Curcumin protects against stroke and increases levels of Notch intracellular domain

Liu, Shuang; Cao, Yungang; Qu, Man; Zhang, Zheng; Feng, Liang; Ye, Zusen; Xiao, Mingzhao; Hou, Sheng T.; Zheng, Ran; Han, Zhao

doi:10.1080/01616412.2016.1187804

Cited by 41 publications

(34 citation statements)

References 34 publications

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“…Previous studies performed in stroke models have shown that curcumin exerts diverse neuroprotective functions, including antioxidative effects (Thiyagarajan and Sharma, 2004; Yang et al, 2009; Wu et al, 2013), regulation of neuronal (and other cell) apoptosis (Zhao et al, 2008, 2010; Altinay et al, 2017), promotion of mitochondrial biogenesis (Liu et al, 2014), and enhancement of neurogenesis (Liu S. et al, 2016). The present study demonstrates that curcumin reduces ischemic stroke-induced brain damage and improves several functional outcomes.…”

Section: Discussionmentioning

confidence: 99%

“…Curcumin has also been proposed as a promising agent for stroke prevention in humans (Ovbiagele, 2008). Manifold mechanisms are involved in the protective effects of curcumin, including anti-oxidative, anti-inflammatory (Thiyagarajan and Sharma, 2004; Yang et al, 2009; Wu et al, 2013), and anti-apoptotic mechanisms (Zhao et al, 2008, 2010; Altinay et al, 2017), as well as neurogenesis (Liu S. et al, 2016). However, the effect of curcumin on microglial phenotypic polarization after ischemic stroke has not been explored.…”

Section: Introductionmentioning

confidence: 99%

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Curcumin Protects against Ischemic Stroke by Titrating Microglia/Macrophage Polarization

Liu

Ran

Huang

et al. 2017

Front. Aging Neurosci.

145

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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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Curcumin Protects against Ischemic Stroke by Titrating Microglia/Macrophage Polarization

Liu

Ran

Huang

et al. 2017

Front. Aging Neurosci.

145

101

View full text Add to dashboard Cite

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“…In recent years, curcumin has been used in the treatment of cerebrovascular disease due to its good antioxidation and anti-inflammatory effects (Motterlini, Foresti, Bassi, & Green, 2000;Priyadarsini, 1997 pass through the blood-brain barrier of aged rats and is recommended for the prevention and treatment of Alzheimer's disease (Wang et al, 2005;Yang et al, 2005). Nowadays, a number of studies reported that curcumin improves outcomes and attenuates focal cerebral ischemic injury in MCAO rat models (Liu et al, 2016;Miao et al, 2016;Zhao et al, 2010). Similarly, our results showed that curcumin decreased the infarct volume and improved the neurological outcomes in another different MCAO mouse model, which is more and more widely used to investigate the complicated molecular mechanisms of cerebral ischemia in recent years (Evans et al, 2017;H.…”

Section: Discussionmentioning

confidence: 99%

Curcumin protects neural cells against ischemic injury in N2a cells and mouse brain with ischemic stroke

