Journal
INTERNATIONAL IMMUNOPHARMACOLOGY
Volume 29, Issue 2, Pages 722-729Publisher
ELSEVIER
DOI: 10.1016/j.intimp.2015.09.003
Keywords
NHDC; Paraquat; Hepatic injury; Oxidative damage; Inflammation; Apoptosis
Categories
Funding
- National Natural Science Foundation of China [21477098]
- Science and Technology Talent Cultivation Project of Chongqing [cstc2014kjrc-qnrc00001]
- Fundamental Research Funds for the Central Universities [XDJK2014A020, XDJK2015A017]
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The present study evaluated the protective effect of artificial sweetener neohesperidin dihydrochalcone (NHDC) against paraquat (PQ)-induced acute liver injury in mice. A single dose of PQ (75 mg/kg body weight, i.p.) induced acute liver toxicity with the evidences of increased liver damage biomarkers, aspartate transaminase (AST) and alanine transaminase (ALT) activities in serum. Consistently, PQ decreased the antioxidant capacity by reducing glutathione peroxidase (GP-X), glutathione-S-transferase (GST) and catalase (CAT) activities, glutathione (GSH) level and total antioxidant capacity (T-AOC), as well as increasing reactive oxygen species (ROS) and thiobarbituric acid reactive substances (TBARS) levels. Histopathological examination revealed that PQ induced numerous changes in the liver tissues. Immunochemical staining assay indicated the upregulation of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expressions. However, NHDC ameliorates PQ-induced hepatic toxicity in mice by reversing these parameters. Additionally, NHDC significantly inhibited PQ-induced nuclear factor-kappa B (NF-kappa B) expression and mitothondrial-driven apoptotic signaling. TUNEL assay confirmed that PQ-induced apoptosis was relieved by NHDC In conclusion, these findings suggested that NHDC showed potent antioxidant, anti-inflammatory and anti-apoptotic effects against PQ-induced acute liver damage. (C) 2015 Elsevier B.V. All rights reserved.
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