Multifunctional Activities of Green Tea Catechins in Neuroprotection

Abstract

Many lines of evidence suggest that oxidative stress resulting in reactive oxygen species (ROS) generation and inflammation play a pivotal role in the age-associated cognitive decline and neuronal loss in neurodegenerative diseases including Alzheimer’s (AD), Parkinson’s (PD) and Huntington’s diseases. One cardinal chemical pathology observed in these disorders is the accumulation of iron at sites where the neurons die. The buildup of an iron gradient in conjunction with ROS (superoxide, hydroxyl radical and nitric oxide) are thought to constitute a major trigger in neuronal toxicity and demise in all these diseases. Thus, promising future treatment of neurodegenerative diseases and aging depends on availability of effective brain permeable, iron-chelatable/radical scavenger neuroprotective drugs that would prevent the progression of neurodegeneration. Tea flavonoids (catechins) have been reported to possess potent iron- chelating, radical-scavenging and anti-inflammatory activities and to protect neuronal death in a wide array of cellular and animal models of neurological diseases. Recent studies have indicated that in addition to the known antioxidant activity of catechins, other mechanisms such as modulation of signal transduction pathways, cell survival/death genes and mitochondrial function, contribute significantly to the induction of cell viability. This review will focus on the multifunctional properties of green tea and its major component (–)-epigallocatechin-3-gallate (EGCG) and their ability to induce neuroprotection and neurorescue in vitro and in vivo. In particular, their transitional metal (iron and copper) chelating property and inhibition of oxidative stress.

Constitutive Overexpression of Nrf2-dependent Heme Oxygenase-1 in A549 Cells Contributes to Resistance to Apoptosis Induced by Epigallocatechin 3-Gallate

“…2, A, B, and D) sustains high concentration of intracellular iron produced by HO-1 catalytic activity that may result in phosphorylation of PKC␣ and subsequent activation of Nrf2 (48,51). In this scenario, we speculated that EGCG, as an iron chelator (26,33) and not as an ROS generator (36,37), may exert its inhibitory effects on phosphorylation of PKC␣ (Fig.…”

“…observed unexpectedly low levels of ferritin in contrast to overexpression of HO-1 (Fig. 2, B and D), we next focused on the possibility that the occurrence of highly activated PKC␣ may be associated with an accumulation of free iron (48,51) because of the failure of iron sequestering by ferritin, which is concomitantly up-regulated with HO-1 induction (3,54). To verify this hypothesis, we tested the effect of an iron chelator, DFO (26), along with an ROS scavenging agent, NAC (20,21), during EGCG treatment of A549 cells.…”

Neuroprotective Effect of Sanguisorbae Radix against Oxidative Stress-Induced Brain Damage: in Vitro and in Vivo

“…Neuronal cells exposed to H 2 O 2 produce membrane depolarization depending on the increased permeability to Na 14) It could be also suggested that ROS-scavenging activity of SR possibly attributable to catechin played a critical role in neuronal survival, since catechin has been shown to have neuroprotective property directly associated with ROS-scavenging activity. 46,47) Future study to elucidate the precise mechanism should be performed.…”

Screening Camelia sinensis Germplasm Against Grey Leaf Blight of Tea

“…It contains polyphenols and other metabolites, with anti-carcinoma (Wang and Bachrach, 2002;Zhang et al, 2012), anti-oxidative (Rietveld and Wiseman, 2003;Fatima and Rizvi, 2015) and anti-arteriosclerosis (Lee et al, 2015) properties. These polyphenols are also reported to be effective for the prevention of Alzheimer's and Parkinson diseases (Mandel, Amit, Weinreb, Reznichenko, and Youdim, 2008;Anandhan, Tamilselvam, Radhiga, Rao, and Essa, 2012) and for their anti-obesity effects in human and animals (Zhong, Furne, and Levitt, 2006;Ashigai et al, 2016).…”