Neuroprotective and Anti-ageing Effects of Curcumin in Aged Rat Brain Regions

Bala, Kiran; Tripathy, Baishnab C.; Sharma, Deepak

doi:10.1007/s10522-006-6495-x

Cited by 157 publications

(85 citation statements)

References 38 publications

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“…The neuroprotective effect of curcumin is exerted via various intra-and extra-cellular mechanisms in the central nervous system, which are responsible for its antioxidant and anti-inflammatory properties (Bala et al, 2006;Mythri & Bharath, 2012). Curcumin could reduce N-methyl-D-aspartate (NMDA)-mediated excitotoxic cell damage through modulation of NMDA receptor activity and attenuating NMDA receptor-mediated calcium rise, leading to a lower rate of apoptosis and enhancing cell viability (Matteucci et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Antiepileptogenic effect of curcumin on kainate-induced model of temporal lobe epilepsy

Kiasalari

Roghani

Khalili

et al. 2013

Pharmaceutical Biology

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Context: Temporal lobe epilepsy (TLE) is an intractable neurological disorder. Curcumin is the bioactive component of turmeric with anti-epileptic and neuroprotective potential. Objective: The beneficial effect of curcumin on the intrahippocampal kainate-induced model of TLE was investigated. Materials and methods: Rats were divided into sham, curcumin-pretreated sham, kainate and curcumin-pretreated kainate groups. The rat model of TLE was induced by unilateral intrahippocampal injection of 4 mg of kainate. Rats received curcumin p.o. at a dose of 100 mg/kg/d starting 1 week before the surgery. Seizure activity (SE) and oxidative stressrelated markers were measured. Furthermore, the Timm index for evaluation of mossy fiber sprouting (MFS) and number of Nissl-stained neurons were quantified. Results: All rats in the kainate group had SE, while 28.5% of rats showed seizures in the curcumin-pretreated kainate group. Malondialdehyde and nitrite and nitrate levels significantly increased in the kainate group (p50.01 and p50.05, respectively), and curcumin significantly lowered these parameters (p50.05). Superoxide dismutase activity significantly decreased in the kainate group (p50.05) and curcumin did not improve it. Rats in the kainate group showed a significant reduction of neurons in Cornu Ammonis 1 (CA1) (p50.05), CA3 (p50.005) and hilar (p50.01) regions, and curcumin significantly prevented these changes (p50.05-0.005). The Timm index significantly increased in the kainate group (p50.005), and curcumin significantly lowered this index (p50.01). Discussion and conclusion: Curcumin pretreatment can attenuate seizures, lower some oxidative stress markers, and prevent hippocampal neuronal loss and MFS in the kainate-induced model of TLE.

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Section: Discussionmentioning

confidence: 99%

Antiepileptogenic effect of curcumin on kainate-induced model of temporal lobe epilepsy

Kiasalari

Roghani

Khalili

et al. 2013

Pharmaceutical Biology

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“…CUR represents the pungent principle of curry and is used as a food color in various countries [2]. It exhibits an extremely broad spectrum of biological activities [3,4], which comprise anti-inflammatory [5], antioxidant [6], chemosensitizing [7], radiosensitizing [8], antiangiogenic [9], neuroprotective [10], antimicrobial [11], antiviral [12], antifungal [13], and wound-healing [14] properties, among others.…”

Section: Introductionmentioning

confidence: 99%

Metabolism of curcumin and induction of mitotic catastrophe in human cancer cells

