Effect of reduced glutathione on lung injury in rats with acute necrotizing pancreatitis
Jia Bao
Abstract
Jia Bao
Abstract
AIM: To investigate the changes of transcription factor nuclear factor-κB (NF-κB), TNF-α, IL-1β, IL-18, myeloperoxidase (MPO) in the lung of rats with acute necrotizing pancreatitis (ANP) and explore the effects of reduced glutathione (GSH) on lung injury. METHODS: Wistar rats (n=72) were divided into 3 groups at random, ANP group, GSH treated group, and sham operation (SO) group. Animals in the 3 groups were killed 6, 12 and 18 h after operations and lung tissue, pancreas tissue were harvested. The expressions of IL-18, IL-1β, TNF-α in lung tissue were measured by immunohistochemistry. MPO was determined by chromatometry. Intrapulmonary expression of NF-kBp65 mRNA was detected by RT-PCR. The histopathology of lung and pancreas was observed under the light microscope. RESULTS: The expressions of NF-κB mRNA, IL-18, IL-1β, TNF-α and the activity of MPO in lung tissue were much higher at 6, 12, 18 h in ANP group, with statistical significance compared with the SO group (P0.05) and the levels of NF-κB mRNA, IL-1β and TNF-α reached the peak at 12 h. After treatment with GSH, the levels of IL-18, IL-1β, TNF-α became lower at 6, 12, 18 h and NF-κB mRNA, MPO were decreased at 12 h (P0.05 vs ANP group). CONCLUSION: All of NF-κB, TNF-α, IL-1β, IL-18 and MPO have something to do with acute lung injury in experimental acute necrosis pancreatitis. GSH may inhibit the activity of NF-κB and neutrophil in lung tissue, decrease the concentrations of inflammatory cytokines (TNF-α, IL-1β, IL-18), thus exerting the preventive effect against lung injury.
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AIM: To investigate the changes of transcription factor nuclear factor-κB (NF-κB), TNF-α, IL-1β, IL-18, myeloperoxidase (MPO) in the lung of rats with acute necrotizing pancreatitis (ANP) and explore the effects of reduced glutathione (GSH) on lung injury. METHODS: Wistar rats (n=72) were divided into 3 groups at random, ANP group, GSH treated group, and sham operation (SO) group. Animals in the 3 groups were killed 6, 12 and 18 h after operations and lung tissue, pancreas tissue were harvested. The expressions of IL-18, IL-1β, TNF-α in lung tissue were measured by immunohistochemistry. MPO was determined by chromatometry. Intrapulmonary expression of NF-kBp65 mRNA was detected by RT-PCR. The histopathology of lung and pancreas was observed under the light microscope. RESULTS: The expressions of NF-κB mRNA, IL-18, IL-1β, TNF-α and the activity of MPO in lung tissue were much higher at 6, 12, 18 h in ANP group, with statistical significance compared with the SO group (P0.05) and the levels of NF-κB mRNA, IL-1β and TNF-α reached the peak at 12 h. After treatment with GSH, the levels of IL-18, IL-1β, TNF-α became lower at 6, 12, 18 h and NF-κB mRNA, MPO were decreased at 12 h (P0.05 vs ANP group). CONCLUSION: All of NF-κB, TNF-α, IL-1β, IL-18 and MPO have something to do with acute lung injury in experimental acute necrosis pancreatitis. GSH may inhibit the activity of NF-κB and neutrophil in lung tissue, decrease the concentrations of inflammatory cytokines (TNF-α, IL-1β, IL-18), thus exerting the preventive effect against lung injury.
Key concepts: Myeloperoxidase, Glutathione, Lung, Tumor necrosis factor alpha, Pancreatitis, Internal medicine, Acute pancreatitis, Pathology