H2S inhalation-induced energy metabolism disturbance is involved in LPS mediated hepatocyte apoptosis through mitochondrial pathway

Abstract

Hydrogen sulfide (H2S) is a toxic gas and one of the air pollutants of great concern. High-concentrated H2S can induce energy metabolism disturbance and apoptosis. However, the mechanism of H2S-induced liver injuries is unknown. Lipopolysaccharide (LPS), the main component of endotoxin, can cause fulminant hepatitis. Here, we evaluated the effects of H2S 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 H2S group, suggesting that H2S exposure disturbed the energy metabolism in the liver and induced hepatocyte apoptosis through the mitochondrial pathway. In addition, H2S combined with the LPS aggravated the level of energy metabolism disorders and apoptosis, indicating that H2S inhalation-induced energy metabolism disturbance is involved in LPS-mediated hepatocyte apoptosis through the mitochondrial pathway.