Neuroprotective Properties of Gallic Acid from Sanguisorbae Radix on Amyloid .BETA. Protein (25-35)-Induced Toxicity in Cultured Rat Cortical Neurons

Ban, Ju Yeon; Nguyen, Huy Bang; Lee, Hee-Ju; Cho, Soon Ock; Ju, Hyun; Kim, Ju Yeon; Bae, KiHwan; Song, Kyung‐Sik; Seong, Yeon Hee

doi:10.1248/bpb.31.149

Cited by 81 publications

(52 citation statements)

References 38 publications

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“…Gallic acid and vanillic acid showed neuroprotective effect, AchE inhibitory activity and antioxidant effect (Ban et al ., 2008; Ghayur et al ., 2011; Gan et al ., 2011; Weon et al ., 2012). Ferulic acid was also protected against memory and learning deficit induced β-amyloid peptide in mice and had antioxidant activity (Cho et al ; 2005).…”

Section: Disscusionmentioning

confidence: 99%

Neuroprotective Effect of Steamed and Fermented Codonopsis lanceolata

Weon

Yun

Lee

et al. 2014

Biomolecules & Therapeutics

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Codonopsis lanceolata has been used as an herbal medicine for several lung inflammatory diseases, such as asthma, tonsillitis, and pharyngitis. Previously, we showed the neuroprotective effect of steamed and fermented C. lanceolata (SFC) in vitro and in vivo. In the current study, the treatment of HT22 cells with SFC decreased glutamate-induced cell death, suggesting that SFC protected HT22 cells from glutamate-induced cytotoxicity. Based on these, we sought to elucidate the mechanisms of the neuro-protective effect of SFC by measuring the oxidative stress parameters and the expression of Bax and caspase-3 in HT22 cells. SFC reduced contents of ROS, Ca2+ and NO. Moreover, SFC restored contents of glutathione and glutathione reductase as well as inhibited Bax and caspase-3 activity in HT22 cells. These results indicate that steamed and fermented C. lanceolata (SFC) extract protected HT22 cells by anti-oxidative effect and inhibition of the expression of Bax and caspase-3.

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Section: Disscusionmentioning

confidence: 99%

Neuroprotective Effect of Steamed and Fermented Codonopsis lanceolata

Weon

Yun

Lee

et al. 2014

Biomolecules & Therapeutics

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“…36) Gallic acid, which is a main antioxidant in the acorn extract, 15) has been reported to inhibit Aβ(25-35)-induced [Ca 2+ ] i increases in rat cortical neurons. 21) In addition, octyl gallate reportedly inhibits Ca 2+ signaling in PC 12 cells through multiple pathways including voltage-gated Ca 2+ channel and Ca 2+ -permeable-ligand-ion channels. 37) Contents of phenolic compounds and gallic acid in the acorn extract used in this study were 5.43% 22) and 0.27%, 23) respectively.…”

Section: Discussionmentioning

confidence: 99%

“…17) Gallic acid has prevented Aβ(25-35)-induced apoptotic neuronal death by interfering with [Ca 2+ ] i increases in rat cortical neurons. 21) Massive release of glutamate induces [Ca 2+ ] i increases after acute brain injuries such as epilepsy and brain ischemia, which initiate many cellular processes including RoS formation. All these results suggest the possibility that acorn extract can be used as a supplement against glutamate excitotoxicity-related neurologic disorders including epilepsy and ischemia.…”

Section: Discussionmentioning

confidence: 99%

“…20) Gallic acid is one of the main antioxidants in acorn extract, and reportedly prevents amyloid beta (Aβ) (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)-induced apoptotic neuronal death by interfering with [Ca 2+ ] i increases in rat cortical neurons. 21) However, there are no reports on the effect of acorn extract against glutamate-induced Ca 2+ signaling in cultured rat hippocampal neurons.…”

