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

Kiasalari, Zahra; Roghani, Mehrdad; Khalili, Mohsen; Rahmati, Batool; Baluchnejadmojarad, Tourandokht

doi:10.3109/13880209.2013.803128

Cited by 60 publications

(35 citation statements)

References 53 publications

(59 reference statements)

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“…Curcumin a enuated the spinal cord ischemia-reperfusion injury in rabbits by reducing the oxidative damage (10). It inhibited hippocampal neuronal loss (11) and bipolar disorder (12). In conjunction with stem cell therapy, curcumin synergistically improved recovery from acute traumatic spinal cord injury (SCI) (13), underlying the potential regenerative action of curcumin if appropriately mediated by the neural stem cells.…”

Section: Introductionmentioning

confidence: 99%

Curcumin-Protected PC12 Cells Against Glutamate-Induced Oxidative Toxicity

Chang

Chen

Yü

et al. 2014

Food. Technol. Biotechnol.

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SummaryGlutamate is a major excitatory neurotransmi er present in the central nervous system. The glutamate/cystine antiporter system x c -connects the antioxidant defense with neurotransmission and behaviour. Overactivation of ionotropic glutamate receptors induces neuronal death, a pathway called excitotoxicity. Glutamate-induced oxidative stress is a major contributor to neurodegenerative diseases including cerebral ischemia, Alzheimer's and Huntington's disease. Curcuma has a wide spectrum of biological activities regarding neuroprotection and neurocognition. By reducing the oxidative damage, curcumin a enuates a spinal cord ischemia-reperfusion injury, seizures and hippocampal neuronal loss. The rat pheochromocytoma (PC12) cell line exhibits many characteristics useful for the study of the neuroprotection and neurocognition. This investigation was carried out to determine whether the neuroprotective eff ects of curcumin can be observed via the glutamate-PC12 cell model. Results indicate that glutamate (20 mM) upregulated glutathione peroxidase 1, glutathione disulphide, Ca 2+ infl ux, nitric oxide production, cytochrome c release, Bax/Bcl-2 ratio, caspase-3 activity, lactate dehydrogenase release, reactive oxygen species, H 2 O 2 , and malondialdehyde; and downregulated glutathione, glutathione reductase, superoxide dismutase and catalase, resulting in enhanced cell apoptosis. Curcumin alleviates all these adverse eff ects. Conclusively, curcumin can eff ectively protect PC12 cells against the glutamate-induced oxidative toxicity. Its mode of action involves two pathways: the glutathione-dependent nitric oxide-reactive oxygen species pathway and the mitochondria-dependent nitric oxide-reactive oxygen species pathway.

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Section: Introductionmentioning

confidence: 99%

Curcumin-Protected PC12 Cells Against Glutamate-Induced Oxidative Toxicity

Chang

Chen

Yü

et al. 2014

Food. Technol. Biotechnol.

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“…The malondialdehyde (MDA) concentration was measured as described by Kiasalari et al (2013). The results were expressed as MDA equivalents using tetraethoxypropane as a standard.…”

Section: Determination Of Pancreas Malondialdehyde Contentmentioning

confidence: 99%

Antidiabetic potential of salvianolic acid B in multiple low-dose streptozotocin-induced diabetes

Raoufi

Baluchnejadmojarad

Roghani

et al. 2015

Pharmaceutical Biology

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Context: Salvianolic acids are the most abundant water-soluble compounds extracted from the herb Salvia miltiorrhiza L. (Lamiaceae) with antioxidant and protective effects. Objective: This study evaluates the antidiabetic effect of salvianolic acid B (Sal B) in multiple low-dose streptozotocin (MLDS)-induced diabetes in rat. Materials and methods: Rats were divided into control, Sal B40-treated control, diabetic, Sal B20-, and Sal B40-treated diabetic groups. Sal B was daily administered at doses of 20 or 40 mg/kg (i.p.), started on third day post-STZ injection for 3 weeks. Serum glucose and insulin level and some oxidative stress markers in pancreas were measured in addition to the oral glucose tolerance test (OGTT), histological assessment, and apoptosis determination. Results: After 3 weeks, treatment of diabetic rats with Sal B20 and Sal B40 caused a significant decrease of the serum glucose (p50.05-0.01) and improvement of OGTT. Meanwhile, serum insulin was significantly higher in Sal B20-and Sal B40-treated diabetics (p50.01) and treatment of diabetics with Sal B40 significantly lowered malondialdehyde (MDA) (p50.05), raised glutathione (GSH) (p50.05), and activity of catalase (p50.01) with no significant change of nitrite. Furthermore, the number of pancreatic islets (p50.05) and their area (p50.01) was significantly higher and apoptosis reactivity was significantly lower (p50.05) in the Sal B40-treated diabetic group versus diabetics. Discussion and conclusion: Three-week treatment of diabetic rats with Sal B exhibited antidiabetic activity which is partly exerted via attenuation of oxidative stress and apoptosis and augmentation of antioxidant system.

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“…Curcuminoids extracted from C. longa have shown anticonvulsant activity in different epileptic models [72,128,129]. The mechanisms proposed for its action include as an antoxidant, by enhancing GABAergic inhibition, and via a direct or an indirect activation of adenosine A1 [130][131][132][133][134][135]. It has further been discovered that, in addition to curcuminoids, bisabolene sesquiterpenoids also promote anticonvulsant activity and need to be studied further [136].…”

Section: Curcuma Longa L (Haridra)mentioning

confidence: 99%