کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2540663 | 1122603 | 2015 | 10 صفحه PDF | دانلود رایگان |
• Dex exposure leads to splenocytes apoptosis by oxidative damage.
• BA alleviates oxidative stress and splenocytes apoptosis induced by Dex.
• Protective effect of BA on splenocytes via mitochondrial signal pathway
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.
Journal: International Immunopharmacology - Volume 27, Issue 1, July 2015, Pages 85–94