Effects of curcumin on ion channels and pumps: A review

Tabeshpour, Jamshid; Banaeeyeh, Sara; Eisvand, Farhad; Sathyapalan, Thozhukat; Hashemzaei, Mahmoud; Sahebkar, Amirhossein

doi:10.1002/iub.2054

Cited by 19 publications

(5 citation statements)

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“…Moreover, its chemical structure is very closely related to that of chalcone, which moved us to consider curcumin for our purposes, together with curcuminoids, demethoxycurcumin (13), and bisdemethoxycurcumin (14). Additionally, the interaction of curcumin with ion channels was also studied, trying to shed light into the underlying molecular mechanisms, and was broadly reviewed [47,48]. In fact, curcumin itself has recently been reported as an α7 nAChRs PAM, reversing nociception in mouse models [49,50].…”

Section: Evaluation Of Polyhydroxy Natural Products (Nps)mentioning

confidence: 99%

Natural Polyhydroxy Flavonoids, Curcuminoids, and Synthetic Curcumin Analogs as α7 nAChRs Positive Allosteric Modulators

Ximenis

Mulet²,

Sala³

et al. 2021

IJMS

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The α7 nicotinic acetylcholine receptor (α7 nAChR) is a ligand-gated ion channel that is involved in cognition disorders, schizophrenia, pain, and inflammation. Allosteric modulation of this receptor might be advantageous to reduce the toxicity in comparison with full agonists. Our previous results obtained with some hydroxy-chalcones, which were identified as positive allosteric modulators (PAMs) of α7 nAChR, prompted us to evaluate the potential of some structurally related naturally occurring flavonoids and curcuminoids and some synthetic curcumin analogues, with the aim of identifying new allosteric modulators of the α7 nAChR. Biological evaluation showed that phloretin, demethoxycurcumin, and bis-demethoxicurcuming behave as PAMs of α7 nAChR. In addition, some new curcumin derivatives were able to enhance the signal evoked by ACh; the activity values found for the tetrahydrocurcuminoid analog 23 were especially promising.

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Section: Evaluation Of Polyhydroxy Natural Products (Nps)mentioning

confidence: 99%

Natural Polyhydroxy Flavonoids, Curcuminoids, and Synthetic Curcumin Analogs as α7 nAChRs Positive Allosteric Modulators

Ximenis

Mulet²,

Sala³

et al. 2021

IJMS

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“…Thus, knowing that curcumin acts on several biological pathways including oxidative/nitrosative, and in ammatory (Wang et al, 2010;Bhandari, 2015;Tsuda, 2018;Pan et al, 2019), its protective actions are reported in several neurodegenerative and neuropsychiatric disorders (Mythri, Bharath, 2012). This compound can increase the inhibition of DOPA and NE reuptake by different pathways (Tabeshpour, et al, 2019), acting on neurotransmitter imbalances implicated in bipolar disorder (Anderson, Maes, 2015), anxiety disorders (Furtado, Katzman, 2015), schizophrenia (Davis et al, 2014) and autism (Rossignol, Frye, 2014).…”

Section: Discussionmentioning

confidence: 99%

Curcumin for Attention Deficit Hyperactivity Disorder: a Behavioral Preliminary Investigation

Macedo

Antunes

Alvarenga

et al. 2021

Preprint

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Background: Curcumin has protective actions in neuropsychiatric disorders. Its mechanism of action is associated with the restoration of catecholaminergic balance, reduction of oxidative/nitrosative stress, protection against inflammation, and neuroprotection. Objective: In a first approach, the study presents an empty review of the potential effect of curcumin on cognitive performance in attention deficit hyperactivity disorder (ADHD).Methods: On a second moment, seeing the scarcity of studies and knowing that ADHD is related to hyperactive and anxious behavior, 20 spontaneously hypertensive Wistar rats (SHR) were divided into groups that received water (1 mg/kg/day), curcumin (50 mg/kg/day), or methylphenidate (1 mg/kg/day) for 42 days. Behavioral tests to assess activity (Open Field test), anxiety and impulsivity (Elevated Plus Maze, and Social Interaction), and memory (Y Maze and Object Recognition Test) were performed. Results: Animals treated with curcumin showed less anxious and hyperactive behavior. Related to the memory, the results can be related to hyperactivity. Conclusion: Thus, the data suggest that the treatments used here can beneficially modulate the anxious and hyperactive behavior of SHR.