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Inhibitory Effects of Acorn Extract on Glutamate-Induced Calcium Signaling in Cultured Rat Hippocampal Neurons

Lee

Hong

Yang

et al. 2013

Biological & Pharmaceutical Bulletin

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Various effects of acorn extract have been reported including antioxidant activity, cytotoxicity against cancer cells, and the levels of acetylcholine and its related enzyme activities in the dementia mouse models. However, it is unclear whether acorn extract inhibits glutamate-induced calcium signaling in hippocampal neurons. This study was an investigation into the effect of acorn extract on intracellular free Ca ] i ) can also be elevated by the release of Ca 2+ from IP 3 -sensitive intracellular stores through the metabotrophic glutamate receptor-induced activation of phospholipase C (PLC). Ca 2+ plays a role as an intracellular messenger and a key regulatory factor for a large number of cellular processes such as muscle contraction, metabolism, secretion or even cell differentiation and apoptosis.

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“…GA induced apoptosis in human leukemia HL-60RG cells (9), human lung cancer cell lines (10), human stomach cancer KATO III, colon adenocarcinoma COLO 205 cell line (11) and PC12 rat pheochromocytoma cells (12). It was also reported that GA plays an important role in the prevention of malignant transformation (13) and GA prevents amyloid ß-induced apoptotic neuronal death by interfering with the increase of Ca 2+ levels and then by inhibiting glutamate release and generation of ROS (14). GA was shown to have antitumor effects on LL-2 lung cancer cells transplanted in mice (15) and NCI-H460 human lung cancer cells in vitro and in vivo (10).…”

Section: Introductionmentioning

confidence: 94%

Gallic acid induces apoptosis in A375.S2 human melanoma cells through caspase-dependent and -independent pathways

Lai²,

Yang

et al. 2010

Int J Oncol

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Abstract. The natural antioxidant gallic acid (GA) has demonstrated a significant inhibition of cell proliferation and induction of apoptosis in a series of cancer cell lines. However, there is no available information to show whether GA induces apoptosis in human skin cancer cells. In the present study, we report GA-induced apoptosis in A375.S2 human melanoma cells. GA affected morphological changes, decreased the percentage of viable cells and induced apoptosis in A375.S2 cells in a dose-and time-dependent manner. Observation of the molecular mechanism of apoptosis in A375.S2 cells showed that GA up-regulated the proapoptotic proteins such as Bax, and induced caspase cascade activity, but down-regulated antiapoptotic proteins such as Bcl-2. GA induced reactive oxygen species (ROS) and intracellular Ca 2+ productions and decreased the level of mitochondrial membrane potential (Δae m ) in A375.S2 cells in a timedependent manner. GA triggered cytosolic release of apoptotic molecules, cytochrome c, promoted activation of caspase-9 and caspase-3, and ultimately apoptotic cell death. In addition, GA also promoted cytosolic release of apoptosisinducing factor (AIF) and endonuclease G (Endo G). Therefore, GA may also induce apoptosis through a caspaseindependent pathway. Our results suggest that GA might be a potential anticancer compound; however, in depth in vivo studies are needed to elucidate the exact mechanism.

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Neuroprotective Properties of Gallic Acid from Sanguisorbae Radix on Amyloid .BETA. Protein (25-35)-Induced Toxicity in Cultured Rat Cortical Neurons

Abstract: ] c , and then by inhibiting glutamate release and generation of ROS, and that these effects of gallic acid may be partly associated with the neuroprotective effect of Sanguisorbae radix.

Cited by 81 publications

References 38 publications

Neuroprotective Effect of Steamed and Fermented Codonopsis lanceolata

Neuroprotective Effect of Steamed and Fermented Codonopsis lanceolata

Inhibitory Effects of Acorn Extract on Glutamate-Induced Calcium Signaling in Cultured Rat Hippocampal Neurons

Gallic acid induces apoptosis in A375.S2 human melanoma cells through caspase-dependent and -independent pathways

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