Changes in expressions of serum inflammation factor levels and renal tissue immune-associated proteins in multiple factors-caused IgA nephropathymodel rats
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Abstract
Objective To observe the changes in expressions of serum inflammation factors, kidney tissues T cell immune globulin sticky protein 1(TIM-1)and transforming growth factor-beta 1(TGF-beta 1)through multiple factors-caused IgA nephropathy model rats,and to investigate the inflammatory immune mechanism of IgA nephropathy.Methods Twenty healthy male Sprague-Dauley rats were randomly divided(Random number table)into 2 groups with a random digit table:control group(n=10),and model group(n=10).The rats in the model group were administered gastrically with bovine serum albumin solution(400 mg/kg,1 mL/100g)every other day for 6 weeks,and injected subcutaneously with 0.5 mL castor oil and 0.1mL carbon tetrachloride solution once a week for 9 weeks,and injected intravenously through the tail vein with lipopolysaccharide(LPS)solution(0.05 mg/rat)in week 6 and week 8.The rats in the control group were administered gastrically with the same amount of distilled water,and injected subcutaneously with 0.9% sodium chloride solution at a dose of 0.4 mL/rat at the same time points,and injected intravenously through the tail vein with 0.9% sodium chloride solution at a dose of 0.2 mL/rat.The modeling time was 10 weeks.After modeling,urinary microalbumin,24h urine protein and liver and kidney function indices were determined for each group.ELSIA method was used to detect contents of IgA,IFN-γ,IL-4,and IL-6 in the serum,and expressions of TGF-β1 and TIM-1 in rat kidney tissues.Results In the model group,in week 8 after modeling the rats developed less shiny fur color with different severities,listlessness,loose stools.Compared to the rats in the control group,the rats in the model group had significantly increased urinary microalbumin and 24h urine protein(P<0.05),and obviously increased IgA content in the serum and fluorescent expressions of IgA in renal tissues(P<0.05).Compared to the rats in the control group,the rats in the model group showed notably increased serum IL-4 and IL-6 levels(P<0.05),significantly enhanced expressions of GF-β1 and TIM-1 in renal tissues(P<0.05). Conclusion: The multiple factors-caused IgAN model rats have the signs similar to clinical patients with IgAN.Its pathogenesis is closely associated with release of inflammatory factors and expression of TGF-beta 1 and TIM-1.
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