Orally administered epigallocatechin gallate attenuates light-induced photoreceptor damage

Costa, Belmira da Silveira Andrade da Lara; Fawcett, Rebecca; Li, Guangyu; Safa, Rukhsana; Osborne, Neville N.

doi:10.1016/j.brainresbull.2008.01.022

Cited by 45 publications

(26 citation statements)

References 72 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…For these reasons, we confirmed that caspase-3/7 was activated by light injury, being significant at 48 h after light exposure. Costa et al (2008) also reported that caspase-3 was up-regulated at 48 h after light exposure, and our result corresponded with those results. In the present study, SNJ-1945 inhibited caspase-3/7 activation 48 h after light exposure.…”

Section: Discussionsupporting

confidence: 91%

Calpain Inhibitor Protects Cells against Light-Induced Retinal Degeneration

Imai¹,

Shimazawa²,

Nakanishi³

et al. 2010

J Pharmacol Exp Ther

View full text Add to dashboard Cite

Calpains are activated by excessive light exposure and related to retinal degeneration. We investigated the protective effects of ((1S)-1-((((1S)-1-benzyl-3-cyclopropylamino-2,3-di-oxopropyl)amino)carbonyl)-3-methylbutyl)carbamic acid 5-methoxy-3-oxapentyl ester (SNJ-1945), a calpain inhibitor, against lightinduced retinal degeneration in mice. SNJ-1945 was orally administrated at doses of 100 and 200 mg/kg at 30 min before and just after light exposure. Light-induced calpain activation was evaluated by using proteolysis of ␣-spectrin and p35 (a neuron-specific activator for cyclin-dependent kinase 5). The effects of SNJ-1945 against light-induced retinal damage were examined by the thickness of the outer nuclear layer (ONL). Photoreceptor apoptosis was assessed by counting terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL)-positive cells in ONL. Retinal functions were measured in terms of a-and b-wave amplitudes by using an electroretinogram. As the mechanism of SNJ-1945, caspase-3/7 measurement was carried out. SNJ-1945 inhibited the proteolysis of ␣-spectrin and p35 by light exposure and presented a decrease in the numbers of TUNEL-positive cells and ONL atrophy. Furthermore, SNJ-1945 presented a decrease in a-and b-wave amplitude and caspase-3/7 activation induced by light exposure. These findings suggest that the activation of calpain plays a pivotal role in photoreceptor degeneration by light exposure, and SNJ-1945 may be a candidate for effectively treating diseases related to photoreceptor degeneration.

show abstract

Section: Discussionsupporting

confidence: 91%

Calpain Inhibitor Protects Cells against Light-Induced Retinal Degeneration

Imai¹,

Shimazawa²,

Nakanishi³

et al. 2010

J Pharmacol Exp Ther

View full text Add to dashboard Cite

show abstract

“…In vitro and in vivo studies support the neuroprotective activity of polyphenols against diverse neuronal insults, such as ischemia, oxidative-induced damage, and dopamine-induced neurotoxicity (Lau et al, 2005;Mercer et al, 2005;Gottlieb et al, 2006;Costa et al, 2008;Maher, 2008;Rainey-Smith et al, 2008;Vauzour et al, 2008). Administration of the polyphenol epigallocatechin Contract grant sponsor: FAPERJ; Contract grant sponsor: CNPq; Contract grant sponsor: CAPES.…”

mentioning

confidence: 92%

Effects of the flavonoid casticin from Brazilian Croton betulaster in cerebral cortical progenitors in vitro: Direct and indirect action through astrocytes

