| Objective: To investigate immunomodulatory disorders and transforminggrowth factor-β1(TGF-β1) induced response gene to complement-32(RGC-32)expression in renal fibrosis in IgA nephropathy rats, and the effects and themechanism of Rhizoma Imperatae polysaccharide (RIP) on IgA nephropathy.Methods:①Animal parts:.50rats were randomly divided into5groups,including control group, model group, small does RIP group，high does RIPgroup and dexamethasone treated group，IgA nephropathy rat model was builtby bovine serum albumin(BSA) plus lipopolysaccharide (LPS) and carbontetrachloride (CCl4) subcutaneous injection，RIP was orally given at a dose of20,10mg·kg-1·d-1for4weeks.Dexamethasone was used at a dose of2mg·kg-1·d-1as a positive control．Urine red blood cell(URBC),urinary protein (UP),serumcreatinine (Scr),blood ureanitrogen (BUN),serum IL-2, serum IL-6weredetected.Renal specimens were observed by pathological (HE; PASM-Massonstaining;immunofluorescence;electron microscopy), renal tissue contents ofTGF-β1, RGC-32expression were tested by Immunohistochemical and PT-PCR②Cell parts: Renal tubular epithelial cells (RTEC)were divided into differentgroups and treated with IL-2and IL-6by different concentration (IL-2:10,30,90pg/ml; IL-6:100,300,600pg/ml)individually and mixed together， The expression of Transforming growth factor beta1(TGF-β1) in each group wasdetected with immunohistochemical methods. Results:①Fluoroscope suggestedthat the model establishing was succeeded.Compared with the model group：URBC, UP, Scr,BUN were significantly decreased in treatment group (P<0.01)；Electron dense deposition,mesangioproliferative, podocyte fusionand IgA deposition were not remarkable by electromicroscopy and Immuno-fluorescence in treatment group； IL-2,and IL-6were significantly reduced inhigh does RIP group group (P <0.05); immunohistochemistry and PT-PCRresults showed that TGF-β1, RGC-32protein expression levels weresignificantly lower in RIP group group(P <0.01).②IL-2had no effect on theexpression of TGF-β1in RTEC individually (p>0.05). However, IL-6couldaffect RTEC TGF-β1expression directly (p <0.01). IL-2combined with IL-6had interaction on rat kidney TGF-β1expression. When the concentration ofIL-2was90pg/ml together with IL-6was300pg/ml, TGF-β1had highestexpression levels (p <0.01). Conclusions:Serum IL-2and IL-6changes,especially IL-6increased，may promote the development of IgA nephropathyTGF-β1-mediated renal fibrosis.Rhizoma Imperatae polysaccharide byreducing rat IgA nephropathy model of serum IL-2and IL-6levels, therebyreducing kidney TGF-β1expression and suppression of RGC-32-mediatedfibrosis Rhizoma Imperatae polysaccharide may be he treatment of rats with IgAone of the mechanisms.Rhizoma Imperatae polysaccharides can reduce IgAdeposition in the mesangial area and improve renal function, which may relateto its immune regulation by degrade IL-2and IL-6,reducing TGF-β1expressionand suppression of RGC-32-mediated fibrosis in IgA nephropathy. The... |
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