Curcumin reverses impaired cognition and neuronal plasticity induced by chronic stress

Xu, Ying; Lin, Dan; Li, Shan; Li, Gaowen; Shyamala, Subramaniam G.; Barish, Philip A.; Vernon, Matthew M.; Pan, Jianchun; Ogle, William O.

doi:10.1016/j.neuropharm.2009.06.010

Cited by 111 publications

(75 citation statements)

References 40 publications

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“…Other studies found that curcumin inhibited histone deacetylase (Liu et al, 2005;Chen et al, 2007Chen et al, , 2013Lee et al, 2011). It has also been suggested that curcumin blocked corticosterone-induced phosphorylation of CaMKII in cultured hippocampal neurons (Xu et al, 2009) and inhibited CaMKII autophosphorylation in vitro (Mayadevi et al, 2012), although such a mechanism has not been studied in vivo. Since we have previously found a critical role of CaMKIIa in opioid tolerance and dependence, we tested the hypothesis that curcumin's inhibitory action on CaMKIIa may be a mechanism attenuating the initiation or maintenance of opioid tolerance and dependence.…”

Section: Discussionmentioning

confidence: 99%

Curcumin Attenuates Opioid Tolerance and Dependence by Inhibiting Ca²⁺/Calmodulin-Dependent Protein Kinase II α Activity

Huang

Szymusiak

et al. 2014

J Pharmacol Exp Ther

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Chronic use of opioid analgesics has been hindered by the development of opioid addiction and tolerance. We have reported that curcumin, a natural flavonoid from the rhizome of Curcuma longa, attenuated opioid tolerance, although the underlying mechanism remains unclear. In this study, we tested the hypothesis that curcumin may inhibit Ca 21 /calmodulin-dependent protein kinase II a (CaMKIIa), a protein kinase that has been previously proposed to be critical for opioid tolerance and dependence. In this study, we used state-of-the-art polymeric formulation technology to produce poly(lactic-co-glycolic acid) (PLGA)-curcumin nanoparticles (nanocurcumin) to overcome the drug's poor solubility and bioavailability, which has made it extremely difficult for studying in vivo pharmacological actions of curcumin. We found that PLGAcurcumin nanoparticles reduced the dose requirement by 11-to 33-fold. Pretreatment with PLGA-curcumin (by mouth) prevented the development of opioid tolerance and dependence in a dosedependent manner, with ED 50 values of 3.9 and 3.2 mg/kg, respectively. PLGA-curcumin dose-dependently attenuated already-established opioid tolerance (ED 50 5 12.6 mg/kg p.o.) and dependence (ED 50 5 3.1 mg/kg p.o.). Curcumin or PLGA-curcumin did not produce antinociception by itself or affect morphine (1-10 mg/kg) antinociception. Moreover, we found that the behavioral effects of curcumin on opioid tolerance and dependence correlated with its inhibition of morphine-induced CaMKIIa activation in the brain. These results suggest that curcumin may attenuate opioid tolerance and dependence by suppressing CaMKIIa activity.

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Section: Discussionmentioning

confidence: 99%

Curcumin Attenuates Opioid Tolerance and Dependence by Inhibiting Ca²⁺/Calmodulin-Dependent Protein Kinase II α Activity

Huang

Szymusiak

et al. 2014

J Pharmacol Exp Ther

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“…These results are similar to the changes elicited by the immobilization stress, which was previously reported (Suenaga et al, 2004). This elevation of pCaMKII was reversed by curcumin administration at different dose ranges from 0.62 to 2.5 mM (Ying Xu et al, 2009). …”

Section: Camk Pathwaymentioning

confidence: 91%

“…However, CaMKII over phosphorylation may produce some degree of neurotoxicity to the cells and alter some biochemical pathways involved in memory processing. It should be noted that mice that expressed a constitutively active CaMKII lacked low frequency LTP and were not able to form stable place cells within the hippocampus (Ying Xu et al, 2009). In hippocampal neurons, pCaMKII levels were significantly increased in response to corticosterone exposure, though no changes were found in total CaMKII levels.…”

Section: Camk Pathwaymentioning

confidence: 96%

“…One such nutraceutical is turmeric, which has been used throughout Asia as a food additive and a traditional herbal medicine. The active substance in turmeric is curcumin, the yellow pigment extracted from the rhizoma of Curcuma longa (Ying Xu et al, 2009). In this study, the effects of curcumin on restraint stress-induced spatial learning and memory dysfunction in a water maze task were investigated, and related neuroendocrine and plasticity changes were measured.…”

