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Abstract Title:

Betulinic acid attenuates dexamethasone-induced oxidative damage through the JNK-P38 MAPK signaling pathway in mice.

Abstract Source:

Biomed Pharmacother. 2018 Apr 17 ;103:499-508. Epub 2018 Apr 17. PMID: 29677535

Abstract Author(s):

Lijuan Zhu, Xianglian Yi, Jing Zhao, Zhihang Yuan, Lixin Wen, Blazej Pozniak, Bozena Obminska-Mrukowicz, Yanan Tian, Zhuliang Tan, Jing Wu, Jine Yi

Article Affiliation:

Lijuan Zhu

Abstract:

Dexamethasone (Dex), a potent anti-inflammatory/immunosuppressive agent, has been shown to induce oxidative stress. Betulinic acid (BA) is a pentacyclic lupane triterpene with a potent antioxidant activity. The aim of this study was to investigate the ameliorative effect and underlying mechanisms of BA on Dex-induced oxidative damage. Mice were pretreated with BA orally (0, 0.25, 0.5, and 1.0 mg/kg) daily for 14 days, and then a single dose of Dex (25 mg/kg body weight) was administered intraperitoneally 8 h after the last administration of BA to induce oxidative stress. BA pretreatment significantly alleviated Dex-induced changes of blood biochemical indices, increased the totalantioxidant capacity (T-AOC), the activity of superoxide dismutase (SOD), and the ability of inhibiting hydroxyl radical (AIHR), reduced the level of malondialdehyde (MDA) in serum. Moreover, BA pretreatment enhanced the T-AOC, AIHR and the activity of peroxidase (POD) in liver, spleen and thymus. Concomitant with these biochemical parameters, BA pretreatment significantly reduced gene and protein expressions of apoptosis signal-regulating kinase 1 (ASK1), c-Jun N-terminal kinase (JNK) and P38 mitogen-activated protein kinase (P38 MAPK) in the lymphatic organs of Dex-treated mice. BA was foundto effectively attenuate Dex-induced oxidative damage. These protective effects may be mediated in part through the JNK-P38 MAPK signaling transduction pathway and BA may be a potential therapeutic agent due to its anti-oxidative properties.

Study Type : Animal Study

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