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“…High voltage-gated Ca 2+ channels [152] Cav2.2 and Cav2.1 [152,153] Ca 2+ release-activated Ca 2+ (CRAC) channels [152,153] Cystic fibrosis transmembrane conductance regulator (CFTR) [152] Aquaporin 4 (AQP-4) [152] Voltage-Gated Potassium Channel Kv1.3 (Kv1.3) [152,154] ATP-binding cassette drug transporter [152] Glucose transporter protein 2 GLUT2 [152] Glucose transporter protein 4 (GLUT4) [152] Transient receptor potential cation channel, subfamily M, member 2 (TRPM2) [119] Studies with rat hepatocytes and neuroblastoma cells have provided evidence that curcumin inhibits TRPM2 channels [119,155]. Oz and Celik investigated the actions of curcumin on TRPM2 channels in SH-SY5Y neuroblastoma cells heterologously expressing TRPM2 [155].…”

Section: Examples Of Proteins That Have Beenmentioning

confidence: 99%

TRPM2 Non-Selective Cation Channels in Liver Injury Mediated by Reactive Oxygen Species

2021

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TRPM2 channels admit Ca2+ and Na+ across the plasma membrane and release Ca2+ and Zn2+ from lysosomes. Channel activation is initiated by reactive oxygen species (ROS), leading to a subsequent increase in ADP-ribose and the binding of ADP-ribose to an allosteric site in the cytosolic NUDT9 homology domain. In many animal cell types, Ca2+ entry via TRPM2 channels mediates ROS-initiated cell injury and death. The aim of this review is to summarise the current knowledge of the roles of TRPM2 and Ca2+ in the initiation and progression of chronic liver diseases and acute liver injury. Studies to date provide evidence that TRPM2-mediated Ca2+ entry contributes to drug-induced liver toxicity, ischemia–reperfusion injury, and the progression of non-alcoholic fatty liver disease to cirrhosis, fibrosis, and hepatocellular carcinoma. Of particular current interest are the steps involved in the activation of TRPM2 in hepatocytes following an increase in ROS, the downstream pathways activated by the resultant increase in intracellular Ca2+, and the chronology of these events. An apparent contradiction exists between these roles of TRPM2 and the role identified for ROS-activated TRPM2 in heart muscle and in some other cell types in promoting Ca2+-activated mitochondrial ATP synthesis and cell survival. Inhibition of TRPM2 by curcumin and other “natural” compounds offers an attractive strategy for inhibiting ROS-induced liver cell injury. In conclusion, while it has been established that ROS-initiated activation of TRPM2 contributes to both acute and chronic liver injury, considerable further research is needed to elucidate the mechanisms involved, and the conditions under which pharmacological inhibition of TRPM2 can be an effective clinical strategy to reduce ROS-initiated liver injury.

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Effects of curcumin on ion channels and pumps: A review

Cited by 19 publications

References 100 publications

Natural Polyhydroxy Flavonoids, Curcuminoids, and Synthetic Curcumin Analogs as α7 nAChRs Positive Allosteric Modulators

Natural Polyhydroxy Flavonoids, Curcuminoids, and Synthetic Curcumin Analogs as α7 nAChRs Positive Allosteric Modulators

Curcumin for Attention Deficit Hyperactivity Disorder: a Behavioral Preliminary Investigation

TRPM2 Non-Selective Cation Channels in Liver Injury Mediated by Reactive Oxygen Species

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