Lihua Zhang1, Huiqing He2, Jing Wang1, Deqiao Sheng3. 1. Department of Pediatrics of The Second People's Hospital of Yichang Yichang, Hubei Province, China. 2. Department of Public Health of The Second People's Hospital of Yichang Yichang, Hubei Province, China. 3. Department of Biochemistry of Medical Science College of China Three Gorges University Yichang 443000, Hubei Province, China.
Abstract
OBJECTIVE: To investigate Cartilage glycoprotein 39 (Cgp-39) expression in peripheral blood monocytes of septic rats, and analyze the relationship between Toll-like receptor 4 (TLR4)-NF-κB signalling pathway and Cgp-39 expression. METHODS: The ligation puncture was performed to establish rat sepsis model, and ELISA was used to measure serum Cgp-39 concentration. Peripheral blood mononuclear cells was isolated and cultured for 72 h. RNA interference technology was used to inhibit TLR4 and NF-κB gene expression, and real-time PCR and Western blot were performed to detect mRNA and protein expression of TLR4 and NF-κB. RESULTS: At 1 h, there was no significant differences in serum Cgp-39 concentration between sepsis group and the control group (P > 0.05), however, at 6 h, 12 h, 24 h and 48 h, serum Cgp-39 concentrations in sepsis group were significantly higher than those in the control group at the corresponding time points (P < 0.05). Compared with the control group, TLR4 mRNA and protein expression were increased significantly in sepsis group and sepsis NF-κB interference group; NF-κB mRNA and protein expression were increased significantly in sepsis group and sepsis TLR4 interference group. However, compared with sepsis group, Cgp-39 concentrations decreased significantly in either sepsis TLR4 interference group or NF-κB interference group (P < 0.05 for both). CONCLUSION: Cgp-39 is highly expressed in peripheral blood monocytes of septic rat and TLR4-NF-κB signalling pathways may be involved in the regulation of Cgp-39 expression.
OBJECTIVE: To investigate Cartilage glycoprotein 39 (Cgp-39) expression in peripheral blood monocytes of septic rats, and analyze the relationship between Toll-like receptor 4 (TLR4)-NF-κB signalling pathway and Cgp-39 expression. METHODS: The ligation puncture was performed to establish ratsepsis model, and ELISA was used to measure serum Cgp-39 concentration. Peripheral blood mononuclear cells was isolated and cultured for 72 h. RNA interference technology was used to inhibit TLR4 and NF-κB gene expression, and real-time PCR and Western blot were performed to detect mRNA and protein expression of TLR4 and NF-κB. RESULTS: At 1 h, there was no significant differences in serum Cgp-39 concentration between sepsis group and the control group (P > 0.05), however, at 6 h, 12 h, 24 h and 48 h, serum Cgp-39 concentrations in sepsis group were significantly higher than those in the control group at the corresponding time points (P < 0.05). Compared with the control group, TLR4 mRNA and protein expression were increased significantly in sepsis group and sepsis NF-κB interference group; NF-κB mRNA and protein expression were increased significantly in sepsis group and sepsisTLR4 interference group. However, compared with sepsis group, Cgp-39 concentrations decreased significantly in either sepsisTLR4 interference group or NF-κB interference group (P < 0.05 for both). CONCLUSION:Cgp-39 is highly expressed in peripheral blood monocytes of septic rat and TLR4-NF-κB signalling pathways may be involved in the regulation of Cgp-39 expression.
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