phagocytic form of microglia in the stratum pyramidale and reactive astrocytes in the stratum radiatum and oriens.…”

Section: Discussionsupporting

confidence: 90%

Neuroprotective Effects of Purpurin Against Ischemic Damage via MAPKs, Bax, and Oxidative Stress Cascades in the Gerbil Hippocampus

et al. 2022

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Purpurin has various effects, including anti-inflammatory effects, and can efficiently cross the blood–brain barrier. In the present study, we investigated the effects of purpurin on oxidative stress in HT22 cells and mild brain damage in the gerbil hippocampal CA1 region induced by transient forebrain ischemia. Oxidative stress induced by H2O2 was significantly ameliorated by treatment with purpurin, based on changes in cell death, DNA fragmentation, formation of reactive oxygen species, and pro-apoptotic (Bax)/anti-apoptotic (Bcl-2) protein levels. In addition, treatment with purpurin significantly reduced the phosphorylation of c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase 1/2 (ERK), and p38 signaling in HT22 cells. Transient forebrain ischemia in gerbils led to a significant increase in locomotor activity 1 day after ischemia and significant decrease in number of surviving cells in the CA1 region 4 days after ischemia. Administration of purpurin reduced the travel distance 1 day after ischemia and abrogates the neuronal death in the hippocampal CA1 region 4 days after ischemia based on immunohistochemical and histochemical staining for NeuN and Fluoro-Jade C, respectively. Purpurin treatment significantly decreased the activation of microglia and astrocytes as well as the increases of nuclear factor kappa-light-chain-enhancer of activated B cells p65 in the hippocampal CA1 region 4 days after ischemia and ameliorated the ischemia-induced transient increases of interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α in the hippocampus 6 h after ischemia. In addition, purpurin significantly alleviated the ischemia-induced phosphorylation of JNK, ERK, and p38 in the hippocampus 1 day after ischemia. Furthermore, purpurin treatment significantly mitigated the increases of Bax in the hippocampus 1 day after ischemia and the lipid peroxidation based on malondialdehyde and hydroperoxides levels 2 days after ischemia. These results suggest that purpurin can be one of the potential candidates to reduce neuronal damage and inflammatory responses after oxidative stress in HT22 cells or ischemic damage in gerbils.

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“…In addition, acute or chronic demyelination can be triggered by toxins such as lysophosphatidylcholine (LPC) and cuprizone, which induce local inflammation or directly induce OL apoptosis, respectively [29,30]. Lastly, myelin loss can be induced by physical injury (as observed in SCI) and hypoxia (either induced directly or indirectly as a result of ischemia) [31,32]. Collectively, these ani-mal models allow us to test, both in vitro and in vivo, the factors and cellular mechanisms that may progress myelin pathology or that, conversely, may aid in myelin repair.…”

Section: Steroid Hormonesmentioning

confidence: 99%

Hormonal Regulation of Oligodendrogenesis II: Implications for Myelin Repair

Breton¹,

Long²,

Barraza³

et al. 2021

Preprint

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Alterations in myelin, the protective and insulating sheath surrounding axons, affect brain function, as is evident in demyelinating diseases where the loss of myelin leads to cognitive and motor dysfunction. Recent evidence suggests that changes in myelination, including both hyper- and hypo-myelination, may also play a role in numerous neurological and psychiatric diseases. Protecting myelin and promoting remyelination is thus crucial for a wide range of disorders. Oligodendrocytes (OLs) are the cells that generate myelin, and oligodendrogenesis (OLgenesis), the creation of new OLs, continues throughout life and is necessary for myelin plasticity and remyelination. Understanding the regulation of OLgenesis and myelin plasticity within disease contexts is therefore critical for the development of novel therapeutic targets. In our companion manuscript [1], we review literature demonstrating that multiple hormone classes are involved in the regulation of OLgenesis under physiological conditions. The majority of hormones enhance OLgenesis, increasing oligodendrocyte precursor cell differentiation and inducing maturation and myelin production in OLs. Thus, hormonal treatments present a promising route to promote remyelination. Here, we review literature on hormonal regulation of OLgenesis within the context of disorders. We focus on steroid hormones, including glucocorticoids and sex hormones, peptide hormones such as insulin-like growth factor 1, and thyroid hormones. For each hormone, we describe whether they aid in OL survival, differentiation, or remyelination, and we discuss their mechanisms of action, if known. Several of these hormones have yielded promising results in both animal models and in human conditions; however, a better understanding of hormonal effects, interactions, and their mechanisms will ultimately lead to more targeted therapeutics for myelin repair.

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Neurodegeneration, Myelin Loss and Glial Response in the Three-Vessel Global Ischemia Model in Rat

Cited by 13 publications

References 81 publications

Neuroprotective Effects of Purpurin Against Ischemic Damage via Anti-inflammatory and MAPK Pathway

Neuroprotective Effects of Purpurin Against Ischemic Damage via Anti-inflammatory and MAPK Pathway

Neuroprotective Effects of Purpurin Against Ischemic Damage via MAPKs, Bax, and Oxidative Stress Cascades in the Gerbil Hippocampus

Hormonal Regulation of Oligodendrogenesis II: Implications for Myelin Repair

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