Oleoylethanolamide inhibits glial activation via moudulating PPARα and promotes motor function recovery after brain ischemia

Luo, Doudou; Zhang, Yali; Yuan, Xiaoqian; Pan, Yilin; Yang, Lichao; Zhao, Yun; Zhuo, Rengong; Chen, Caixia; Lu, Peng; Li, Wenjun; Jin, Xin; Zhou, Yu

doi:10.1016/j.phrs.2019.01.027

Cited by 38 publications

(31 citation statements)

References 60 publications

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“…Among the TGF-β family members, TGF-β1 is a cytokine that is generated in the brain in response to ischemia. TGF-β1 is a master regulator of glial activation and scar formation after brain ischemia (Luo et al, 2019). In addition, TGF-β1 also has been shown to protect hippocampal neurons from injuries, including neurotoxins, as well as excitotoxic and hypoxia/ischemia ingury (Cho et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Propolis ameliorates cerebral injury in focal cerebral ischemia/reperfusion (I/R) rat model via upregulation of TGF-β1

Abdel-Rahman

Alqasoumi

Ogaly

et al. 2020

Saudi Pharmaceutical Journal

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Neuroprotective impact of transforming growth factor β1 (TGF-β1) is increasingly recognized in different brain injuries. Propolis exhibits a broad spectrum of biological and pharmacological properties including neuroprotective action. The objective of the investigation was to explore the involvement of TGF-β1 signaling in the neuroprotective mechanism of propolis in I/R rats. In this study, focal cerebral ischemia model was built by middle cerebral artery occlusion (MCAO) for 2 h followed by reperfusion. The investigation was carried out on 48 rats that were arranged into four groups (n = 12): the sham group, I/R control group, I/R + propolis (50 mg/kg) group and I/R + propolis (100 mg/kg) group. The results revealed that propolis preserved rats against neuronal injury induced by cerebral I/R. It significantly reduced neurological deficit scores and improved motor coordination and locomotor activity in I/R rats. Propolis antagonized the damage induced by cerebral I/R through suppression of malondialdehyde (MDA) and elevation of reduced glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), brain-derived neurotropic factor (BDNF) and dopamine levels in the brain homogenates of I/R rats. Other ameliorations were also observed based on reduction of neurodegeneration and histological alterations in the brain tissues. These results also proposed that the neuroprotective effect of propolis might be related to upregulation of TGF-β1 and suppressed matrix metallopeptidase-9 (MMP9) mRNA expression.

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Section: Discussionmentioning

confidence: 99%

Propolis ameliorates cerebral injury in focal cerebral ischemia/reperfusion (I/R) rat model via upregulation of TGF-β1

Abdel-Rahman

Alqasoumi

Ogaly

et al. 2020

Saudi Pharmaceutical Journal

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“…PEA is also suggested to improve neuronal survival by possibly counteracting reactive astrogliosis [ 159 , 160 ]. PEA- and OEA-mediated inhibition of astrocyte activation seems to involve PPAR-α [ 161 , 162 ]. Furthermore, AEA has been shown to elicit glutamate release through astrocytic CB 1 receptor activation in the core of nucleus accumbens in rats [ 163 ].…”

Section: Neuroinflammation-induced Synaptopathy and Neurodegenerative Diseasesmentioning

confidence: 99%

Neuroprotective and Immunomodulatory Action of the Endocannabinoid System under Neuroinflammation

Kasatkina

Rittchen

Sturm

2021

IJMS

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Endocannabinoids (eCBs) are lipid-based retrograde messengers with a relatively short half-life that are produced endogenously and, upon binding to the primary cannabinoid receptors CB1/2, mediate multiple mechanisms of intercellular communication within the body. Endocannabinoid signaling is implicated in brain development, memory formation, learning, mood, anxiety, depression, feeding behavior, analgesia, and drug addiction. It is now recognized that the endocannabinoid system mediates not only neuronal communications but also governs the crosstalk between neurons, glia, and immune cells, and thus represents an important player within the neuroimmune interface. Generation of primary endocannabinoids is accompanied by the production of their congeners, the N-acylethanolamines (NAEs), which together with N-acylneurotransmitters, lipoamino acids and primary fatty acid amides comprise expanded endocannabinoid/endovanilloid signaling systems. Most of these compounds do not bind CB1/2, but signal via several other pathways involving the transient receptor potential cation channel subfamily V member 1 (TRPV1), peroxisome proliferator-activated receptor (PPAR)-α and non-cannabinoid G-protein coupled receptors (GPRs) to mediate anti-inflammatory, immunomodulatory and neuroprotective activities. In vivo generation of the cannabinoid compounds is triggered by physiological and pathological stimuli and, specifically in the brain, mediates fine regulation of synaptic strength, neuroprotection, and resolution of neuroinflammation. Here, we review the role of the endocannabinoid system in intrinsic neuroprotective mechanisms and its therapeutic potential for the treatment of neuroinflammation and associated synaptopathy.

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“…HE Et al ischemia. [47][48][49] Our data showed a robust increase in GFAP and S100β double-positive cells in the thalamus started from first week postirradiation, suggesting the reactive astrocytes were induced at very early stage in our gamma ray irradiation mouse model. In our model, both microglia and astrocytes proliferated and activated before the occurrence of radiation-induced neuronal loss and brain necrosis.…”

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confidence: 58%

Gamma ray‐induced glial activation and neuronal loss occur before the delayed onset of brain necrosis

Wang

et al. 2020

FASEB j.

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Radiotherapy is one of the most effective treatments for head and neck tumors. However, delayed radiation‐induced brain necrosis (RN) remains a serious issue due to the lack of satisfying prevention and effective treatment. The pathological role of radiation in the delayed onset of brain necrosis is still largely unknown, and the traditional animal model of whole brain irradiation, although being widely used, does not produce reliable and localized brain necrosis mimicking clinical features of RN. In this study, we demonstrated a successful RN mouse model using optimized gamma knife irradiation in male C57BL/6 mice. On the premise that brain necrosis started to appear at 6 weeks postirradiation in our RN model, as confirmed by both MRI and histopathological examinations, we systematically examined different time points before the onset of RN for the histopathological changes and biochemical indicators. Our initial results demonstrated that in the ipsilateral hemisphere of the irradiated brains, a significant decrease in neuronal numbers that occurred at 4 weeks and a sustained increase in TNF‐α, iNOS, and other inflammatory cytokines beginning at 1‐week postirradiation. Changes of cell morphology and cell numbers of both microglia and astrocytes occurred as early as 1‐week postirradiation, and intervention by bevacizumab administration resulted in reduced microglia activation and reduction of radiation‐induced lesion volume, indicating that chronic glial activation may result in subsequent elevation of inflammatory factors, which led to the delayed onset of neuronal loss and brain necrosis. Since C57BL/6 is the most widely used strain of genetic engineered mouse model, our data provide an invaluable platform for the mechanistic study of RN pathogenesis, identification of potential imaging and biological biomarkers, and the development of therapeutic treatment for the disease.

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Oleoylethanolamide inhibits glial activation via moudulating PPARα and promotes motor function recovery after brain ischemia

Cited by 38 publications

References 60 publications

Propolis ameliorates cerebral injury in focal cerebral ischemia/reperfusion (I/R) rat model via upregulation of TGF-β1

Propolis ameliorates cerebral injury in focal cerebral ischemia/reperfusion (I/R) rat model via upregulation of TGF-β1

Neuroprotective and Immunomodulatory Action of the Endocannabinoid System under Neuroinflammation

Gamma ray‐induced glial activation and neuronal loss occur before the delayed onset of brain necrosis

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