Effect of curcumin on acute spinal cord injury in mice via inhibition of inflammation and TAK1 pathway

Zhang, Nanwen; Wei, Guicai; Ye, Jian; Yang, Lin; Hong, Yunda; Liu, Guisheng; Zhong, Huifen; Cai, Xinyi

doi:10.1016/j.pharep.2017.02.012

Cited by 32 publications

(16 citation statements)

References 21 publications

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“…Curcumin attenuated hyperglycemia-mediated TAK1 protein expression in cerebrum of streptozotocin-induced diabetic rat [29]. Moreover, curcumin decreased the phosphorylation levels of TAK1 protein and p38 MAPK in mice with acute spinal cord injury [30]. The roles of TAK1 signal pathway in EMT and peritoneal fibrosis of PMCs are in accordance with a previous report [17].…”

Section: Discussionsupporting

confidence: 86%

Curcumin suppresses epithelial-to-mesenchymal transition of peritoneal mesothelial cells (HMrSV5) through regulation of transforming growth factor-activated kinase 1 (TAK1)

et al. 2019

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Objective Peritoneal fibrosis remains a serious complication of long-term peritoneal dialysis (PD) leading to peritoneal membrane ultrafiltration failure. Epithelial–mesenchymal transition (EMT) of peritoneal mesothelial cells (PMCs) is a key process of peritoneal fibrosis. Curcumin has been previously shown to inhibit EMT of renal tubular epithelial cells and prevent renal fibrosis. There are only limited reports on inhibition of PMCs-EMT by curcumin. This study aimed to investigate the effect of curcumin on the regulation of EMT and related pathway in PMCs treated with glucose-based PD. Methods EMT of human peritoneal mesothelial cells (HMrSV5) was induced with glucose-based peritoneal dialysis solutions (PDS). Cells were divided into a control group, PDS group, and PDS group receiving varied concentrations of curcumin. Cell Counting Kit-8 (CCK-8) assay was used to measure cell viability, and a transwell migration assay was used to verify the capacity of curcumin to inhibit EMT in HMrSV5 cells. Real-time quantitative PCR and western blot were used to detect the expression of genes and proteins associated with the EMT. Results High glucose PDS decreased cell viability and increased migratory capacity. Curcumin reversed growth inhibition and migration capability of human peritoneal mesothelial cells (HPMCs). In HMrSV5 cells, high glucose PDS also decreased expression of epithelial markers, and increased expression of mesenchymal markers, a characteristic of EMT. Real-time RT-PCR and western blot revealed that, compared to the 4.25% Dianeal treated cells, curcumin treatment resulted in increased expression of E-cadherin (epithelial marker), and decreased expression of α-SMA (mesenchymal markers) ( P < 0.05). Furthermore, curcumin reduced mRNA expression of two extracellular matrix protein, collagen I and fibronectin. Curcumin also reduced TGF-β1 mRNA and supernatant TGF-β1 protein content in the PDS-treated HMrSV5 cells ( P < 0.05). Furthermore, it significantly reduced protein expression of p-TAK1, p-JNK and p-p38 in PDS-treated HMrSV5 cells. Conclusions Our results demonstrate that curcumin showed an obvious protective effect on PDS-induced EMT of HMrSV5 cells and suggest implication of the TAK1, p38 and JNK pathway in mediating the effects of curcumin in EMT of MCs.

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Section: Discussionsupporting

confidence: 86%

Curcumin suppresses epithelial-to-mesenchymal transition of peritoneal mesothelial cells (HMrSV5) through regulation of transforming growth factor-activated kinase 1 (TAK1)

et al. 2019

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“…Therefore, NF-κB activity at least in glial cells contributes to the pathogenesis of SCI. Subsequently, it has been demonstrated that curcumin ameliorates secondary damage (e.g., production of IL-6, TNF-α, IL-1β, and nitric oxide) presumably through inhibiting both the TAK1/MKK6/p38 pathway and the NF-κB pathway, which may contribute to the improvement of locomotor recovery after SCI [ 76 ].…”

