AIM: To observe the variation in expression of AP-1 and TGF-beta1 in rat kidney of iodine deficiency, to explore the nosogenesis of renal damage in the region of iodine deficiency. METHODS: The models of deficient iodine rats were established by treatment with low iodine diet, wistar rats were divided into gentle low iodine group(GLIG), dense low iodine group(DLIG) and control group(CL). Serum levels of thyroid humone were determined by chemiluminescent immunoassay. To observe the gene expression of c-Jun by using RT-PCR, observe the expression of TGF-beta1 by using immunohistochemistry. RESULTS: Compared with CL, the FT3, FT4 of DLIG were significantly decreased(P<0.01), the FT3 of GLIG were significantly decreased(P<0.01), the FT4 of GLIG were not significantly decreased(P>0.05). Compared with GLIG, the FT3, FT4 of DLIG were significantly decreased(P<0.01). Compared with CL, GLIG group, the gene expression of c-Jun was significantly increased(P<0.01) in DLIG group. Compared with CL group, the level of c-Jun was slightly increased(P>0.05)in GLIG group. Compared with CL, the TGF-beta1 of DLIG was significantly increased, the TGF-beta1 of GLIG was significantly increased. Compared with GLIG, the TGF-beta1 of DLIG was significantly increased. CONCLUSION: Iodine deficiency can decrease the secretion of thyroid humone, can lead the activation of c-Jun and TGF-beta1 in kidney. This finding suggest that AP-1 signal transduction pathway participate in the nosogenesis of renal damage.
AIM: To observe the variation in expression of AP-1 and TGF-beta1 in ratkidney of iodine deficiency, to explore the nosogenesis of renal damage in the region of iodine deficiency. METHODS: The models of deficient iodinerats were established by treatment with low iodine diet, wistar rats were divided into gentle low iodine group(GLIG), dense low iodine group(DLIG) and control group(CL). Serum levels of thyroid humone were determined by chemiluminescent immunoassay. To observe the gene expression of c-Jun by using RT-PCR, observe the expression of TGF-beta1 by using immunohistochemistry. RESULTS: Compared with CL, the FT3, FT4 of DLIG were significantly decreased(P<0.01), the FT3 of GLIG were significantly decreased(P<0.01), the FT4 of GLIG were not significantly decreased(P>0.05). Compared with GLIG, the FT3, FT4 of DLIG were significantly decreased(P<0.01). Compared with CL, GLIG group, the gene expression of c-Jun was significantly increased(P<0.01) in DLIG group. Compared with CL group, the level of c-Jun was slightly increased(P>0.05)in GLIG group. Compared with CL, the TGF-beta1 of DLIG was significantly increased, the TGF-beta1 of GLIG was significantly increased. Compared with GLIG, the TGF-beta1 of DLIG was significantly increased. CONCLUSION:Iodine deficiency can decrease the secretion of thyroid humone, can lead the activation of c-Jun and TGF-beta1 in kidney. This finding suggest that AP-1 signal transduction pathway participate in the nosogenesis of renal damage.