Identification of proteins regulated by curcumin in cerebral ischemia

Shah, Fawad Ali; Gim, Sang-Ah; Sung, Jin-Hee; Jeon, Seong-Jun; Kim, Myeong-Ok; Koh, Phil-Ok

doi:10.1016/j.jss.2015.10.025

Cited by 32 publications

(24 citation statements)

References 33 publications

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“…In animal focal cerebral ischemia, curcumin reduced both the volume of brain infarction [109][110][111][112][113][114][115][116][117][118][119] and brain edema [109,110,[113][114][115]120,121] and gave better neurological outcomes than in the vehicle group [112,114,117,122]. Curcumin improved sensory, motor, and locomotor activity, both smaller neurobehavioral and neurological deficits [111,115,117,119,120,123,124].…”

Section: Neuroprotection and Neurogenesismentioning

confidence: 96%

Substantiation for the Use of Curcumin during the Development of Neurodegeneration after Brain Ischemia

Ułamek-Kozioł

Czuczwar

Januszewski

et al. 2020

IJMS

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Currently available pharmacological treatment of post-ischemia-reperfusion brain injury has limited effectiveness. This review provides an assessment of the current state of neurodegeneration treatment due to ischemia-reperfusion brain injury and focuses on the role of curcumin in the diet. The purpose of this review was to provide a comprehensive overview of what was published about the benefits of curcumin influence on post-ischemic brain damage. Some data on the clinical benefits of curcumin treatment of post-ischemic brain in terms of clinical symptoms and adverse reactions have been reviewed. The data in this review contributes to a better understanding of the potential benefits of curcumin in the treatment of neurodegenerative changes after ischemia and informs scientists, clinicians, and patients, as well as their families and caregivers about the possibilities of such treatment. Due to the pleotropic properties of curcumin, including anti-amyloid, anti-tau protein hyperphosphorylation, anti-inflammatory, anti-apoptotic, and neuroprotective action, as well as increasing neuronal lifespan and promoting neurogenesis, curcumin is a promising candidate for the treatment of post-ischemic neurodegeneration with misfolded proteins accumulation. In this way, it may gain interest as a potential therapy to prevent the development of neurodegenerative changes after cerebral ischemia. In addition, it is a safe substance and inexpensive, easily accessible, and can effectively penetrate the blood–brain barrier and neuronal membranes. In conclusion, the evidence available in a review of the literature on the therapeutic potential of curcumin provides helpful insight into the potential clinical utility of curcumin in the treatment of neurological neurodegenerative diseases with misfolded proteins. Therefore, curcumin may be a promising supplementary agent against development of neurodegeneration after brain ischemia in the future. Indeed, there is a rational scientific basis for the use of curcumin for the prophylaxis and treatment of post-ischemic neurodegeneration.

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Section: Neuroprotection and Neurogenesismentioning

confidence: 96%

Substantiation for the Use of Curcumin during the Development of Neurodegeneration after Brain Ischemia

Ułamek-Kozioł

Czuczwar

Januszewski

et al. 2020

IJMS

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“…A number of studies have demonstrated that curcumin can protect against ischemic stroke in experimental models (Thiyagarajan and Sharma, 2004; Lapchak, 2011; Shah et al, 2016). Pre-/post-stroke treatment with curcumin was found to effectively reduce infarct volumes and improve functional outcomes.…”

Section: Introductionmentioning

confidence: 99%

Curcumin Protects against Ischemic Stroke by Titrating Microglia/Macrophage Polarization

Liu

Ran

Huang

et al. 2017

Front. Aging Neurosci.

