Role of Reactive Oxygen Species in Gallic Acid-Induced Apoptosis.

Inoue, Makoto; Sakaguchi, Nahoko; Isuzugawa, Kazuto; Tani, Hiroyuki; Ogihara, Yukio

doi:10.1248/bpb.23.1153

Cited by 144 publications

(110 citation statements)

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“…Increasing evidence suggests that apoptosis induced by GA is associated with oxidative stresses derived from ROS (11,27). According to our results, ROS (DCF) level such as H 2 O 2 was not altered in GA-treated CPAEC and was decreased in 400 μM GA-treated HUVEC.…”

Section: Discussionsupporting

confidence: 66%

“…Anticancer activity of GA has been reported in various cancer cells, such as prostate cancer (6), lung cancer (7,8), gastric, colon, breast, cervical and esophageal cancer (9). Apoptosis induced by GA is associated with oxidative stresses derived from reactive oxygen species (ROS), mitochondrial dysfunction and an increase in intracellular Ca 2+ level (10,11). Controversially, GA has been suggested to have both pro-oxidant and antioxidant properties depending on iron or H 2 O 2 in medium and plasma (12,13).…”

Section: Introductionmentioning

confidence: 99%

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p38 inhibitor enhances growth inhibition and death in gallic acid-treated endothelial cells

Yang

Park²

2010

Int J Mol Med

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Abstract. Gallic acid (GA) found in various plants, fruits and foods has various biological effects including apoptosis. However, little is known about the relationship between reactive oxygen species (ROS) and p38 signaling in GAtreated endothelial cells (ECs). In this study, we investigated the effects of p38 inhibitor on GA-induced calf pulmonary artery endothelial cells (CPAEC) and human umbilical vein endothelial cell (HUVEC) death in view of ROS and glutathione (GSH). GA inhibited the growth of both ECs and induced apoptosis, which was accompanied by the loss of mitochondrial membrane potential (MMP; Δae m ). The susceptibility of CPAEC to GA is higher than that of HUVEC. GA differently increased or decreased ROS levels in ECs. GA increased GSH depleted cell numbers in ECs. p38 inhibitor seemed to enhance cell growth inhibition and cell death in GA-treated ECs. This inhibitor increased or decreased ROS levels in GA-treated ECs. p38 inhibitor to some extent enhanced GSH depletion in GA-treated CPAEC but it clearly increased GSH depletion cell numbers in GAtreated and -untreated HUVEC. In conclusion, p38 inhibitor appeared to enhance growth inhibition and death in GAtreated ECs, which were partially influenced by the changes of ROS and GSH depletion levels.

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Section: Discussionsupporting

confidence: 66%

Section: Introductionmentioning

confidence: 99%

p38 inhibitor enhances growth inhibition and death in gallic acid-treated endothelial cells

Yang

Park²

2010

Int J Mol Med

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“…This suggested that both GDs were able to stimulate caspase-3 in a way similar to GA, as reported elsewhere. 18) ROS and intracellular Ca 2ϩ play important roles in GA-induced apoptosis. Therefore, we first examined the effects of various kinds of inhibitors on GA, hydrogen peroxide or hypoxanthine-xanthine oxidase (HX/XO)-elicited PARP cleavage (Fig.…”

Section: Resultsmentioning

confidence: 99%

Ca2+-Dependent Caspase Activation by Gallic Acid Derivatives.

Isuzugawa

Ogihara

2001

Biological & Pharmaceutical Bulletin

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“…Some results have shown that GT causes apoptosis via inhibition of glutathione (GSH) production and synthesis of reactive oxygen species (Inoue et al 2000). Also, GT decreased the gene expression and production of phorbol 12Ámyristate 13Áacetate-stimulated pro-inflammatory cytokines such as TNF-alpha and IL-6 in human mast cells ).…”

Section: Discussionmentioning

confidence: 99%

Gallotannin regulates apoptosis and COX-2 expression via Akt and p38kinase pathway in human lung cancer cell line, A549

Gweon

Chung

et al. 2012

Animal Cells and Systems

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Gallotannin (GT) is derived from plant poly phenol and is associated with biological actions in a wide range of cells. In this study, we evaluated the effect of GT on apoptosis and cyclooxygenase-2 (COX-2) expression and attempted to shed light on the mechanism of action in A549 human lung carcinoma cells. We found that GT dramatically induced apoptosis as demonstrated by expression of p53 and active caspase-3 via western blot analysis and fragmented DNA as detected by DNA fragmentation and DAPI staining. We also observed that GT significantly causes COX-2 expression in a dose-dependent manner determined by western blot analysis. Phosphorylation of Akt and p38 was considerably increased by GT in A549 human lung carcinoma cells. Inhibition of Akt and p38kinase with LY294002 or SB203580 suppressed GT-induced apoptosis and COX-2 expression. Furthermore, we have shown that prevention of COX-2 with NS398 or indomethacin does not any effects on apoptosis induced by GT. Taken together, our present results suggest that GT regulates apoptosis and COX-2 expression through Akt and p38kinase pathway in A549, human lung carcinoma cells.

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Role of Reactive Oxygen Species in Gallic Acid-Induced Apoptosis.

Cited by 144 publications

References 0 publications

p38 inhibitor enhances growth inhibition and death in gallic acid-treated endothelial cells

p38 inhibitor enhances growth inhibition and death in gallic acid-treated endothelial cells

Ca2+-Dependent Caspase Activation by Gallic Acid Derivatives.

Gallotannin regulates apoptosis and COX-2 expression via Akt and p38kinase pathway in human lung cancer cell line, A549

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