Chlorogenic acid ameliorates endotoxin-induced liver injury by promoting mitochondrial oxidative phosphorylation
- State Key Laboratory of Food Science and Technology and School of Food Science, Nanchang University, Nanchang 330047 (China)
- College of Food Safety, Guizhou Medical University, Guiyang 550025 (China)
Acute or chronic hepatic injury is a common pathology worldwide. Mitochondrial dysfunction and the depletion of adenosine triphosphate (ATP) play important roles in liver injury. Chlorogenic acids (CGA) are some of the most abundant phenolic acids in human diet. This study was designed to test the hypothesis that CGA may protect against chronic lipopolysaccharide (LPS)-induced liver injury by modulating mitochondrial energy generation. CGA decreased the activities of serum alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase. The contents of ATP and adenosine monophosphate (AMP), as well as the ratio of AMP/ATP, were increased after CGA supplementation. The activities of enzymes that are involved in glycolysis were reduced, while those of enzymes involved in oxidative phosphorylation were increased. Moreover, phosphorylated AMP-activated protein kinase (AMPK), and mRNA levels of AMPK-α, peroxisome proliferator-activated receptor-gamma coactivator 1α (PGC-1α), nuclear respiratory factor 1, and mitochondrial DNA transcription factor A were increased after CGA supplementation. Collectively, these findings suggest that the hepatoprotective effect of CGA might be associated with enhanced ATP production, the stimulation of mitochondrial oxidative phosphorylation and the inhibition of glycolysis. - Highlights: • Dietary supplementation with chlorogenic acid (CGA) improved endotoxin-induced liver injury. • Chlorogenic acid enhances ATP increase and shifts energy metabolism, which is correlated with up-regulation AMPK and PGC-1α. • The possible mechanism of CGA on mitochondrial biogenesis was correlated with up-regulation AMPK and PGC-1α.
- OSTI ID:
- 22594197
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 469, Issue 4; Other Information: Copyright (c) 2015 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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Related Subjects
ADENOSINE
ALANINES
ALKALINE PHOSPHATASE
AMINOTRANSFERASES
AMP
ATP
DNA
ENDOTOXINS
GLYCOLYSIS
INHIBITION
INJURIES
LIPOPOLYSACCHARIDES
LIVER
MESSENGER-RNA
MITOCHONDRIA
OXIDATION
PATHOLOGY
PHENOLS
PHOSPHORYLATION
RECEPTORS
RESPIRATION
STIMULATION
TRANSCRIPTION
TRANSCRIPTION FACTORS