Effects of acute and chronic quercetin administration on methylphenidate-induced hyperlocomotion and oxidative stress

Abstract

These results suggest that chronic quercetin treatment has antimanic-like and antioxidant effects, thus encouraging further studies of quercetin as a putative new antimanic drug.

Crocin acts as a neuroprotective mediator against methylphenidate-induced neurobehavioral and neurochemical sequelae: Possible role of the CREB-BDNF signaling pathway

“…Other experimental studies have also established that the observed anti-oxidative properties of crocin in neurodegenerative disorders and diseases are mediated by an increase in activity of GR and GPx (Bors et al, 1984;Ochiai et al, 2004a). Moreover, a similar previous study demonstrated that prolonged quercetin treatment blocked the MPH-induced increase in oxidative stress (Kanazawa et al, 2017). Also, our results confirm prior studies showing a decrease in SOD action following MPH abuse (Lagace et al, 2006;Martins et al, 2006).…”

“…It has been previously proposed that crocin can modulate cortical excitability, motor activity, and reaction speed in depressed individuals (Jam et al, 2017). A related study demonstrated that chronic administration of quercetin blocked MPH-stimulated hyper-locomotion in mice, which may reflect an antimanic-like effect (Kanazawa et al, 2017).…”

“…Previous research demonstrates that treatment with crocin can counteract oxidative stress by lipid peroxidation reduction, and can improve the functioning of antioxidant enzymes such as superoxide dismutase (SOD) and catalase in some neurodegenerative disorders El-Beshbishy et al, 2012). Also, one previous study indicated that chronic treatment of quercetin -an agent that is structurally similar to crocin -can inhibit the manic-like and antioxidant effects of MPH treatment (Kanazawa et al, 2017). Additionally, prolonged treatment with crocin decreased the alcohol-induced increase in levels of interleukin 1 beta (IL-1β) and tumor necrosis factor alpha (TNF-α) (El-Maraghy et al, 2015).…”

Role of Protein Kinase C in Bipolar Disorder: A Review of the Current Literature

“…AMPH-induced hyperlocomotion has been shown to be reversed [7] and prevented [49] by intraperitoneal administration of lithium or tamoxifen (TMX), a selective estrogen receptor modulator with PKC inhibitory activity [8,50]. Similarly, intraperitoneal administration of quercetin, a nonspecific PKC inhibitor, also prevented methylphenidate-induced hyperlocomotion [51]. Not only in the presence of pharmacological intervention, daily intraperitoneal administration of lithium or TMX alone for 7 days significantly decreases phosphorylated PKC (pPKC) in the hippocampus, PFC, amygdala, and striatum [7].…”

“…Kanazawa et al [53] showed that the quercetin administration was able to reverse the increase in lipid peroxidation in PFC, hippocampus, and striatum in a mouse model of mania induced by PSD. Quercetin also blocked methylphenidate-induced hyperlocomotion and oxidative stress in PFC, hippocampus, and striatum of mice [51]. It appears that oxidative stress is downstream to PKC signaling as TMX, a selective PKC inhibitor, also prevented and reversed oxidative stress in AMPH-treated rats [50].…”