Betulin inhibited cigarette smoke-induced COPD in mice

详细信息    查看全文

• 作者：Ma Chunhua ; Hongyan Long ; ^{longhongyantcm@163.com} ; Weina Zhu ; Zheng Liu ; Ruan Jie ; Yajie Zhang ; Yarui Wang
• 关键词：Betulin ; COPD ; ROCK/NF-κB
• 刊名：Biomedicine & Pharmacotherapy
• 出版年：2017
• 出版时间：January 2017
• 年：2017
• 卷：85
• 期：Complete
• 页码：679-686
• 全文大小：1674 K
• 卷排序：85

文摘

The purpose of the present study was to evaluate the protective effect of betulin (BE) on CS (cigarette smoke)-induced COPD in mice and explore its underlying mechanisms. 60 male ICR mice were randomly assigned to five groups: control group, model group, dexamethasone (2 mg/kg) group, BE (20 mg/kg) group and BE (40 mg/kg) group. The COPD mice were induced by cigarette smoke exposure for 8 weeks. The result of H&E staining demonstrated that BE inhibited CS-induced pathological injury in lung tissue. Besides, BE could restore the activities of superoxide dismutase (SOD) in serum and in lung, catalase (CAT) in serum and reduce the content of malondialdehyde (MDA) in serum and in lung. BE also inhibited the overproductions of pro-inflammatory cytokines including tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β). Furthermore, the administration of BE significantly inhibited the protein expression of ROCK/NF-κB pathway in CS-induced mice. Our findings suggested that BE might effectively ameliorate the progression of COPD via ROCK/NF-κB pathway in mice.