Effects of Tanshinone IIA sodium sulfonate on LPS-induced acute lung injury in mice

被引:2
作者
Qian, Jinxian [1 ,2 ,4 ]
Yang, Xinjing [3 ]
Wu, Jian [4 ]
Yang, Aixiang [4 ]
Tao, Weiyi [4 ]
Ling, Chunhua [1 ,2 ]
Zhang, Guoxing [5 ]
机构
[1] Soochow Univ, Affiliated Hosp 1, Dept Resp, 188 Shizi Rd, Suzhou 215006, Jiangsu, Peoples R China
[2] Soochow Univ, Affiliated Hosp 1, Dept Crit Care Med, 188 Shizi Rd, Suzhou 215006, Jiangsu, Peoples R China
[3] Soochow Univ, Affiliated Hosp 1, Intens Care Unit, Suzhou 215006, Jiangsu, Peoples R China
[4] Nanjing Med Univ, Suzhou Municipal Hosp, Affiliated Suzhou Hosp, Dept Intens Care Unit, Suzhou, Jiangsu, Peoples R China
[5] Soochow Univ, Med Coll, Dept Physiol, 199 Renai Rd, Suzhou 215123, Jiangsu, Peoples R China
关键词
Tanshinone IIA sodium sulfonate; lipopolysaccharide; acute lung injury; autophagy; ACUTE RESPIRATORY-DISTRESS; INDUCED INFLAMMATION; CARDIAC CONTRACTILE; AUTOPHAGY; SEPSIS; DYSFUNCTION; ACTIVATION; RATIONALE; PROTECTS; SURVIVAL;
D O I
暂无
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Objective: The study investigated the protective effect of Tanshinone IIA sodium sulfonate (TSS) on lipopolysaccharide (LPS)-induced acute lung injury (ALI), and the underlying mechanisms. Methods: Male C57/black mice were subjected to LPS (10 mg/kg, i.p.) administration to induce acute lung injury. Half an hour before LPS injection, mice were pretreated with TSS (30 mg/kg, i.p.). One hour, six and twelve hours later, mice were sacrificed. Lung edema and inflammatory cell infiltration were observed. Expression of pro-inflammatory factors (TNF alpha, IL-1 beta, IL-6) were measured by RT-PCR and ELISA in lung tissues. Markers of autophagy including LC3 and Beclin-1 expression were determined by RT-PCR and Western blot. Number of autophagosomes was observed by electron microscope. Results: Our results showed that TSS did not ameliorate the LPS-induced lung edema, but significantly reduced pro-inflammatory cell infiltration. LPS increased mRNA and protein expression of inflammatory factors (TNF alpha, IL-1 beta, IL-6) at all observed time. TSS markedly reduced the protein expression of IL-6 but not TNF alpha and IL-1 beta. In addition, LPS increased tissue autophagic levels (expression of Beclin-1, LC3 and number of autophagosomes) and TSS treatment further increased the autophagic levels. Conclusion: TSS exerts certain anti-inflammation and enhancing autophagy effects in LPS-induced ALI.
引用
收藏
页码:4605 / 4613
页数:9
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