Section: Involvement Of P38 In the Pathogenesis Of Scimentioning

confidence: 99%

Stress-Activated Protein Kinases in Spinal Cord Injury: Focus on Roles of p38

Kasuya

Umezawa

Hatano

2018

IJMS

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Spinal cord injury (SCI) consists of three phases—acute, secondary, and chronic damages—and limiting the development of secondary damage possibly improves functional recovery after SCI. A major component of the secondary phase of SCI is regarded as inflammation-triggered events: induction of cytokines, edema, microglial activation, apoptosis of cells including oligodendrocytes and neurons, demyelination, formation of the astrocytic scar, and so on. Two major stress-activated protein kinases (SAPKs)—c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38 MAPK)—are activated in various types of cells in response to cellular stresses such as apoptotic stimuli and inflammatory waves. In animal models of SCI, inhibition of either JNK or p38 has been shown to promote neuroprotection-associated functional recovery. Here, we provide an overview on the roles of SAPKs in SCI and, in particular, the pathological role of p38 will be discussed as a promising target for therapeutic intervention in SCI.

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“…Additionally, curcumin reduced reactive gliosis in the rat brain stem after ethidium bromide injection yielding smaller GFAP+ glial scar regions. [26][27][28][29]61,62 However, like a multitude of other drugs, curcumin is quite instable and poorly bioavailable so that the systemic application of the native drug will hardly achieve therapeutically relevant local concentrations. 63 In first attempts to apply curcumin locally to the brain, poly (vinyl alcohol) (PVA) based implants were loaded with curcumin and implanted into the rodent brain.…”

Section: Discussionmentioning

confidence: 99%

<p>Liposomal Encapsulated Curcumin Effectively Attenuates Neuroinflammatory and Reactive Astrogliosis Reactions in Glia Cells and Organotypic Brain Slices</p>

Schmitt¹,

Lechanteur²,

Cossais³

et al. 2020

IJN

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Introduction: The polyphenolic spice and food coloring ingredient curcumin has beneficial effects in a broad variety of inflammatory diseases. Amongst them, curcumin has been shown to attenuate microglia reaction and prevent from glial scar formation in spinal cord and brain injuries. Methods: We developed a protocol for the efficient encapsulation of curcumin as a model for anti-inflammatory drugs yielding long-term stable, non-toxic liposomes with favorable physicochemical properties. Subsequently, we evaluate the effects of liposomal curcumin in experimental models for neuroinflammation and reactive astrogliosis. Results: We could show that liposomal curcumin can efficiently reduce the reactivity of human microglia and astrocytes and preserve tissue integrity of murine organotypic cortex slices. Discussion and Perspective: In perspective, we want to administer this curcumin formulation in brain implant coatings to prevent neuroinflammation and glial scar formation as foreign body responses of the brain towards implanted materials.

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Effect of curcumin on acute spinal cord injury in mice via inhibition of inflammation and TAK1 pathway

Abstract: Curcumin restores mice hind-limb function that has been reduced by SCI. This occurs by inhibition of TAK1/MKK6/p38MAPK via the TAK1 and NFκB pathways and inflammation. These results suggest the therapeutic potential for curcumin in the treatment of SCI.

Cited by 32 publications

References 21 publications

Curcumin suppresses epithelial-to-mesenchymal transition of peritoneal mesothelial cells (HMrSV5) through regulation of transforming growth factor-activated kinase 1 (TAK1)

Curcumin suppresses epithelial-to-mesenchymal transition of peritoneal mesothelial cells (HMrSV5) through regulation of transforming growth factor-activated kinase 1 (TAK1)

Stress-Activated Protein Kinases in Spinal Cord Injury: Focus on Roles of p38

<p>Liposomal Encapsulated Curcumin Effectively Attenuates Neuroinflammatory and Reactive Astrogliosis Reactions in Glia Cells and Organotypic Brain Slices</p>

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