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Objective:To explore the role of activated liver X receptor a (LXRα) on the expressions of interleukin-1 receptor associated kinase-4 (IRAK-4) and NF-kappaB (NF-κB) in the inflammatory response which induced by LPS in the Kupffer cells and to investigate the possible mechanisms of LXRαnegative regulation of inflammatory response. Methods:The Kupffer cells were isolated from male Kunming mice by collagen perfusion in situ.And these cells were divided into 4 groups:normal control group,LPS treatment group,LXRαagonist T0901317 treatment group,LPS and T0901317 combined treatment group.The LPS treatment group were treated with a final concentration of 1μg/ml LPS in RPMI 1640 and cultured for 6 h,the T0901317 treatment group were treated with a final concentration of 5μg/ml in RPMI 1640 and cultured for 24 h,and the combined treatment group received pre-culture for 24 h with a final concentration of 1μg/ml T0901317 in RPMI 1640 and then cultured for 6 h with a final concentration of 5μg/ml LPS in RPM! 1640.All groups were cultured for 30 h.The expression of LXRα,IRAK-4 and NF-κB at mRNA and protein levels were detected by real-time PCR and Western blotting,and the TNF-αand IL-1βlevels were detected by ELISA. Results:The levels of LXRαmRNA and protein were highest in T0901317 group,and lowest in LPS group (P<0.05). The level of IRAK4 and NF-κB mRNAs and proteins were evidently lower in the Combined-treated group than in LPS group (P<0.05).And the level of TNF-αand IL-1 were observed highest in LPS group (P<0.05),but no difference among the Control group,T0901317 group and Combined-treated group (P>0.05).Conclusion:These date suggest that the LXR agonists can effectively up-regulate the expressions of LXRαmRNA and protein and inhibit the inflammatory response.This may be via down-regulating the expressions of IRAK4 and NF-κB at mRNA and protein levels.
Objective: To explore the role of activated liver X receptor a (LXRα) on the expressions of interleukin-1 receptor associated kinase-4 (IRAK-4) and NF-κB in the inflammatory response which induced by LPS in the Kupffer cells and to investigate the possible mechanisms of LXR [alpha] negative regulation of inflammatory response. Methods: The Kupffer cells were isolated from male Kunming mice by collagen perfusion in situ. These cells were divided into 4 groups: normal control group, LPS treatment group, LXRαagonist T0901317 treatment group, LPS and T0901317 combined treatment group. LPS treatment group were treated with a final concentration of 1 μg / ml LPS in RPMI 1640 and cultured for 6 h, the T0901317 treatment group were treated with a final concentration of 5 μg / ml in RPMI 1640 and cultured for 24 h, and the combined treatment group received pre-culture for 24 h with a final concentration of 1 μg / ml T0901317 in RPMI 1640 and then cultured for 6 h with a final concentration of 5 μg / ml LPS in RPM! 1640. All groups were cultured for 30 h. The expression of LXRα, IRAK-4 and NF-κB at mRNA and protein levels were detected by real-time PCR and Western blotting, and the TNF- IL-1βlevels were detected by ELISA. Results: The levels of LXRα mRNA and protein were highest in T0901317 group, and lowest in LPS group (P <0.05). The levels of IRAK4 and NF- κB mRNAs and proteins were evidently lower in the Combined -treated group than in LPS group (P <0.05) .And the level of TNF-αand IL-1 was highest in LPS group (P <0.05), but no difference among the Control group, T0901317 group and Combined-treated group (P> 0.05) .Conclusion: These date suggest that the LXR agonists can effectively up-regulate the expressions of LXRα mRNA and protein and inhibit the inflammatory response. This may be via down-regulating the expressions of IRAK4 and NF-κB at mRNA protein levels.