Xie

Cai

et al. 2018

Brain and Behavior

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Background and PurposeCurcumin, a natural antioxidant isolated from Curcuma longa, has been reported to exert neuroprotective effect in animal models of ischemic stroke. However, the underlying mechanism is still not fully understood. The purpose of this study was to investigate the effect of curcumin treatment on neuronal apoptosis in the periinfarct cortex after cerebral ischemia/reperfusion (I/R) injury and in mouse N2a cells after oxygen‐glucose deprivation/reoxygenation (OGD/R) injury and its underlying mechanism.MethodsThe cerebral I/R injury was established by 1‐hr middle cerebral artery occlusion (MCAO) and reperfusion in mice. Infarct volume was determined by TTC staining, and neurological score was evaluated by mNSS. Cell morphology in the ischemic boundary zone were detected by HE staining. The number and apoptotic rate of neurons in ischemic boundary zone were assayed by immunohistochemistry and TUNEL, respectively. Mouse neuroblastoma N2a cells were subjected to OGD/R. Cell viability was assessed with CCK‐8. The mitochondrial membrane potential was measured using JC‐1 staining. The expression of Bax, Bcl‐2, and caspase‐3 was detected using Western blotting. Besides, cellular distribution of Bax was determined by immunofluorescence assays.ResultsCurcumin treatment reduced infarct volume, improved neurological function, alleviated the morphological damage of neurons, and increased neuronal survival rate after I/R injury in vivo. Moreover, curcumin treatment improved cell viability, reduced cell apoptosis, increased Bcl‐2 protein levels while decreased Bax and caspase‐3 expressions in mouse N2a cells after OGD/R injury. Besides, curcumin treatment inhibited Bax activation and maintained mitochondrial membrane integrity.ConclusionCurcumin promotes neuron survival in vivo and in vitro to exert neuroprotective effects against ischemia injury. Moreover, our results for the first time demonstrated curcumin inhibited ischemia‐induced mitochondrial apoptosis via restricting Bax activation, which may be one of the possible mechanisms underlying the neuroprotective effects of curcumin.

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“…In addition, curcumin protected against alcohol-induced neurodegeneration in the hippocampal area [16]. Furthermore, curcumin may stimulate neurogenesis and prevent focal cerebral ischemia reperfusion injury [17]. However, the specific underlying mechanism remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Protective Effect of Curcumin Against Oxidative Stress-Induced Injury in Rats with Parkinson’s Disease Through the Wnt/ β-Catenin Signaling Pathway

Wang

Zhang

et al. 2017

Cell Physiol Biochem

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Background/Aims: The study aimed to investigate the protective effect of curcumin against oxidative stress-induced injury of Parkinson’s disease (PD) through the Wnt/β-catenin signaling pathway in rats. Methods: The successfully established PD rat models and normal healthy rats were randomly assigned into the 6-hydroxydopamine (6-OHDA), the curcumin (Cur) and the control groups. Immunohistochemistry was used to detect the positive expression of tyrosine hydroxylase (TH), dopamine transporter (DAT) and glial fibrillary acidic protein (GFAP). Deutocerebrum primary cells were extracted and classified into the control, 6-OHDA, Cur (5, 10, 15 µmol/L), Dickkopf-1 (DKK-1) and Cur + DKK-1 groups. MTT assays, adhesion tests and TUNEL staining were used to assess cell viability, adhesion and apoptosis, respectively. Western blotting and qRT-PCR were used to examine the protein and mRNA expressions of Wnt3a and β-catenin and the c-myc and cyclinD1 mRNA expressions. Results: TH and DAT expressions in the Cur group were elevated and GFAP was reduced compared with the 6-OHDA group. Curcumin enhanced viability, survival and adhesion and attenuated apoptosis of deutocerebrum primary cells by activating the Wnt/β-catenin signaling pathway. Higher Wnt3a and β-catenin mRNA and protein expressions and c-myc and cyclinD1 mRNA expressions, enhanced superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) contents, decreased malondialdehyde (MDA) content and elevated mitochondrial membrane potential (∆ψm) were found in the 10 and 15 µmol/L Cur groups compared with the 6-OHDA group. However, opposite tendencies were found in the Cur + DKK-1 group compared to the 10 µmol/L Cur group. Conclusion: This study suggests that curcumin could protect against oxidative stress-induced injury in PD rats via the Wnt/β-catenin signaling pathway.

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Curcumin protects against stroke and increases levels of Notch intracellular domain

Abstract: Curcumin may protect from focal cerebral ischemia reperfusion injury as well as stimulate neurogenesis by activating the Notch signaling pathway.

Cited by 41 publications

References 34 publications

Curcumin Protects against Ischemic Stroke by Titrating Microglia/Macrophage Polarization

Curcumin Protects against Ischemic Stroke by Titrating Microglia/Macrophage Polarization

Curcumin protects neural cells against ischemic injury in N2a cells and mouse brain with ischemic stroke

Protective Effect of Curcumin Against Oxidative Stress-Induced Injury in Rats with Parkinson’s Disease Through the Wnt/ β-Catenin Signaling Pathway

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