Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0019158 (
hepatitis
)
30,205
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Hydrogen sulfide (H
2
S) is a toxic gas and one of the air pollutants of great concern. High-concentrated H
2
S can induce energy metabolism disturbance and apoptosis. However, the mechanism of H
2
S-induced liver injuries is unknown. Lipopolysaccharide (LPS), the main component of endotoxin, can cause fulminant
hepatitis
. Here, we evaluated the effects of H
2
S combined with LPS on the energy metabolism and apoptosis pathway in the liver using a one-day-old chicken as a model. Our results showed that the expression levels of energy metabolism-related genes (AMP-activated protein kinase (AMPK), Hypoxia-inducible factor-1 (HIF-1),
aconitase 2
(
ACO2
), hexokinase1 (HK1), hexokinase 2 (HK2), lactate dehydrogenase A (LDHA), lactate dehydrogenase B (LDHB), phosphofructokinase (PFK), pyruvate kinase (PK) and succinate dehydrogenase B (SDHB)) tended to decrease, that the status of apoptosis increased, and that the expression levels of apoptosis-related genes (caspase3, BCL2, and bax) increased in H
2
S group, suggesting that H
2
S exposure disturbed the energy metabolism in the liver and induced hepatocyte apoptosis through the mitochondrial pathway. In addition, H
2
S combined with the LPS aggravated the level of energy metabolism disorders and apoptosis, indicating that H
2
S inhalation-induced energy metabolism disturbance is involved in LPS-mediated hepatocyte apoptosis through the mitochondrial pathway.
...
PMID:H
2
S inhalation-induced energy metabolism disturbance is involved in LPS mediated hepatocyte apoptosis through mitochondrial pathway. 3071 28
