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Objective To investigate the effect of transmembrane activator and calcium modulator cy- clophilin ligand interactor-immunoglobulin (TACI-Ig) on renal damage in rats with IgA nephropathy(IgAN). Methods A total of 24 SD rats were randomly divided into the normal control, the model, the TACI-Ig,and the drug control groups with six rats per group. The normal control and model groups received saline, the TACI-Ig group received TACI-Ig(14.36 mg/kg), and the drug control group received prednisolone acetate (5 mg/kg). Twenty-four-hour urinary protein (24h-UP), serum creatinine (Scr), blood urea nitrogen (BUN),ga- lactose-deficient IgA1 (Gd-IgA1), Toll-like receptor 4(TLR4), Myeloid differentiation factor 88 (MyD88), Nu- clear factor kapра В(NF-кВ) protein and mRNA levels were compared among groups to analyze the influence of TACI-Ig on renal damage. Results The 24h-UP levels in the model group were significantly higher than those in the normal control group, while levels in the TACI-Ig and drug control groups were significantly lower than those in the model group (P<0.05). Serum CRE levels in the TACI-Ig group were lower than those in the model group(P<0.05). Deposition of immune complexes in the mesangial area of renal tissues was significantly inhibited in the TACI-Ig and drug control groups. Serum Gd-IgAl levels in the model group were higher than those in the normal control group but lower than those in the TACI-Ig group (P<0.01). Se- rum Gd-IgAl levels in the drug control group were lower than those in the model group but higher than those in the TACI-Ig group (P<0.01). TLR4, MyD88, and NF-kB protein levels in the TACI-Ig group were lower than those in the model group(P<0.05). TLR4, MyD88 protein levels in the drug control group were higher than those in the TACI-Ig group (P<0.05). TLR4, MyD88, and NF-KB mRNA levels in the TACI-Ig group were lower than those in the model group (P<0.05). Conclusion TACI-Ig exhibits therapeutic efficacy in IgAN, improving renal function in rats and inhibiting mesangial matrix expansion and mesangial cell proliferation. [ABSTRACT FROM AUTHOR]

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