Ameliorative effect of betulinic acid on oxidative damage and apoptosis in the splenocytes of dexamethasone treated mice
- PMID: 25959028
- DOI: 10.1016/j.intimp.2015.04.050
Ameliorative effect of betulinic acid on oxidative damage and apoptosis in the splenocytes of dexamethasone treated mice
Abstract
Betulinic acid (BA) is a bioactive pentacyclic triterpene that exhibits a variety of biological activities including antioxidative and immunomodulative properties. The objective of this study was to investigate the potential splenocytes protective effect and underlying mechanism of BA using dexamethasone (Dex)-induced mice as a model system. Pretreatment with BA (0.25, 0.5, and 1.0 mg/kg) dose-dependently ameliorated Dex-induced oxidative damage and apoptosis after 14 days of feeding. In addition to reactive oxygen species scavenging activity in Dex-induced splenocytes, BA administration up-regulated antioxidant enzymes, decreased lipid peroxidation, restored mitochondrial function, decreased the expression of pro-apoptotic protein Bax, prevented the decline of anti-apoptotic protein Bcl-2, inhibited caspase-9 and caspase-3 activation, and improved cell survival. These findings reveal that BA was able to mitigate Dex-induced oxidative stress and might play an important role in repairs of oxidative damage in immunological system.
Keywords: Apoptosis; Betulinic acid; Dexamethasone; Oxidative stress; Splenocytes.
Copyright © 2015 Elsevier B.V. All rights reserved.
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