Rosiglitazone Attenuates Cerebral Vasospasm and Provides Neuroprotection in an Experimental Rat Model of Subarachnoid Hemorrhage

Lin, Bo-Feng; Kuo, Chan-Yang; Wen, Li-Li; Chen, Chunmei; Chang, Ya-Feng; Wong, Chih‐Shung; Cherng, Chen‐Hwan; Chuang, Mei-Yu

doi:10.1007/s12028-014-0010-z

Cited by 14 publications

(8 citation statements)

References 49 publications

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“…A study indeed showed rosiglitazone‐mediated GFAP increase, but in terms of restored astrocyte activity in subarachnoid hemorrhage (Lin et al . ). On the other hand, our observations in the diabetic brain closely emulated the effects of rosiglitazone against striatal dopaminergic neurodegeneration (Lee et al .…”

Section: Discussionmentioning

confidence: 97%

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Rosiglitazone up‐regulates glial fibrillary acidic protein via HB‐EGF secreted from astrocytes and neurons through PPARγ pathway and reduces apoptosis in high‐fat diet‐fed mice

Kushwaha

Mishra

Gupta

et al. 2018

Journal of Neurochemistry

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The anti-diabetic drug and peroxisome proliferator-activated receptor-gamma (PPARc) agonist, rosiglitazone, alters astrocyte activation; however, its mechanism remains less-known. We hypothesized participation of epidermal growth factor receptor (EGFR), known to control astrocyte reactivity. We first detected that rosiglitazone promoted glial fibrillary acidic protein (GFAP) expression in primary astrocytes as well as the mouse cerebral cortex, associated with increased EGFR activation. Screening for EGFR ligands revealed a rosiglitazone-mediated increase of heparin-binding epidermal growth factor (HB-EGF) in astrocytes, resulting in HB-EGF release into culture medium and mouse cerebrospinal fluid too. Treatment with HB-EGF-siRNA and EGFR inhibitors showed that the rosiglitazone-induced HB-EGF and p-EFGR were interdependent, which participated in GFAP increase. Interestingly, we observed that rosiglitazone could induce cellular and secreted-HB-EGF in neurons also, contributing toward the activated EGFR-induced GFAP in astrocytes. Probing whether these effects of rosiglitazone were PPARc-linked, revealed potential PPARc-responsive elements within HB-EGF gene. Moreover, gel-shift, site-directed mutagenesis, chromatinimmunoprecipitation and luciferase-reporter assays demonstrated a PPARc-dependent HB-EGF transactivation. Subsequently, we examined effects of rosiglitazone in a high-fat diet-fed diabetes mouse model, and supporting observations in the normal cortical cells, identified a rosiglitazone-induced GFAP, astrocyte and neuronal HB-EGF and secreted-HB-EGF in the cerebral cortex of diabetic mice. Moreover, assessing relevance of increased HB-EGF and GFAP revealed an anti-apoptotic role of rosiglitazone in the cerebral cortex, supported by a GFAP-siRNA as well as HB-EGF-siRNA-mediated increase in cleaved-caspase 3 and 9 levels in the rosiglitazone-treated astrocyte-neuron coculture. Overall, our study indicates that rosiglitazone may protect the brain, via a PPARc-dependent HB-EGF/EGFR signaling and increased GFAP.

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Section: Discussionmentioning

confidence: 97%

“…Additionally, roziglitazone attenuated GFAP loss and enhanced astrocyte activity after cerebral hemorrhage (Lin et al . ). Nonetheless, rosiglitazone‐induced mechanism in astrocytes remains less investigated.…”

mentioning

confidence: 97%

Rosiglitazone up‐regulates glial fibrillary acidic protein via HB‐EGF secreted from astrocytes and neurons through PPARγ pathway and reduces apoptosis in high‐fat diet‐fed mice

Kushwaha

Mishra

Gupta

et al. 2018

Journal of Neurochemistry

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“…Rosiglitazone is a highly selective and potent agonist to peroxisome proliferator-activated receptor γ . Continuous treatment with 6 mg/kg rosiglitazone for 6 days reduces glutamate level, upregulates GLT-1 expression, reduces MDA and catalase levels, and ameliorates vasospasm following SAH, exhibiting a protective role in the brain [ 161 ]. Treatment with rosiglitazone in cerebral hemorrhage regulates antioxidation and anti-inflammatory effects, possibly through the interaction of Nrf-2, retinoid X receptor (RXR), and NF- κ B and reduces SBI [ 162 ].…”

