Curcumin Provides Neuroprotection After Spinal Cord Injury

Lin, Muh-Shi; Lee, Yi‐Hsuan; Chiu, Wen Ta; Hung, Kuo Sheng

doi:10.1016/j.jss.2009.07.001

Cited by 114 publications

(81 citation statements)

References 36 publications

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“…Inhibition of GFAP expression following CNS injury was also observed in several other investigations using Cur 9,13,15 . Cur was able to reduce the expression of both GFAP mRNA and GFAP protein, as well as to induce autophagy and to rescue the filamentous organization of the GFAP mutant protein in an in vitro model of Alexander disease, in which heterozygous mutations of the GFAP gene are responsible for the intracytoplasmic accumulation of fibrous eosinophilic deposits known as Rosenthal fibers in dystrophic astrocytes 28 .…”

Section: Discussionsupporting

confidence: 77%

“…Astroglial cells respond to CNS injury and other neuro-disturbing conditions by undergoing "reactive astrogliosis", a process whereby astrocytes undergo cellular hypertrophy and proliferation 19,20,21,22,23,24 . Increased GFAP is a hallmark of reactive astrocytes and this cytoskeletal protein contributes to the barrier effect produced by the glial scar that mitigates axonal extension and CNS repair 9 . Astrocyte precursors and immature astrocytes present principally nestin and vimentin and, during development as astrocytes mature, nestin expression disappears, GFAP becomes increasingly expressed and vimentin decreases to undetectable levels 21 .…”

Section: Discussionmentioning

confidence: 99%

“…Recently, Cur has been shown to exhibit proven therapeutic benefits (including antioxidant, anti-inflammatory, anti-cancer and anti-fibrotic effects) in many pathological conditions, such as Alzheimer' s disease, Parkinson' s disease, multiple sclerosis, epilepsy, cerebral injury, cancer, allergy, asthma, bronchitis, colitis, rheumatoid arthritis, renal ischemia, psoriasis, scleroderma, diabetes, obesity, depression, fatigue and acquired immunodeficiency disease 6,7,8 . Specifically regarding the CNS, Cur was capable of providing neuroprotection after spinal cord injury, inhibiting apoptosis and neuron loss and attenuating oxidative stress in astrocytes and reactive astrogliosis 9,10,11,12,13 , suggesting that Cur might beneficially affect astrocyte population in the CNS inflammatory environment by regulating both NF-κβ and SOX9 signaling pathways 14,15 . In this context, the aim of this study was to evaluate whether Cur had the capacity to affect astrocyte response during the process of demyelination and remyelination following gliotoxic injury induced by ethidium bromide (EB).…”

mentioning

confidence: 99%

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Curcumin decreases astrocytic reaction after gliotoxic injury in the rat brainstem

Bondan

Cardoso

Martins

2017

Arq. Neuro-Psiquiatr.

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Recent studies have demonstrated that curcumin (Cur) has antioxidant, anti-inflammatory and anti-fibrotic effects. Ethidium bromide (EB) injections into the central nervous system (CNS) are known to induce local oligodendroglial and astrocytic loss, resulting in primary demyelination and neuroinflammation. Peripheral astrogliosis is seen around the injury site with increased immunoreactivity to glial fibrillary acidic protein (GFAP). This investigation aimed to evaluate the effect of Cur administration on astrocytic response following gliotoxic injury. Wistar rats were injected with EB into the cisterna pontis and treated, or not, with Cur (100 mg/kg/day, intraperitoneal route) during the experimental period. Brainstem sections were collected at 15, 21 and 31 days after EB injection and processed for GFAP immunohistochemical staining. Astrocytic reactivity was measured in a computerized system for image analysis. In Cur-treated rats, the GFAP-stained area around the lesion was significantly smaller in all periods after EB injection compared to untreated animals, showing that Cur reduces glial scar development following injury.Keywords: astrocytes; curcumin; ethidium; gliosis; gliotoxin. RESUMOEstudos recentes têm demonstrado que a curcumina (Cur) possui efeitos antioxidantes, anti-inflamatórios e antifibróticos. Sabe-se que a injeção de brometo de etídio (EB) no sistema nervoso central induz a perda oligodendroglial e astrocitária, resultando em desmielinização primária e neuroinflamação. Astrogliose periférica é observada ao redor da lesão com aumento da imunorreatividade à proteína glial fibrilar ácida (GFAP). A presente investigação objetivou avaliar o efeito da Cur sobre a resposta astrocitária após injúria gliotóxica. Ratos Wistar foram injetados com EB na cisterna basal e tratados ou não com Cur (100 mg/kg/dia, via intraperitoneal) durante o período experimental. Amostras do tronco encefálico foram coletadas aos 15, 21 e 31 dias pós-injeção de EB e processadas para estudo imuno-histoquímico para a GFAP. A reatividade astrocitária foi medida em um sistema computadorizado para análise de imagem. Nos ratos tratados com Cur, a área marcada para GFAP foi significantemente menor em todos os períodos pós-injeção de EB, indicando que a Cur reduz o desenvolvimento da cicatriz glial após injúria.