Dempe

Pfeiffer

Grimm

et al. 2008

Molecular Nutrition Food Res

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In cultured cells, curcumin (CUR) causes cell death by interfering with mitosis and leading to fragmented nuclei and disrupted microtubules, a process named mitotic catastrophe. In order to clarify the role of the known CUR metabolites hexahydro-CUR (HHC) and CUR-glucuronide (CUR-gluc) in mitotic catastrophe, the effects of CUR were studied in three human cancer cell lines with different metabolism of CUR. In Ishikawa and HepG2 cells, CUR was metabolized to HHC and small amounts of octahydro-CUR (OHC), whereas the only metabolism in HT29 cells was the formation of CUR-gluc. Despite their different metabolism, all three cell systems responded to CUR with arrest in G2/M phase and mitotic catastrophe. Fractionation of the cells showed that concentrations of CUR were higher in the ER and cytosol than in the incubation medium by a factor of up to about 150 and 8, respectively. In contrast to CUR, the metabolite HHC and the products of spontaneous degradation did not elicit any effects in Ishikawa cells. These results imply that the causative agent of mitotic catastrophe is the parent CUR molecule, whereas reductive metabolism and chemical degradation render CUR inactive.

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“…Tumeric contains curcumin, demethoxycurcumin and bisdemethoxycurcumin which is potential as antioxidant and neuroprotective agent. [14][15][16] Its highly lipophylic character would increase curcumin disposition in the brain. 17 In vitro and in vivo studies showed that curcumin could prevent neurodegenerative process caused by oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Tumeric Rhizome (Curcuma Longa L) on Radial Arm Maze and Passive Avoidance Test in Trimetiline-Induced Rat Models

Yuliani

Setiani

2017

JKKI

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Backround:Oxidative stress can cause death of hippocampal cells associated to the deficit of learning and memory function. Turmeric rhizome contains curcuminoid which has antioxidant activity that can prevent oxidative stress, thus it was expected to prevent the deficit of learning and memory function on trimethyltin (TMT)-induced rat models. Objectve: This study aimed to determine the effect of turmeric rhizome extract on cognitive learning and memory fuction which was tested using radial arm maze and passive avoidance tests on Wistar rats injected with TMT. Methods: A total of 30 Wistar rats, male, 8-12 weeks of age were divided into 6 groups. The first (normal) group was given CMC-Na, the second (TMT) group was given CMC-Na, the third-the fifth groups were given turmeric rhizome extract (TRE) orally in the dosage of 120mg/kgBW (TRE120), 240 mg/kgBW (TRE240) and 480 mg/kgBW (TRE480), respectivelly. The sixth (P500) group was given piracetam in the dosage of 500 mg/kgBW. Treatments were given for 8 days orally. At day-9th, excluding the first group, all rats were injected with 12 mg/kgBW TMT solution intraperitoneally. One day after TMT injection, the cognitive learning and memory function was measured using radial maze and passive avoidance tests. The datas of cognitve function tests were analyzed statistically by ANOVA test followed by LSD test at significance level 0.05. Results:The results of radial maze and passive avoidance tests showed that the TRE240 group was not statistically significant different with TMT group(p>0.05). However there were significant difference between TRE120 and TMT groups, as well as between TRE480 and TMT groups (p<0.05). The administration of 480 mg/kgBW of TRE showed that its cognitive function was not significantly different with the administration of Piracetam (p>0.05). Conclusion: It can be concluded that the administration of 480 mg/kgBW of TRE can improve cognitive learning and memory function of Wistar rats injected by TMT. Latar Belakang: Stres oksidatif dapat menyebabkanterjadinya kematian sel hippocampus yang dapat berakibat terhadap penurunan fungsi kognitif belajar dan mengingat. Rimpang kunyit (Curcuma longa L) mengandung kurkuminoid yang memiliki aktifitas antioksidan sehingga dapat mencegah stres oksidatif dan diharapkan dapat mencegah penurunan kemampuan belajar dan mengingat pada tikus yang diinduksi zat neurotoksik trimetiltin (TMT).

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Neuroprotective and Anti-ageing Effects of Curcumin in Aged Rat Brain Regions

Cited by 157 publications

References 38 publications

Antiepileptogenic effect of curcumin on kainate-induced model of temporal lobe epilepsy

Antiepileptogenic effect of curcumin on kainate-induced model of temporal lobe epilepsy

Metabolism of curcumin and induction of mitotic catastrophe in human cancer cells

The Effect of Tumeric Rhizome (Curcuma Longa L) on Radial Arm Maze and Passive Avoidance Test in Trimetiline-Induced Rat Models

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