OBJECTIVE: To investigate the effects of tumor necrosis factor α (TNF α) and inhibitor protein of nuclear factor κB (IκBα) on pulmonary hemorrhage (PH) of neonatal rats induced by lipopolysaccharide (LPS). METHODS: Seven to ten days old Wistar rats were randomly separated into 2 groups: LPS group, the rats of which were injected with LPS intraperitoneally at the dosage of 5 mg/kg, and they were sacrificed 30 min, 1, 2, 4, 8, 16 and 24 hs after injection of LPS, respectively; normal saline (NS) group, where equal amount of NS was injected intraperitoneally. The number of each time point was 6. The lungs of the rats were examined by eyes and microscope. The protein and mRNA of TNF α in the lung tissues were detected by the method of ELISA and reverse transcription polymerase chain reaction. The expression of IκBα protein was measured by Western Blot. RESULTS: One hour after administration of LPS, patch like bleeding was observed in more than two lobes of the lung. From the 1st h after injection of LPS, TNF α protein increased and was significantly higher than that of NS control group (P< 0.01 ), it peaked at the 2nd h. TNF α mRNA increased 30 min after injection of LPS and was significantly higher than NS control (P< 0.01 ) and the peak was reached 2 hs after injection of LPS. The expression of IκBα quickly weakened from the 1st h after injection of LPS (P< 0.05 ), it was the lowest at the 8th h. CONCLUSIONS: LPS may lead to lung hemorrhage in the neonatal rats, which may be associated with the decrease of IκBα protein in the lung tissue and activation of NF κB, up regulation of the transcription of TNF α gene."/>
Effects of Tumor Necrosis Factor α and IκBα on Pulmonary Hemorrhage of Neonatal Rats Induced by Lipopolysaccharide
Effects of Tumor Necrosis Factor α and IκBα on Pulmonary Hemorrhage of Neonatal Rats Induced by Lipopolysaccharide
CAI Xu-Xu, WU Wen-Bin, DU Yue, LIU Chun-Feng, ZHANG Hong, LU Yan
Department of Pediatrics, Second Affiliated Hospital, China Medical Universit y, Shenyang 110004, China; 2. Department of Pediatrics, Central Hospital of Tiex i District, Shenyang 110021, China
Abstract OBJECTIVE: To investigate the effects of tumor necrosis factor α (TNF α) and inhibitor protein of nuclear factor κB (IκBα) on pulmonary hemorrhage (PH) of neonatal rats induced by lipopolysaccharide (LPS). METHODS: Seven to ten days old Wistar rats were randomly separated into 2 groups: LPS group, the rats of which were injected with LPS intraperitoneally at the dosage of 5 mg/kg, and they were sacrificed 30 min, 1, 2, 4, 8, 16 and 24 hs after injection of LPS, respectively; normal saline (NS) group, where equal amount of NS was injected intraperitoneally. The number of each time point was 6. The lungs of the rats were examined by eyes and microscope. The protein and mRNA of TNF α in the lung tissues were detected by the method of ELISA and reverse transcription polymerase chain reaction. The expression of IκBα protein was measured by Western Blot. RESULTS: One hour after administration of LPS, patch like bleeding was observed in more than two lobes of the lung. From the 1st h after injection of LPS, TNF α protein increased and was significantly higher than that of NS control group (P< 0.01 ), it peaked at the 2nd h. TNF α mRNA increased 30 min after injection of LPS and was significantly higher than NS control (P< 0.01 ) and the peak was reached 2 hs after injection of LPS. The expression of IκBα quickly weakened from the 1st h after injection of LPS (P< 0.05 ), it was the lowest at the 8th h. CONCLUSIONS: LPS may lead to lung hemorrhage in the neonatal rats, which may be associated with the decrease of IκBα protein in the lung tissue and activation of NF κB, up regulation of the transcription of TNF α gene.
CAI Xu-Xu,WU Wen-Bin,DU Yue et al. Effects of Tumor Necrosis Factor α and IκBα on Pulmonary Hemorrhage of Neonatal Rats Induced by Lipopolysaccharide[J]. 中国当代儿科杂志, 2003, 5(4): 301-305.
CAI Xu-Xu,WU Wen-Bin,DU Yue et al. Effects of Tumor Necrosis Factor α and IκBα on Pulmonary Hemorrhage of Neonatal Rats Induced by Lipopolysaccharide[J]. CJCP, 2003, 5(4): 301-305.