142

101

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Stroke is the most common type of cerebrovascular disease and is a leading cause of disability and death. Ischemic stroke accounts for approximately 80% of all strokes. The remaining 20% of strokes are hemorrhagic in nature. To date, therapeutic options for acute ischemic stroke are very limited. Recent research suggests that shifting microglial phenotype from the pro-inflammatory M1 state toward the anti-inflammatory and tissue-reparative M2 phenotype may be an effective therapeutic strategy for ischemic stroke. The dietary phytochemical curcumin has shown promise in experimental stroke models, but its effects on microglial polarization and long-term recovery after stroke are unknown. Here we address these gaps by subjecting mice to distal middle cerebral artery occlusion (dMCAO) and administering curcumin intraperitoneally (150 mg/kg) immediately after ischemia and 24 h later. Histological studies revealed that curcumin post-treatment significantly reduced cerebral ischemic damage 3 days after dMCAO. Sensorimotor functions—as measured by the adhesive removal test and modified Garcia scores—were superior in curcumin-treated mice at 3, 5, 7 and 10 days after stroke. RT-PCR measurements revealed an elevation of M2 microglia/macrophage phenotypic markers and a reduction in M1 markers in curcumin-treated brains 3 days after dMCAO. Immunofluorescent staining further showed that curcumin treatment significantly increased the number of CD206+Iba1+ M2 microglia/macrophages and reduced the number of CD16+Iba1+ M1 cells 10 days after stroke. In vitro studies using the BV2 microglial cell line confirmed that curcumin inhibited lipopolysaccharide (LPS) and interferon-γ (IFN-γ)-induced M1 polarization. Curcumin treatment concentration-dependently reduced the expression of pro-inflammatory cytokines, including TNF-α, IL-6 and IL-12p70, in the absence of any toxic effect on microglial cell survival. In conclusion, we demonstrate that curcumin has a profound regulatory effect on microglial responses, promoting M2 microglial polarization and inhibiting microglia-mediated pro-inflammatory responses. Curcumin post-treatment reduces ischemic stroke-induced brain damage and improves functional outcomes, providing new evidence that curcumin might be a promising therapeutic strategy for stroke.

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“…Proteomic analysis was performed according to a previously described method [25]. Right cerebral cortex tissues were homogenized in lysis buffer (8 M urea, 4% CHAPS, ampholytes and 40 mM Tris-HCl).…”

Section: Methodsmentioning

confidence: 99%

Hyperglycemia aggravates decreases of PEA-15 and its two phosphorylated forms in cerebral ischemia

Sung

Koh

2017

The Journal of Veterinary Medical Science

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Diabetes is a metabolic health disorder and an important risk factor for stroke. Phosphoprotein enriched in astrocytes 15 (PEA-15) is a multifunctional protein modulating cell proliferation, survival, apoptosis and glucose metabolism. This study investigated whether diabetes modulates the expression of PEA-15 and two phosphorylated forms (Ser 104 and Ser 116) in middle cerebral artery occlusion (MCAO)-induced brain injury. Male Sprague-Dawley rats were administrated with streptozotocin (40 mg/kg) and were underwent right middle cerebral artery occlusion (MCAO) 4 weeks after streptozotocin injection. Brain tissues were collected 24 hr after MCAO and stained using triphenyltetrazolium chloride. Western blot analysis was performed to elucidate the expression of PEA-15 and two phosphorylated forms (Ser 104 and Ser 116) in right cerebral cortex. Infarct volume during MCAO injury was severely increased in diabetic animals compared to non-diabetic animals. We identified the decrease in PEA-15 in animals that underwent MCAO using proteomic approach. PEA-15 expression during MCAO was strongly decreased in diabetic animals compared to non-diabetic animals. Western blots analysis confirmed that diabetes exacerbated the decrease in PEA-15 expression after MCAO. Moreover, decrease in expression of phospho-PEA-15 (Ser 104 and Ser 116) was greater in diabetic than in non-diabetic animals. These results suggested that a diabetic condition may aggravate brain damage through decreasing expression of PEA-15 and phospho-PEA-15 (Ser 104 and Ser 116) in ischemic brain injury.

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Identification of proteins regulated by curcumin in cerebral ischemia

Cited by 32 publications

References 33 publications

Substantiation for the Use of Curcumin during the Development of Neurodegeneration after Brain Ischemia

Substantiation for the Use of Curcumin during the Development of Neurodegeneration after Brain Ischemia

Curcumin Protects against Ischemic Stroke by Titrating Microglia/Macrophage Polarization

Hyperglycemia aggravates decreases of PEA-15 and its two phosphorylated forms in cerebral ischemia

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