Platonin mitigates acute lung injury induced by bilateral lower limb ischemia-reperfusion in rats.
BACKGROUND
Oxidative stress and inflammatory response are crucial in mediating the development of acute lung injury induced by bilateral lower limb ischemia-reperfusion (I/R). Platonin, a potent antioxidant, possesses anti-inflammation capacity. We sought to elucidate whether platonin could mitigate acute lung injury induced by lower limb I/R.


METHODS
Forty-eight adult male rats were allocated to receive I/R, I/R plus platonin (100 μg/kg intravenous injection immediately after reperfusion), sham instrumentation, or sham instrumentation plus platonin (denoted as the I/R, I/R-platonin, Sham, or Sham-platonin group, respectively; n = 12 in each group). Bilateral hind limb I/R was induced by applying rubber band tourniquets high around each thigh for 3 h followed by reperfusion for 3 h. After sacrifice, the degree of lung injury was determined.


RESULTS
Histologic findings revealed moderate inflammation in lung tissues of the I/R group and mild inflammation in those of the I/R-platonin group. Total cell number and protein concentration in bronchoalveolar lavage fluid as well as the leukocyte infiltration and myeloperoxidase activity in lung tissues of the I/R group were significantly higher than those of the I/R-platonin group. The pulmonary concentrations of macrophage inflammatory protein-2, interleukin-6, and prostaglandin E(2) of the I/R group were significantly higher than those of the I/R-platonin group. Moreover, the plasma nitric oxide concentration as well as the nitric oxide and malondialdehyde concentrations in lung tissues of the I/R group were significantly higher than those of the I/R-platonin group.


CONCLUSIONS
Platonin mitigates acute lung injury induced by bilateral lower limb I/R in rats.
Hsu
Kuei-Yao
KY
Department of Anesthesiology, Buddhist Tzu Chi General Hospital, Taipei Branch, Taipei, Taiwan.
Tsai
Pei-Shan
PS
Lee
Jie-Jen
JJ
Wang
Tao-Yeuan
TY
Huang
Chun-Jen
CJ
D055371:Acute Lung Injury / Q000209:etiology* / Q000378:metabolism / Q000517:prevention & control*; D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D054426:Chemokine CXCL2 / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism; D007275:Injections, Intravenous; D015850:Interleukin-6 / Q000378:metabolism; D007962:Leukocytes / Q000473:pathology; D035002:Lower Extremity / Q000098:blood supply*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D023421:Models, Animal; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D013844:Thiazoles / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*
D000975:Antioxidants; D054426:Chemokine CXCL2; C513296:Cxcl2 protein, rat; D015850:Interleukin-6; D013844:Thiazoles; C032149:platonin; D009569:Nitric Oxide; D008315:Malondialdehyde; D015232:Dinoprostone