Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
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Enzyme
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Query: UMLS:C0242706 (
hyperoxia
)
5,219
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Lung tissues are frequently exposed to a
hyperoxia
environment, which leads to oxidative stress injuries. Hydrogen sulfide (H
2
S) is widely implicated in physiological and pathological processes and its antioxidant effect has attracted much attention. Therefore, in this study, we used hydrogen peroxide (H
2
O
2
) as an oxidative damage model to investigate the protective mechanism of H
2
S in lung injury. Cell death induced by H
2
O
2
treatment could be significantly attenuated by the pre-treatment of H
2
S, resulting in a decrease in the Bax/Bcl-2 ratio and the inhibition of caspase-3 activity in human lung epithelial cell line A549 cells. Additionally, the results showed that H
2
S decreased reactive oxygen species (ROS), as well as neutralized the damaging effects of H
2
O
2
in mitochondria energy-producing and cell metabolism. Pre-treatment of H
2
S also decreased H
2
O
2
-induced suppression of endogenous H
2
S production enzymes,
cystathionine-beta-synthase
(
CBS
), cystathionine-gamma-lyase (CSE), and 3-mercapto-pyruvate sulfurtransferase (MPST). Furthermore, the administration of H
2
S attenuated [Ca
2+
] overload and endoplasmic reticulum (ER) stress through the mitogen-activated protein kinase (MAPK) signaling pathway. Therefore, H
2
S might be a potential therapeutic agent for reducing ROS and ER stress-associated apoptosis against H
2
O
2
-induced lung injury.
...
PMID:Hydrogen Sulfide Attenuates Hydrogen Peroxide-Induced Injury in Human Lung Epithelial A549 Cells. 3144 88
