OBJECTIVE: To observe the mRNA and protein expression of TLR9, NF-κB and serum level of Th1/Th2 cytokines when stimulated with different concentration of CpG-ODN in STZ-induced diabetic rats. METHODS: 40 SD male rats were randomly divided into four groups:normal control group (Group I), type 1 diabetes control group (Group II), low-dose CpG-ODN treated type 1 diabetes group (Group III), high dose CpG-ODN treated type 1 diabetes group (Group IV). 60 µg /kg and 120 µg /kg CpG-ODN were injected to rats of Group III and IV when inducing type 1 diabetes model.mRNA and protein levels of TLR9 and NF-κB in spleen and pancreas were detected by fluorescence quantitative PCR and Western blotting.Serum TNF-α, IL-6 and IFN-γ were measured by ELISA. RESULTS: TLR9 protein expression levels were much higher in spleen than in the pancreas among these four groups. In spleen, TLR9 and NF-κB mRNA and protein level were significantly higher in Group III and IV than those in Group I and II, and the expression level was higher in Group IV than in Group III. In pancreas, TLR9 and NF-κB protein level were significantly higher in Group III and IV than those in Group I and II, and the expression level was also higher in Group IV than Group III.Serum TNF-α and IFN-γ level in Group III and IV significantly higher than in Group I and II, and serum levels of TNF-α and IFN-γ in Group IV was higher than in Group III. CONCLUSIONS: CpG-ODN activation of TLR9-MyD88 signaling pathways results in dose-effect NF-κB stimulation in STZ-induced diabetic rats.
OBJECTIVE: To observe the mRNA and protein expression of TLR9, NF-κB and serum level of Th1/Th2 cytokines when stimulated with different concentration of CpG-ODN in STZ-induced diabeticrats. METHODS: 40 SD male rats were randomly divided into four groups:normal control group (Group I), type 1 diabetes control group (Group II), low-dose CpG-ODN treated type 1 diabetes group (Group III), high dose CpG-ODN treated type 1 diabetes group (Group IV). 60 µg /kg and 120 µg /kg CpG-ODN were injected to rats of Group III and IV when inducing type 1 diabetes model.mRNA and protein levels of TLR9 and NF-κB in spleen and pancreas were detected by fluorescence quantitative PCR and Western blotting.Serum TNF-α, IL-6 and IFN-γ were measured by ELISA. RESULTS:TLR9 protein expression levels were much higher in spleen than in the pancreas among these four groups. In spleen, TLR9 and NF-κB mRNA and protein level were significantly higher in Group III and IV than those in Group I and II, and the expression level was higher in Group IV than in Group III. In pancreas, TLR9 and NF-κB protein level were significantly higher in Group III and IV than those in Group I and II, and the expression level was also higher in Group IV than Group III.Serum TNF-α and IFN-γ level in Group III and IV significantly higher than in Group I and II, and serum levels of TNF-α and IFN-γ in Group IV was higher than in Group III. CONCLUSIONS: CpG-ODN activation of TLR9-MyD88 signaling pathways results in dose-effect NF-κB stimulation in STZ-induced diabeticrats.