[Protective effects of melatonin in acute lung injury rats caused by LPS].

Zhongguo Ying Yong Sheng Li Xue Za Zhi

Department of Pathophysiology, Hebei Medical University, Shijiazhuang 050017, China.

Published: November 2010

AI Article Synopsis

  • The study investigates the expression of p-p38 MAPK in lung tissues of rats with acute lung injury induced by lipopolysaccharide (LPS), assessing the potential protective effects of melatonin (MT).
  • Rats were divided into three groups: control, LPS, and LPS + MT, with various methods used to measure p-p38 MAPK expression and observe lung tissue changes.
  • Results show increased p-p38 MAPK expression in the LPS group compared to the control group, while MT treatment significantly reduced this expression, indicating that MT may protect against inflammation in acute lung injury by inhibiting p38 MAPK activation.

Article Abstract

Objective: To observe the expression of p-p38 mitogen-activated protein kinase in lung tissues of acute lung injury rat model induced by lipopolysaccharide (LPS) and to explore the protective effects of melatonin (MT) in lung tissues in rats.

Methods: Seventy-two rats was randomly assigned to three groups, control group, LPS group and LPS + MT group. Rat model of ALI was established by instilling LPS intratracheally. We used immunohistochemical SP and Western blot method to detect the expression of p-p38 mitogen-activated protein kinase in lung tissues and used light microscope to observe morphological changes.

Results: There were rare p-p38 mitogen-activated protein kinase positive cells scattered in alveolar and airway epithelial cells in control group (P < 0.01). The positive p-p38 mitogen-activated protein kinase cells in LPS group increased obviously than those in control group (P < 0.01), and were mainly distributed in infiltrative inflammatory cells, airway epithelial cells, alveolar epithelial cells and pleurames epithelial cells. In MT group, the p-p38 mitogen-activated protein kinase positive cells in airway and lung tissues were much less than those in the LPS group (P < 0.05). The Western blot results were consistent with those of immunohistochemical method.

Conclusion: The expression of p-p38 mitogen-activated protein kinase increases in alveolar and airway epithelial cells in acute lung injury rat models induced by LPS. The activation of p-p38 mitogen-activated protein kinase is found in most lung tissues, suggesting that p-p38 mitogen-activated protein kinase participates in the signal transduction in inflammatory and noninflammatory cells. MT is an effective antioxidant, which relieves the inflammation in acute lung injury rats, possibly through the inhibition of the pathway of p38 MAPK over activation.

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