Andrographolide ameliorates OVA-induced lung injury in mice by suppressing ROS-mediated NF-κB signaling and NLRP3 inflammasome activation
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- 英文论文题名：Andrographolide ameliorates OVA-induced lung injury in mice by suppressing ROS-mediated NF-κB signaling and NLRP3 inflammasome activation
- 论文作者：Gao Jian ; Peng Shuang ; Liu Wen ; Jiang Chunhong ; Yang Xiaolin ; Sun Yang ; Guo Wenjie
- 英文论文作者：Gao Jian ; Peng Shuang ; Liu Wen ; Jiang Chunhong ; Yang Xiaolin ; Sun Yang ; Guo Wenjie ; State Key Laboratory of Pharmaceutical Biotechnology ; School of Life Sciences ; Nanjing University
- 年：2016
- 作者机构：State Key Laboratory of Pharmaceutical Biotechnology,School of Life Sciences,Nanjing University;
- 英文论文关键词：Andrographolide ; asthma ; NF-κB ; NLRP3 ; ROS
- 会议召开时间：2016-11-04
- 会议录名称：第十一届全国免疫学学术大会摘要汇编
- 英文会议录名称：Abstracts of 2016 CSI Congress on Immunology
- 语种：英文
- 分类号：R285.5
- 学会代码：IGMD
- 会议名称：第十一届全国免疫学学术大会
- 会议地点：中国安徽合肥
- 主办单位：中国免疫学会
- 学会名称：中国免疫学会
- 页数：2
- 文件大小：1334k
- 原文格式：D
- 会议级别：全国
摘要
Andrographolide, a natural diterpenoid, found in Andrographis paniculata, has been reported to have anti-inflammatory property. In the present study, we aimed to examine the effect and possible mechanism of Andrographolide on asthma. Asthma was induced by OVA intraperitoneal injection followed by repetitive OVA challenge for 4 weeks. OVA-inducedairway inflammatory cell recruitment and lung histological alterations were significantly ameliorated by Andrographolide. The protein levels of pro-inflammatory cytokines in bron-choalveolar fluid(BALF) and serum were reduced by Andrographolide administration as well as the mRNA levels in lung tissue. Mechanically, Andrographolide markedly suppressed the activation of nuclear factor-κB(NF-κB) and NLRP3 inflammasome both in vivo and vitro thus decreased the level of inflammation cytokines including TNF-α and IL-1β. Finally, ROS scavenging was responsible for Andrographolide's inactivation of NF-κB and NLRP3 inflammasome signaling. In summary, these results suggest that Andrographolide ameliorated OVA-induced asthma in mice through inhibition of NF-κB and NLRP3-mediated inflammatory response. Our study suggests Andrographolide may represent a new therapeutic approach for treating asthma.
Andrographolide, a natural diterpenoid, found in Andrographis paniculata, has been reported to have anti-inflammatory property. In the present study, we aimed to examine the effect and possible mechanism of Andrographolide on asthma. Asthma was induced by OVA intraperitoneal injection followed by repetitive OVA challenge for 4 weeks. OVA-inducedairway inflammatory cell recruitment and lung histological alterations were significantly ameliorated by Andrographolide. The protein levels of pro-inflammatory cytokines in bron-choalveolar fluid(BALF) and serum were reduced by Andrographolide administration as well as the mRNA levels in lung tissue. Mechanically, Andrographolide markedly suppressed the activation of nuclear factor-κB(NF-κB) and NLRP3 inflammasome both in vivo and vitro thus decreased the level of inflammation cytokines including TNF-α and IL-1β. Finally, ROS scavenging was responsible for Andrographolide's inactivation of NF-κB and NLRP3 inflammasome signaling. In summary, these results suggest that Andrographolide ameliorated OVA-induced asthma in mice through inhibition of NF-κB and NLRP3-mediated inflammatory response. Our study suggests Andrographolide may represent a new therapeutic approach for treating asthma.
Andrographolide, a natural diterpenoid, found in Andrographis paniculata, has been reported to have anti-inflammatory property. In the present study, we aimed to examine the effect and possible mechanism of Andrographolide on asthma. Asthma was induced by OVA intraperitoneal injection followed by repetitive OVA challenge for 4 weeks. OVA-inducedairway inflammatory cell recruitment and lung histological alterations were significantly ameliorated by Andrographolide. The protein levels of pro-inflammatory cytokines in bron-choalveolar fluid(BALF) and serum were reduced by Andrographolide administration as well as the mRNA levels in lung tissue. Mechanically, Andrographolide markedly suppressed the activation of nuclear factor-κB(NF-κB) and NLRP3 inflammasome both in vivo and vitro thus decreased the level of inflammation cytokines including TNF-α and IL-1β. Finally, ROS scavenging was responsible for Andrographolide's inactivation of NF-κB and NLRP3 inflammasome signaling. In summary, these results suggest that Andrographolide ameliorated OVA-induced asthma in mice through inhibition of NF-κB and NLRP3-mediated inflammatory response. Our study suggests Andrographolide may represent a new therapeutic approach for treating asthma.
引文