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Previous study has found that RAS blockers can reduce proteinuria and tubulointerstitial fibrosis not only through their hemodynamic/antihypertensive effects but also through the inhibition of NF-B, MCP1 gene expression, and macrophage infiltration, thereby exerting anti-inflammatory/antifibrotic effects in the STZ-induced diabetic rat model (194)

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When induced in this way, renal failure strongly correlates with corresponding human disturbance