Spohr

Stipursky

Sasaki

et al. 2009

J of Neuroscience Research

View full text Add to dashboard Cite

Neurodegenerative diseases are a major constraint on the social and economic development of many countries. Evidence has suggested that phytochemicals have an impact on brain pathology; however, both their mechanisms of action and their cell targets are incompletely known. Here, we investigated the effects of the flavonoid casticin, extracted from Croton betulaster, a common plant in the state of Bahia in Brazil, on rat cerebral cortex neurons in vitro. Treatment of neural progenitors with 10 microM casticin increased the neuronal population positive for the neuronal marker beta-tubulin III and the neuronal transcriptional factor Tbr2 by approximately 20%. This event was followed by a 50% decrease in neuronal death. Pools of astrocyte (GFAP and S100beta), neural (nestin), and oligodendrocyte (Olig2 and NG2) progenitors were not affected by casticin. Neither neuronal commitment nor proliferation of progenitors was affected by casticin, suggesting a neuroprotective effect of this compound. Culture of neural progenitors on casticin-treated astrocyte monolayers increased the neuronal population by 40%. This effect was reproduced by conditioned medium derived from casticin-treated astrocytes, suggesting the involvement of a soluble factor. ELISA assays of the conditioned medium revealed a 20% increase in interleukin-6 level in response to casticin. In contrast to the direct effect, neuronal death was unaffected, but a 52% decrease in the death of nestin-positive progenitors was observed. Together our data suggest that casticin influences the neuronal population by two mechanisms: 1) directly, by decreasing neuronal death, and 2) indirectly, via astrocytes, by modulating the pool of neuronal progenitors.

show abstract

“…In neuropathology, studies have also reported the beneficial effects of these substances, such as in AD, PD, Huntington's disease, and ALS [103,[121][122][123][124]. In vitro and in vivo studies support the neuroprotective activity of polyphenols against diverse neuronal insults such as ischemia, oxidative-induced damage, and dopamineinduced neurotoxicity [121][122][123][124][125][126][127]. The best-known effect of flavonoids on the nervous system is related to the ability of these substances to protect neurons from oxidative stress.…”

Section: Flavonoids and Neurodegenerative Diseasesmentioning

confidence: 94%

“…These substances have attracted increasing interest because numerous epidemiological studies have suggested associations between the consumption of polyphenol-rich foods or beverages and the prevention of certain chronic diseases such as cancers and cardiovascular pathologies [118][119][120]. In neuropathology, studies have also reported the beneficial effects of these substances, such as in AD, PD, Huntington's disease, and ALS [103,[121][122][123][124]. In vitro and in vivo studies support the neuroprotective activity of polyphenols against diverse neuronal insults such as ischemia, oxidative-induced damage, and dopamineinduced neurotoxicity [121][122][123][124][125][126][127].…”

Section: Flavonoids and Neurodegenerative Diseasesmentioning

confidence: 98%

Flavonoids and Astrocytes Crosstalking: Implications for Brain Development and Pathology

et al. 2010

View full text Add to dashboard Cite

Flavonoids are naturally occurring polyphenolic compounds that are present in a variety of fruits, vegetables, cereals, tea, and wine, and are the most abundant antioxidants in the human diet. Evidence suggests that these phytochemicals might have an impact on brain pathology and aging; however, neither their mechanisms of action nor their cell targets are completely known. In the mature mammalian brain, astroglia constitute nearly half of the total cells, providing structural, metabolic, and trophic support for neurons. During the past few years, increasing knowledge of these cells has indicated that astrocytes are pivotal characters in neurodegenerative diseases and brain injury. Most of the physiological benefits of flavonoids are generally thought to be due to their antioxidant and free-radical scavenging effects; however, emerging evidence has supported the hypothesis that their mechanism of action might go beyond these properties. In this review, we focus on astrocytes as targets for flavonoids and their implications in brain development, neuroprotection, and glial tumor formation. Finally, we will briefly discuss the emerging view of astrocytes as essential characters in neurodegenerative diseases, and how a better understanding of the action of flavonoids might open new avenues to develop therapeutic approaches to these pathologies.

show abstract

Orally administered epigallocatechin gallate attenuates light-induced photoreceptor damage

Cited by 45 publications

References 72 publications

Calpain Inhibitor Protects Cells against Light-Induced Retinal Degeneration

Calpain Inhibitor Protects Cells against Light-Induced Retinal Degeneration

Effects of the flavonoid casticin from Brazilian Croton betulaster in cerebral cortical progenitors in vitro: Direct and indirect action through astrocytes

Flavonoids and Astrocytes Crosstalking: Implications for Brain Development and Pathology

Contact Info

Product

Resources

About