The significance and mechanism of propofol on treatment of ischemia reperfusion induced lung injury in rats.

Abstract

This study is aimed to investigate the efficacy and underlying the mechanism of propofol in treatment of ischemia reperfusion (IR)-induced lung injury in rats, providing a novel insight of therapeutic strategy for IR-induced lung injury. 120 healthy SD rats were selected and randomly divided into sham operation group, IR group, and propofol group (40 rats per group). Bronchoalveolar lavage fluid (BALF) protein content, serum protein content, lung permeability index, lung water content rate, methane dicarboxylic aldehyde (MDA) in lung tissue, superoxide dismutase (SOD), nitric oxide (NO), endothelin (ET-1), toll-like receptor 4 (TLR4), nuclear factor (NF-κB), and tumor necrosis factor-α (TNF-α) were examined and compared among different groups to evaluate the therapeutical effects of propofol on IR-induced lung injury and analyze the mechanism. In sham operation group, neither change in lung tissue nor pulmonary interstitial edema or alveolar wall damage was found under microscope; in IR group, marked pulmonary interstitial edema and alveolar wall damage complicated with inflammatory cell infiltration and hemorrhage were found; in propofol group, alveolar wall widening was observed, however, hemorrhage in alveolar cavity, inflammatory infiltration and tissue damage were less significant than in IR group. At 3 h after reperfusion, BALF protein content, lung permeability index, and lung water content rate were all significantly increased in IR group and propofol group, while the serum protein content was significantly lower than sham operation group (p < 0.05). Moreover, we found that the change of above parameters in propofol group was less significant than in IR group (p < 0.05). No statistically significant difference was found in ET-1 levels in different groups (p > 0.05). In contrast, MDA and NO in IR group and propofol group were significantly increased, while SOD activity was significantly decreased (p < 0.05). Furthermore, the change of above parameters in propofol group was less significant than in IR group (p < 0.05). In addition, mRNAs of TLR4, NF-κB, and TNF-α were significantly increased in IR group and propofol group (p < 0.05) with more significant change in IR group compared with propofol group (p < 0.05). Propofol has protective effects against IR-induced lung injury by improving activity of oxygen radical and restoring NO/ET-1 dynamic balance. Besides, regulation of TLR4, NF-κB, and TNF-α by propofol also play important role in alleviating IR-induced lung injury.

• Authors: Pei Yang, Nengli Yang, Xuezheng Zhang, Xuzhong Xu
• Journal: Cell biochemistry and biophysics (Cell Biochem Biophys) Vol. 70 Issue 3 Pg. 1527-32 (Dec 2014) ISSN: 1559-0283 [Electronic] United States
• PMID: 25074530 (Publication Type: Journal Article)

Chemical References

• Cytokines
• Respiratory System Agents
• Propofol

Topics

• Animals
• Cytokines (immunology)
• Female
• Lung (drug effects, pathology, physiopathology)
• Lung Injury (drug therapy, pathology, physiopathology)
• Male
• Propofol (administration & dosage)
• Rats
• Rats, Sprague-Dawley
• Reperfusion Injury (drug therapy, pathology, physiopathology)
• Respiratory System Agents (administration & dosage)
• Treatment Outcome