PT  - JOURNAL ARTICLE
AU  - Meng, Qing-Tao
AU  - Xia, Zhong-Yuan
AU  - Luo, Tao
AU  - Cao, Chen
AU  - Zhao, Bo
AU  - Wu, Yang
AU  - Wu, Xiaojin
AU  - Chen, Xiangdong
TI  - Ligustrazine attenuates acute lung injury induced by blunt chest trauma.
DP  - 2012 Feb 01
TA  - Saudi Medical Journal
PG  - 139--145
VI  - 33
IP  - 2
4099  - http://smj.org.sa/content/33/2/139.short
4100  - http://smj.org.sa/content/33/2/139.full
SO  - Saudi Med J2012 Feb 01; 33
AB  - OBJECTIVES: To investigate the effects of ligustrazine on acute lung injury induced by blunt chest trauma.METHODS: This study was performed in the Animal Center of Renmin Hospital of Wuhan University, Wuhan, China between September 2009 and September 2010. Male Sprague-Dawley rats were randomly allocated into 4 groups: sham control group (group C, n=60), ligustrazine treatment group (group C+L, n=60), blunt chest trauma model group (group T, n=60), and the trauma plus ligustrazine treatment group (group T+L, n=60). The lung contusion was induced as previously described. Animals of the T+L group were intraperitoneally injected with ligustrazine. Acute lung injury was evaluated by histopathology of the lung, and apoptosis was determined by terminal dUTP nick-labeling. Pulmonary edema was estimated using Evans blue dye extravasation and wet/dry ratios of lung tissue. The expression of caspase-3, Bcl-2, and Bax in the lung, as well as blood plasma tumor necrosis factor (TNF)-alpha were also measured.RESULTS: The ligustrazine treatment significantly attenuated lung injury induced by blunt chest trauma, as shown by decreased apoptosis index, and pulmonary edema (p=0.04). The blood plasma TNF-alpha level after blunt chest trauma significantly deceased after the administration of ligustrazine (p=0.03). In addition, the ligustrazine treatment significantly alleviated the expression of caspase-3 (p=0.03), and increased the ratio of Bcl-2 to Bax (p<0.03).CONCLUSIONS: Ligustrazine effectively protects lung injury induced by blunt chest trauma, and the protective effects seem to be mediated by attenuation of cell apoptosis via an increased ratio of Bcl-2/Bax and decreased caspase-3 activity.