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Section: Discussionsupporting

confidence: 77%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Curcumin decreases astrocytic reaction after gliotoxic injury in the rat brainstem

Bondan

Cardoso

Martins

2017

Arq. Neuro-Psiquiatr.

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“…Both PTEN/Akt/mTOR signaling and neuronal activity play a role in phosphorylation and, [38,39]. Relevant to this study, it is interesting to note that in distinct type of cancer cells, curcumin increased levels of phospho-eIF4e [37], which we found to be downregulated in sensorimotor neocortices after SCI.…”

Section: Discussionsupporting

confidence: 67%

Acute adaptive responses of central sensorimotor neurons after spinal cord injury

Thompson

DiBona

Dubey

et al. 2010

Translational Neuroscience

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Spinal cord injury (SCI) can be a lifelong, devastating condition for both the patient and the caregiver, with a daunting incidence rate. Still, there are only limited available therapies and the effectiveness of precise regeneration within the central nervous system is minimal throughout postnatal life. Recently, improved regeneration after SCI was seen by manipulating a pathway in sensorimotor neocortices that is involved in phosphorylation of an RNA binding protein (RBP) required for mRNA translation, the Eukaryotic translation initiation factor 4E (eIF4E). Our data identifies rapid molecular alterations of eIF4E in the sensorimotor neocortices 1 and 3 days after a lateral hemisection SCI, used as a model for Brown-Séquard syndrome. The function of an RBP depends on both its distribution sites within the cell and its phosphorylation states. Indeed, we found both to be affected after SCI. There was a distinct subcellular redistribution of eIF4E and phosphorylated-eIF4E was reduced, indicating that the eIF4E's translation was disrupted. Upon identification and analysis of the mRNA cargo of eIF4E in uninjured sensorimotor neocortices, we found that eIF4E binds both Importin-13 (Ipo13) and Parvalbumin (Pv) mRNAs, indicating a role in their translation. Remarkably, eIF4E's interaction with both Ipo13 and Pv mRNAs was disrupted 1 and 3 days after SCI, despite preservation of total Ipo13 and Pv mRNA levels. Finally, we detected a selective loss of expression of both IPO13 and PV proteins in projection neurons of sensorimotor neocortices, as well as their disrupted dendritic polarity. Since IPO13 is predominantly expressed in neocortical projection neurons and PV in a subset of neocortical interneurons, these data suggest a strong acute effect of SCI on neocortical microcircuitry. Taken together, these data indicate that neocortical eIF4E and a subset of mRNAs may be rapidly recruited to translational machinery after SCI to promote adaptive regeneration response of sensorimotor neurons.

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“…By down-regulating glial fibrillary acidic protein expression, curcumin seems to diminish astrocyte reactivation, which may be useful for neuronal survival. [19] The objective of our study was to determine the antioxidant effects of curcumin in rats with SCI. We also aimed to compare the effects of curcumin with those of methylprednisolone.…”

Section: Resultsmentioning

confidence: 99%

Antioxidant effects of curcumin in spinal cord injury in rats

Kavakli

Koca²,

Alıcı³

2011

Ulus Travma Acil Cerrahi Derg

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AMAÇBu deneysel çalışma, sıçanlarda spinal kord yaralanmasın-da curcuminin antioksidan etki yoluyla faydasını araştır-mak için yapıldı. GEREÇ VE YÖNTEMYirmi dört adet Wistar albino sıçan 3 gruba randomize edildi. Spinal kord yaralanması ağırlık düşürme modeliyle gerçekleştirildi. Grup 1'e laminektomi ardından spinal kord yaralanması uygulandı ve herhangi bir tedavi verilmedi. Grup 2'ye laminektomi ardından spinal kord yaralanması uygulandı ve curcumin verildi (200 mg/kg/gün ağızdan). Grup 3'e laminektomi ardından spinal kord yaralanması uygulandı ve metilprednizolon verildi (30 mg/kg periton içine), 24 saat sonra tüm sıçanlardan kan örnekleri alındı, sonra serum süperoksit dismutaz (SOD) ve malondialdehit (MDA) düzeyleri belirlendi ve elde edilen sonuçlar karşılaştırıldı. BULGULARCurcumin grubunda SOD düzeyi kontrol ve metilprednizolon grubundan daha yüksekti (p<0,001 ve p<0,012). Curcumin grubunda MDA düzeyi kontrol grubundan daha düşüktü (p<0,042). Benzer şekilde metilprednizolon grubunda MDA düzeyi kontrol grubundan daha düşüktü (p<0,001). SONUÇBu çalışmanın sonuçları curcuminin etkin biçimde oksidatif hasara karşı spinal kord dokularını koruduğunu gös-terir.Anahtar Sözcükler: Antioksidan; curcumin; malondialdehit; spinal kord yaralanması; süperoksit dismutaz.

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Curcumin Provides Neuroprotection After Spinal Cord Injury

Cited by 114 publications

References 36 publications

Curcumin decreases astrocytic reaction after gliotoxic injury in the rat brainstem

Curcumin decreases astrocytic reaction after gliotoxic injury in the rat brainstem

Acute adaptive responses of central sensorimotor neurons after spinal cord injury

Antioxidant effects of curcumin in spinal cord injury in rats

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