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Annals of Clinical & Laboratory Science 37:356-361 (2007)
© 2007 Association of Clinical Scientists

Alterations of Pulmonary Zinc Homeostasis and Cytokine Production Following Traumatic Brain Injury in Rats

Lin Zhu1, Wei Yan1, Meng Qi1, Ze Lan Hu2, Ting Jia Lu2, Min Chen2, Jin Zhou2, Chun Hua Hang1 and Ji Xin Shi1
1 Department of Neurosurgery, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu Province, China; 2 Institute of Neuroscience of Shanghai, Chinese Academy of Science, Shanghai, China

Address correspondence to Dr Ji Xin Shi, Department of Neurosurgery, Jinling Hospital, 305 East Zhongshan Road, Nanjing, 210002, P.R. China; tel 86 25 8668 8895; fax 86 25 8481 7581; e-mail shijixin52{at}163.com.

Previous studies have shown that labile zinc and inflammatory mediators participate in many pathophysiological processes. The present study investigated the effects of traumatic brain injury (TBI) on the levels of labile zinc and certain proinflammatory factors in rat lung. Male Wistar rats were randomly assigned to 7 groups as follows: normal group, group with sham operation, and TBI groups that were sacrificed respectively at 1, 6, 24, and 72 hr, and on day 7 post-injury. Pulmonary labile zinc, tumor necrosis factor alpha (TNF-{alpha}), interleukin (IL)-8, and wet/dry weight ratio were measured at the specified time intervals. TBI caused a gradual increase of pulmonary labile zinc as demonstrated by fluorescence staining with Zinpyr-4 (ZP4). The levels of TNF-{alpha} and IL-8 and the lung wet/dry weight ratios were higher in the TBI groups compared to the normal and sham-operated groups (p <0.05). There were highly positive correlations between the intensity of ZP4 fluorescence and the pulmonary levels of TNF-{alpha} and IL-8. The results suggest that TBI induces rapid increases of labile zinc and inflammatory mediators in lung, which may participate in the pathogenesis of acute lung injury.

Keywords: brain trauma, lung, zinc, cytokines, TNF-{alpha}, IL-8






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