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  • Curcumin is found safe in several human studies Chainani Wu


    Curcumin is found safe in several human studies (Chainani-Wu, 2003; Cheng et al., 2001; Dcodhar et al., 2013), in contrary, the toxicity of curcumin has also been reported under some specific conditions (Burgos-Morón et al., 2010). Moreover, it TNF-alpha, recombinant human protein australia was also reported that curcumin induced some types of carcinomas in animal models (Dance-Barnes et al., 2009; “NTP Toxicology and Carcinogenesis Studies of Turmeric Oleoresin (CAS No. 8024-37-1) (Major Component 79%–85% Curcumin, CAS No. 458-37-7) in F344/N Rats and B6C3F1 Mice (Feed Studies).,” 1993). There are proofs on curcumin pharmacokinetic alterations, regarding concomitant use of curcumin with different pharmacological agents such as antidepressants, cardiovascular drugs, chemotherapeutic agents, antibiotics, anticoagulants and antihistamines. These deviations are mainly observed in form of changes in the Cmax and AUC, which is mediated by inhibition of cytochrome and P-glycoprotein (Bahramsoltani et al., 2017). This resembles that although the daily intake of turmeric whole powder seems safe as is evident by Asian diet, conversely, the credibility of its safety is not very much clear. Of note, this also depends on the dose of curcumin administered. In sense of flavonoids safety, there are very few affirmations and further preclinical and clinical explorations are necessary to be performed.
    Neuropsycopharmacological mechanisms of flavonoids in neurodegeneration The anti-amyloid feature of flavonoids is assumed to be an utmost score. The protective role of polyphenols against neurodegenerative disorders has been documented in several in vitro and in vivo studies (Molino et al., 2016) and this is mainly due to the prevention of the onset or delayed progression of age related neurodegenerative disorders (Williams and Spencer, 2012). This potential owes to the multiple interactions with different glial signaling pathways and intracellular neurons, which affects the cerebral and peripheral vascular system, improves neuronal functions and stimulates neuronal regeneration (Moreno et al., 2017; Spencer, 2009). Polyphenols and in particular, resveratrol, curcumin and catechins exhibit their neuroprotective effects through diverse mechanisms, which comprises their anti-inflammatory properties, antioxidant and chelation effects, also may come from their interactions with several cell signaling pathways (Molino et al., 2016). Age related diseases like PD and AD can also be initiated by dysfunctional mitochondrial process (van Loo et al., 2002). An assortment of studies conveyed that flavonoids such as quercetin, EGCG and genistein manipulate mitochondrial dysfunctions (de Oliveira et al., 2016; Gao et al., 2012; Karuppagounder et al., 2013; Oliveira et al., 2016; Valenti et al., 2013). Resveratrol augmented the mitochondrial and vascular activities, likewise exhibited protecting influence on ischemia reperfusion when evaluated in rats (Lin et al., 2013; Menzies et al., 2013). The inductive effect of resveratrol on improvement of the spatial memory performance was proved in a primate study (Dal-Pan et al., 2011), since the action was correlated with decreasing of oxidative damage, chronic inflammation and mitochondrial dysfunction and also by sirtuins activation (Witte et al., 2014). Resveratrol attenuated ageing dependent decline in cognitive function in animal models of AD by lessening plaque formation, which was evident by decreased glutathione and increased cysteine levels (Karuppagounder et al., 2009; Marambaud et al., 2005). In a rotenone-induced rat model of PD, quercetin showed the capability of revamping electron transport defect of mitochondria and upregulation of Complex I, also this effect was assigned to the free radical scavenging activity of quercetin (Karuppagounder et al., 2013; Magalingam et al., 2015). Recently, nanoencapsulated quercetin in zein nanoparticles was prepared to enhance the low oral bioavailability of this compound (Moreno et al., 2017). These nanoparticles when administered orally, ameliorated the memory and cognitive impairments by inhibition of glial fibrillary acidic protein expression in SAMP8 mice (Moreno et al., 2017). Quercetin improved the emotional and cognitive impairments in AD TNF-alpha, recombinant human protein australia models and also found to reverse the histopathological hallmarks of AD (Sabogal-Guaqueta et al., 2015).