Section: Curcuminmentioning

confidence: 99%

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The Serotonergic System and Neuroplasticity are Implicated in the Effect of Phytochemicals on Mood and Cognitive Disorders

Xu¹,

Zhang²,

Ogle³

2012

Recent Advances in Theories and Practice of Chinese Medicine

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“…The results of our study are in good agreement with those of previous studies, which showed that curcumin regulates CaMKII action and effectively cures hippocampal neuronal loss induced by chronic stress. 45 CaMKII is an ubiquitous, multifunctional serine-threonine protein kinase that regulates a variety of neuronal functions. 9,46,47 An overexpression of CaMKII can trigger caspase-3-dependent cell death in damaged retinas.…”

Section: Curcumin Inhibits Retinal Neuronal Lossmentioning

confidence: 99%

Curcumin Inhibits Neuronal Loss in the Retina and Elevates Ca²⁺/Calmodulin-Dependent Protein Kinase II Activity in Diabetic Rats

Wang

Yang

et al. 2015

Journal of Ocular Pharmacology and Therapeutics

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Purpose: To determine whether curcumin offers neuroprotection to minimize the apoptosis of neural cells in the retina of diabetic rats. Methods: Streptozotocin (STZ)-induced diabetic rats and control rats were used in this study. A subgroup of STZ-induced diabetic rats were treated with curcumin for 12 weeks. Retinal histology, apoptosis of neural cells in the retina, electroretinograms, and retinal glutamate content were evaluated after 12 weeks. Retinal levels of Ca 2 + /calmodulin-dependent protein kinase II (CaMKII), phospho-CaMKII (p-CaMKII), and cleaved caspase-3 were determined by Western blot analysis. Results: The amplitudes a-wave, b-wave, and oscillatory potential were reduced by diabetes, but curcumin treatment suppressed this reduction of amplitudes. Curcumin also prevented cell loss from the outer nuclear, inner nuclear, and ganglion cell layers. Apoptosis of retinal neurons was detected in diabetic rats. The concentration of glutamate in the retina was higher in diabetic rats, but was significantly reduced in the curcumintreated group. Furthermore, p-CaMKII and cleaved caspase-3 expression were upregulated in the diabetic retina, but reduced in curcumin-treated rats. Conclusions: Curcumin attenuated diabetes-induced apoptosis in retinal neurons by reducing the glutamate level and downregulating CaMKII. Thus, curcumin might be used to prevent neuronal damage in the retina of patients with diabetes mellitus.

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Curcumin reverses impaired cognition and neuronal plasticity induced by chronic stress

Cited by 111 publications

References 40 publications

Curcumin Attenuates Opioid Tolerance and Dependence by Inhibiting Ca²⁺/Calmodulin-Dependent Protein Kinase II α Activity

Curcumin Attenuates Opioid Tolerance and Dependence by Inhibiting Ca²⁺/Calmodulin-Dependent Protein Kinase II α Activity

The Serotonergic System and Neuroplasticity are Implicated in the Effect of Phytochemicals on Mood and Cognitive Disorders

Curcumin Inhibits Neuronal Loss in the Retina and Elevates Ca²⁺/Calmodulin-Dependent Protein Kinase II Activity in Diabetic Rats

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Curcumin reverses impaired cognition and neuronal plasticity induced by chronic stress

Cited by 111 publications

References 40 publications

Curcumin Attenuates Opioid Tolerance and Dependence by Inhibiting Ca2+/Calmodulin-Dependent Protein Kinase II α Activity

Curcumin Attenuates Opioid Tolerance and Dependence by Inhibiting Ca2+/Calmodulin-Dependent Protein Kinase II α Activity

The Serotonergic System and Neuroplasticity are Implicated in the Effect of Phytochemicals on Mood and Cognitive Disorders

Curcumin Inhibits Neuronal Loss in the Retina and Elevates Ca2+/Calmodulin-Dependent Protein Kinase II Activity in Diabetic Rats

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Product

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Curcumin Attenuates Opioid Tolerance and Dependence by Inhibiting Ca²⁺/Calmodulin-Dependent Protein Kinase II α Activity

Curcumin Attenuates Opioid Tolerance and Dependence by Inhibiting Ca²⁺/Calmodulin-Dependent Protein Kinase II α Activity

Curcumin Inhibits Neuronal Loss in the Retina and Elevates Ca²⁺/Calmodulin-Dependent Protein Kinase II Activity in Diabetic Rats