Cytoprotective effects of eupatilin, a novel antioxidative flavone, in oxidative stress-induced gastric mucosal cell damage

We examined the role of reduced glutathione as a defense mechanism against acid-induced gastric mucosal cell damage in vitro. Cellular stores of reduced glutathione were depleted by reaction with diethyl maleate (DEM) or 1-chloro-2,4-dinitrobenzene (CDNB) and increased by reaction with L-cysteine. Depletion of cellular glutathione by reaction with DEM or CDNB potentiated gastric mucosal cell lysis by acid. Increase of cellular glutathione by L-cysteine decreased cell lysis by acid. Altering the cellular reduced-to-oxidized glutathione ratio by tert-butyl hydroperoxide or diamide increased cellular susceptibility to acid. Reduced glutathione is essential for glutathione peroxidase to catalyze hydrogen peroxide. We further studied whether oxygen free radicals were involved in the pathogenesis of acid-induced gastric mucosal injury in vitro. Neither superoxide dismutase, catalase, nor dimethyl sulfoxide decreased acid-induced gastric mucosal cell damage. We conclude that reduced glutathione plays an important role as a defense mechanism against acid-induced injury in cultured rat gastric mucosal cells. Production of oxygen radical in response to acid exposure may occur intracellularly, since exogenous oxygen radical scavengers, which do not gain access to the interior of cells, had no protective effect. Reduced glutathione might protect gastric mucosal cells by mechanisms other than the elimination of oxygen free radicals.

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Oxidative Stress and Mitochondrial Damage Precedes Gastric Mucosal Cell Death Induced by Ethanol Administration

Alcoholism Clinical and Experimental Research ◽

10.1097/00000374-199803001-00007 ◽

1998 ◽

Vol 22 (Supplement 1) ◽

pp. 111 ◽

Cited By ~ 32

Author(s):

M. Hirokawa ◽

S. Miura ◽

H. Yoshida ◽

I. Kurose ◽

T. Shigematsu ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Death ◽

Mitochondrial Damage ◽

Ethanol Administration ◽

Mucosal Cell ◽

Gastric Mucosal Cell

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Sodium sulfite causes gastric mucosal cell death by inducing oxidative stress

Free Radical Research ◽

10.1080/10715762.2021.1937620 ◽

2021 ◽

pp. 1-29

Author(s):

Moeri Oshimo ◽

Fumie Nakashima ◽

Kenji Kai ◽

Hirofumi Matsui ◽

Takahiro Shibata ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Death ◽

Sodium Sulfite ◽

Mucosal Cell ◽

Gastric Mucosal Cell

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Neuroprotective Effects of Extracts from the Radix Curcuma aromatica on H2O2-induced Damage in PC12 Cells

Combinatorial Chemistry & High Throughput Screening ◽

10.2174/1386207321666181005121457 ◽

2018 ◽

Vol 21 (8) ◽

pp. 571-582 ◽

Cited By ~ 1

Author(s):

Juxiang Liu ◽

Lianli Zhang ◽

Dan Liu ◽

Baocai Li ◽

Mi Zhang

Keyword(s):

Oxidative Stress ◽

Pc12 Cells ◽

Caspase 3 ◽

Cell Damage ◽

Positive Control ◽

Neuroprotective Activity ◽

Antioxidant Enzyme Activities ◽

Morphologic Change ◽

Neuroprotective Effects ◽

Etoh Extract

Aim & Objectives: Curcuminoids are characteristic constituents in Curcuma, displaying obviously neuroprotective activities against oxidative stress. As one of the Traditional Chinese Medicines from Curcuma, the radix of Curcuma aromatica is also rich in those chemicals, but its neuroprotective activity and mechanism remain unknown. The aim of the current study is to evaluate the neuroprotective effects of extracts from the radix of C. aromatica (ECAs) on H2O2-damaged PC12 cells. Material and Methods: The model of oxidative stress damage was established by treatment of 400 µM H2O2 on PC12 to induce cell damage. After the treatment of ECWs for 24 h, the cell viability, LDH, SOD, CAT and GSH were measured to evaluate the neuroprotection of ECAs on that model. The potential action mechanism was studied by measurement of level of ROS, cell apoptosis rate, mitochondrial membrane potential (MMP), morphologic change, the intracellular Ca2+ content (F340/F380) and the expressions of Bcl-2, Bax and Caspase-3. Additionally, the constituents from tested extracts were analyzed by HPLC-DAD-Q-TOF-MS method. Results: Compared with a positive control, Vitamin E, 10 µg/ml of 95% EtOH extract (HCECA) and 75% EtOH extract (MCECA) can markedly increase the rate of cell survival and enhance the antioxidant enzyme activities of SOD, CAT, increase the levels of GSH, decrease LDH release and the level of ROS, attenuate the intracellular Ca2+ overloading, reduce the cell apoptotic rate and stabilize MMP, down-regulate Bcl-2 expression, up-regulate Bax and caspase-3 expression, and improve the change of cell morphology. The chemical analysis showed that diarylheptanoids and sesquiterpenoids are the major chemicals in tested extracts and the former were richer in HCECA and MCECA than others. Conclusions: These findings indicated that the effects of HCECA and MCECA on inhibiting the cells damage induced by H2O2 in PC12 are better than other extracts from the radix of C. aromatica, and the active constituents with neuroprotective effects consisting in those two active extracts are diarylheptanoids.

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