Propyl gallate inhibits the growth of HeLa cells via regulating intracellular GSH level

Han, Yong Hwan; Park, Woo Hyun

doi:10.1016/j.fct.2009.07.013

Cited by 65 publications

(92 citation statements)

References 36 publications

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“…Detection of intracellular ROS levels. Intracellular ROS were detected by means of an oxidation-sensitive fluorescent probe dye, 2',7'-dichlorodihydrofluorescein diacetate (Ex/ Em=495/529 nm; Invitrogen Life Technologies) and dihydroethidium (DHE, Ex/Em=518/605 nm; Invitrogen Life Technologies) as previously described (21,23). DHE is highly selective for O 2…”

Section: Measurement Of the Mitochondrial Membrane Potential (Mmp; ∆ψmentioning

confidence: 99%

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PX-12 inhibits the growth of A549 lung cancer cells via G2/M phase arrest and ROS-dependent apoptosis

You

Shin

Park

2013

International Journal of Oncology

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Abstract. PX-12 (1-methylpropyl 2-imidazolyl disulfide) is an inhibitor of thioredoxin (Trx-1), which has antitumor effects. However, little is known about the toxicological effect of PX-12 on cancer cells. We investigated the anti-growth effects of PX-12 on A549 lung cancer cells in relation to reactive oxygen species (ROS) and glutathione (GSH) levels. Based on MTT assays, PX-12 inhibited the growth of A549 cells with an IC 50 of approximately 20 µM at 72 h. DNA flow cytometric analysis indicated that PX-12 significantly induced the G2/M phase arrest of the cell cycle in A549 cells. This agent also induced apoptotic cell death, as demonstrated by Annexin V-FITC staining cells and the loss of mitochondrial membrane potential MMP (∆Ψ m ). In addition, the administration of Bax siRNA attenuated PX-12-induced A549 cell death. All the tested caspase inhibitors, especially Z-VAD significantly prevented apoptosis induced by PX-12. With respect to ROS and GSH levels, PX-12 increased ROS levels including O 2•-in A549 cells and induced GSH depletion. N-acetyl cysteine (NAC) markedly reduced ROS levels in PX-12-treated A549 cells. NAC also prevented apoptotic cell death and GSH depletion induced by PX-12. This is the first report to show that PX-12 inhibits the growth of A549 cells via G2/M phase arrest, and Bax-mediated and ROS-dependent apoptosis.

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Section: Measurement Of the Mitochondrial Membrane Potential (Mmp; ∆ψmentioning

confidence: 99%

“…Cellular GSH levels were analyzed using a 5-chloromethylfluorescein diacetate dye (CMFDA, Ex/Em=522/595 nm; Invitrogen Life Technologies) as previously described (23,24). In brief, 1ⅹ10…”

Section: Transfection Of Cells Withmentioning

confidence: 99%

PX-12 inhibits the growth of A549 lung cancer cells via G2/M phase arrest and ROS-dependent apoptosis

You

Shin

Park

2013

International Journal of Oncology

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“…Apoptosis was determined by staining HPF cells with Annexin V-fluorescein isothiocyanate (FITC; Ex/Em=488/519 nm; Invitrogen; Thermo Fisher Scientific, Inc.) and PI (Ex/Em=488/617 nm; Sigma-Aldrich; Merck KGaA) as previously described (29). Briefly, 1x10 6 HPF cells in 60 mm culture plates (Nalge Nunc International; Thermo Fisher Scientific, Inc.) were incubated with 0, 50 or 100 µM PG in the presence or absence of each MAPK inhibitor at 37˚C for 24 h. Annexin V/PI staining was analyzed using a FACStar flow cytometer (BD Biosciences, Franklin Lakes, NJ, USA) and CellQuest Pro software (version 5.1; BD Biosciences).…”

Section: Methodsmentioning

confidence: 99%

MAPK inhibitors enhance cell death in pyrogallol-treated human pulmonary fibroblast cells via increasing O2•− levels

Han

Park

2017

Oncology Letters

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Abstract. Pyrogallol (PG) induces apoptosis in lung cancer cells via the overproduction of O 2•-and affects mitogen-activated protein kinases (MAPKs) in these cells. The aim of the present study was to elucidate the effect of PG and/or MAPK inhibitors on human pulmonary fibroblast (HPF) cell viability in relation to reactive oxygen species (ROS) and glutathione (GSH). Treatment with 50 or 100 µM PG inhibited the viability of HPF cells, and induced cell death and the loss of mitochondrial membrane potential (MMP; ΔΨ m ). In particular, treatment with 100 µM PG induced cell death via apoptosis as well as necrosis in HPF cells. PG increased mitochondrial O 2•-levels and the number of GSH-depleted HPF cells. All the MAPK (mitogen-activated protein kinase kinase, c-Jun N-terminal kinase and p38) inhibitors enhanced the inhibition of cell viability, cell death and MMP (ΔΨ m ) loss in 100 µM PG-treated HPF cells. All the inhibitors increased the O 2•-levels in 100 µM PG-treated HPF cells, but none of the inhibitors significantly altered the PG-induced GSH depletion. In conclusion, PG treatment induced cell death via apoptosis and necrosis in HPF cells. Treatment with MAPK inhibitors slightly enhanced cell death in PG-treated HPF cells. HPF cell death induced by PG and/or MAPK inhibitors was at least partially associated with changes in O 2•-levels and GSH content. The present data provided useful information to understand PG-induced normal lung cell death in association with MAPK signaling pathways and ROS levels.

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“…Intracellular GSH levels were determined after staining cell with 5-chloromethylfluorescein diacetate (CMF-DA) [12]. CMF-DA passed freely through cell membranes, but once inside the cell, were transformed into cell-impermeant products and react with the thiol group of GSH.…”

Section: Evaluation Of Glutathione (Gsh) In Clone 9 Cellsmentioning

confidence: 99%

Comparison of the protective effects of seven selected herbs against oxidative stress

Chang¹,

Chu²,

Chu³

et al. 2015

J Coast Life Med

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Propyl gallate inhibits the growth of HeLa cells via regulating intracellular GSH level

Cited by 65 publications

References 36 publications

PX-12 inhibits the growth of A549 lung cancer cells via G2/M phase arrest and ROS-dependent apoptosis

PX-12 inhibits the growth of A549 lung cancer cells via G2/M phase arrest and ROS-dependent apoptosis

MAPK inhibitors enhance cell death in pyrogallol-treated human pulmonary fibroblast cells via increasing O2•− levels

Comparison of the protective effects of seven selected herbs against oxidative stress

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