Section: Antioxidant Therapy After Ichmentioning

confidence: 99%

Intracerebral Hemorrhage, Oxidative Stress, and Antioxidant Therapy

Duan

Wen

Shen

et al. 2016

Oxidative Medicine and Cellular Longevity

230

177

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Hemorrhagic stroke is a common and severe neurological disorder and is associated with high rates of mortality and morbidity, especially for intracerebral hemorrhage (ICH). Increasing evidence demonstrates that oxidative stress responses participate in the pathophysiological processes of secondary brain injury (SBI) following ICH. The mechanisms involved in interoperable systems include endoplasmic reticulum (ER) stress, neuronal apoptosis and necrosis, inflammation, and autophagy. In this review, we summarized some promising advances in the field of oxidative stress and ICH, including contained animal and human investigations. We also discussed the role of oxidative stress, systemic oxidative stress responses, and some research of potential therapeutic options aimed at reducing oxidative stress to protect the neuronal function after ICH, focusing on the challenges of translation between preclinical and clinical studies, and potential post-ICH antioxidative therapeutic approaches.

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“…In the literature, different experimental models have shown that rosiglitazone has protective and antiapoptotic effects on both neural stem cells (NSCs) and mature neurons by preventing the glial-induced inflammation or regulating the intercellular pathways. In ischemia-reperfusion-induced and traumatic brain injury animal models, [22][23][24][25][26][27][28] rosiglitazone has been reported to suppress the glial inflammatory cytokine production (TNFa and IL-1) through the over-activation of glial cells (astrocyte or microglia). This finding correlates with the reduction in neuronal death rates in the hippocampus or other brain areas.…”

Section: Discussionmentioning

confidence: 99%

Effects of prenatal PPAR-γ agonist rosiglitazone exposure on rat hippocampus development in a time-dependent manner: A stereological and histopathological study

et al. 2017

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Rosiglitazone is in the thiazolidinedione class of drugs used in the treatment of type 2 diabetes mellitus. It works as an insulin sensitizer by binding to the peroxisome proliferator-activated receptor gamma. We investigated the effects of prenatally administered rosiglitazone on pyramidal cell numbers and morphologies in the hippocampus at postnatal period using histochemical and stereological techniques, congenital morphological properties and the number of offspring in rats. Eighteen female rats were grouped into control (C), low-dose rosiglitazone (LDR) and high-dose rosiglitazone (HDR). LDR pregnant rats received 2 mg/kg/day of rosiglitazone via oral gavage during the first 16 days of the pregnancy. HDR rats received 5 mg/kg/day. The infants were grouped into newborn (NB), 4 week (4 W) and 12 week (12 W). A side from histopathologic and congenital assessments, stereological analyses were performed using the optical fractionator method. Congenital anomaly was not detected in any of the rosiglitazone treatment groups, and their number of offspring was similar to that of the C group. Stereological counts revealed a significant reduction in the number of hippocampal pyramidal cells in the C and LDR groups but not in the HDR group until birth to 12th week. When NB groups were compared, the number of pyramidal cells in the HDRNB group was less than those in the LDRNB and CNB groups. HDR affected apoptosis or the proliferation and maturation of progenitor cells to the pyramidal neuron during neurodevelopment in the hippocampus, whereas LDR did not adversely affect neuronal development and did not cause congenital anomalies.

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Rosiglitazone Attenuates Cerebral Vasospasm and Provides Neuroprotection in an Experimental Rat Model of Subarachnoid Hemorrhage

Abstract: Rosiglitazone reduced SAH mortality, neurological deficits, body weight loss, GFAP loss, and cerebral vasospasm by preventing the neurotoxicity induced by glutamate and oxidative stress.

Cited by 14 publications

References 49 publications

Rosiglitazone up‐regulates glial fibrillary acidic protein via HB‐EGF secreted from astrocytes and neurons through PPARγ pathway and reduces apoptosis in high‐fat diet‐fed mice

Rosiglitazone up‐regulates glial fibrillary acidic protein via HB‐EGF secreted from astrocytes and neurons through PPARγ pathway and reduces apoptosis in high‐fat diet‐fed mice

Intracerebral Hemorrhage, Oxidative Stress, and Antioxidant Therapy

Effects of prenatal PPAR-γ agonist rosiglitazone exposure on rat hippocampus development in a time-dependent manner: A stereological and histopathological study

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