Protective effects of chlorogenic acid against cyclophosphamide induced liver injury in mice

We investigated possible protective effects of chlorogenic acid (CGA) against cyclophosphamide (CP) induced hepatic injury in mice. We measured aminotransferase alanine transaminase (ALT) and aspartate transaminase (AST) levels in the serum. We assayed catalase (CAT), superoxide dismutase (SOD), reduced glutathione (GSH), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) in hepatic tissue. We assessed expression of nuclear transcription factor 2 (Nrf2) and Kelch sample related protein-1 (keap1) proteins in hepatic tissues using immunohistochemistry. The relative mRNA expression levels of heme oxygenase-1 (HO-1), NADH quinone oxidoreductase 1 (NQO1), tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) were determined using quantitative real-time polymerase chain reaction (qRT-PCR). Hematoxylin & eosin staining was used to assess liver histopathology. We found that administration of CGA prior to induction of injury by CP decreased serum ALT, AST and MDA expressions in hepatic tissue, while CAT, SOD, GSH and GSH-Px concentrations were increased. We found that hepatocytes of animals administered CGA gradually returned to normal morphology. CGA increased the protein expression of Nrf2 in murine hepatic tissue. Administration of CGA up-regulated mRNA expression levels of HO-1, NQO1, TNF-alpha and IL-6 in hepatic tissue. CGA exhibited a marked protective effect on CP induced liver injury in mice.

Automated summary

In this study, we found that chlorogenic acid (CGA) has a significant protective effect against cyclophosphamide (CP) induced liver injury in mice. CGA reduced the levels of liver enzyme in the serum and expressions of malondialdehyde (MDA) in hepatic tissue, while increasing the concentrations of antioxidant enzymes. CGA also increased the protein expression of Nrf2 and up-regulated the mRNA levels of HO-1, NQO1, TNF-α and IL-6 in the liver tissue.