Ligustrazine attenuates acute lung injury induced by blunt chest trauma.
OBJECTIVE
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.
Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.
Qing-Tao
QT
Meng
Zhong-Yuan
ZY
Xia
Tao
T
Luo
Chen
C
Cao
Bo
B
Zhao
Yang
Y
Wu
Xiaojin
X
Wu
Xiangdong
X
Chen
D055371:Acute Lung Injury / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology* / Q000627:therapeutic use; D017209:Apoptosis / Q000187:drug effects; D053148:Caspase 3 / Q000187:drug effects / Q000378:metabolism; D008297:Male; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000187:drug effects / Q000378:metabolism; D011654:Pulmonary Edema / Q000378:metabolism; D011719:Pyrazines / Q000494:pharmacology* / Q000627:therapeutic use; D051381:Rats; D017207:Rats, Sprague-Dawley; D013898:Thoracic Injuries / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000097:blood / Q000187:drug effects; D014949:Wounds, Nonpenetrating / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D051028:bcl-2-Associated X Protein / Q000187:drug effects / Q000378:metabolism
D000894:Anti-Inflammatory Agents, Non-Steroidal; D019253:Proto-Oncogene Proteins c-bcl-2; D011719:Pyrazines; D014409:Tumor Necrosis Factor-alpha; D051028:bcl-2-Associated X Protein; D053148:Caspase 3; C017953:tetramethylpyrazine