The effect of epigallocatechin gallate on suppressing disease progression of ALS model mice

Koh, Seong‐Ho; Lee, Sang Mok; Kim, Ho; Lee, Kyu-Yong; Lee, Young Joo; Kim, Hee-Tae; Kim, Juhan; Kim, Myung Ho; Hwang, Myung-Sil; Song, Chi-Won; Yang, Ki-Wha; Lee, Kwang Woo; Kim, Seung Hyun; Kim, Ok-Hee

doi:10.1016/j.neulet.2005.10.056

Cited by 136 publications

(78 citation statements)

References 25 publications

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“…Consistent with Koh's study [15], We found that EGCG decreased cleaved caspase-3 immunoreactivity (Fig. 5), thereby confirming that EGCG inhibits the caspase-3 pathway in EGCG treated SOD1-G93A mice.…”

Section: Egcg Reduces Activation Of Nf-kb and Diminishes Activated Casupporting

confidence: 91%

Neuroprotective Effects of (-)-Epigallocatechin-3-gallate in a Transgenic Mouse Model of Amyotrophic Lateral Sclerosis

Chen

et al. 2006

Neurochem Res

123

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The purpose of this study is to evaluate neuroprotective effects of (-)-Epigallocatechin-3-gallate (EGCG) in a transgenic mouse model of Amyotrophic lateral sclerosis (ALS). SOD1-G93A transgenic mice and wild-type mice were randomly divided into EGCG-treated groups (10 mg/kg, p.o) and vehicle-treated control groups. Rotarod measurement was performed to assess the motor function of mice starting at the age of 70 days. Nissl staining to examine the number of motor neurons and CD11b immunohistochemical staining to evaluate activation of microglia in the lumbar spinal cords were conducted at the age of 120 days. In addition, for further observation of regulation of cell signaling pathways by EGCG, we used immunohistochemical analysis for nuclear factor kappa B (NF-kappaB) and cleaved caspase-3 as well as western blot analysis to determine the expression of nitric oxide synthase (iNOS) and NF-kappaB in the spinal cord. This study demonstrated that oral administration of EGCG beginning from a pre-symptomatic stage significantly delayed the onset of disease, and extended life span. Furthermore, EGCG-treated transgenic mice showed increased number of motor neurons, diminished microglial activation, reduced immunohistochemical reaction of NF-kappaB and cleaved caspase-3 as well as reduced protein level of iNOS and NF-kappaB in the spinal cords. In conclusion, this study provides further evidences that EGCG has multifunctional therapeutic effects in the mouse model of ALS.

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Section: Egcg Reduces Activation Of Nf-kb and Diminishes Activated Casupporting

confidence: 91%

Neuroprotective Effects of (-)-Epigallocatechin-3-gallate in a Transgenic Mouse Model of Amyotrophic Lateral Sclerosis

Chen

et al. 2006

Neurochem Res

123

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“…Supplementary preclinical models of other neurodegenerative diseases demonstrated that EGCG induced the prolongation of the symptom onset and life span and attenuated death signals in ALS mice model, expressing the human G93A mutated Cu/Zn-superoxide dismutase (SOD1) gene [54,144]. Additionally, EGCG has been shown to be neuroprotective in aged rats [122] and in animal models of focal and global brain ischemia [91,124,125].…”

Section: Preclinical Studiesmentioning

confidence: 99%

Neuroprotective molecular mechanisms of (−)-epigallocatechin-3-gallate: a reflective outcome of its antioxidant, iron chelating and neuritogenic properties

et al. 2009

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Tea, the major source of dietary flavonoids, particularly the epicatechins, signifies the second most frequently consumed beverage worldwide, which varies its status from a simple ancient cultural drink to a nutrient component, endowed possible beneficial neuro-pharmacological actions. Accumulating evidence suggests that oxidative stress, resulting in reactive oxygen species generation, plays a pivotal role in neurodegenerative diseases, supporting the implementation of radical scavengers and metal chelating agents, such as natural tea polyphenols, for therapy. Vast epidemiology data indicate a correlation between occurrence of neurodegenerative disorders, such as Parkinson's and Alzheimer's diseases, and green tea consumption. In particular, recent literature strengthens the perception that diverse molecular signaling pathways, participating in the neuroprotective activity of the major green tea polyphenol, (-)-epigallocatechin-3-gallate (EGCG), renders this natural compound as potential agent to reduce the risk of various neurodegenerative diseases. In the current review, we discuss the studies concerning the mechanisms of action implicated in EGCG-induced neuroprotection and discuss the vision to translate these findings into a lifestyle arena.

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“…EGCG, the most abundant catechin in green tea, is credited with the majority of health benefits associated with green tea consumption. EGCG has demonstrated beneficial effects in studies of Parkinson's disease (Choi et al, 2002), Alzheimer's disease (Choi et al, 2001;Obregon et al, 2006), stroke (Choi et al, 2004;Koh et al, 2006), obesity (Kao et al, 2000), diabetes (Anderson and Polansky, 2002;Tsuneki et al, 2004), chemoprevention (Xu et al, 1992;Katiyar et al, 1993;Kavanagh et al, 2001;Chung et al, 2003) and also possesses antioxidant activity (Guo et al, 1999). In this review, the potential applications of EGCG in the treatment of breast and prostate cancer and its possible mechanisms of action will be discussed.…”

Section: Introductionmentioning

confidence: 99%

Role of epigallocatechin gallate (EGCG) in the treatment of breast and prostate cancer

2006

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The effect of epigallocatechin gallate on suppressing disease progression of ALS model mice

Cited by 136 publications

References 25 publications

Neuroprotective Effects of (-)-Epigallocatechin-3-gallate in a Transgenic Mouse Model of Amyotrophic Lateral Sclerosis

Neuroprotective Effects of (-)-Epigallocatechin-3-gallate in a Transgenic Mouse Model of Amyotrophic Lateral Sclerosis

Neuroprotective molecular mechanisms of (−)-epigallocatechin-3-gallate: a reflective outcome of its antioxidant, iron chelating and neuritogenic properties

Role of epigallocatechin gallate (EGCG) in the treatment of breast and prostate cancer

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