Fig. 6.

Blockade of EV secretion alleviates OTA-induced kidney toxicity. A-B Immunoblotting of the kidney injury markers in control or OTA-exposed NRK52E cells after DMA-mediated inhibition of EV secretion. C Bar diagram representing the kidney and body weight ratio across experimental groups. D-F The level of the classical kidney injury markers serum creatinine (SCr) D, serum urea (SUrea) E, and urinary albumin (UAlb) F, measured in V-control, OTA, OTA + DMA, and DMA-treated rats. G-K Bar diagram representing the concentration of the protein-based urinary kidney injury markers NGAL G, clusterin H, cystatin C (I), TIMP-1 J, and albumin K. L Representative histopathological images showing structural alterations in kidney tissue. H & E staining (left column) illustrating glomerular shrinkage (star symbol), hypercellularity in tubules (thick arrow symbol), proximal epithelial cell degeneration (asterisk symbol); MTS (right column) showing the collagen deposition in the tubulointerstitial space (blue colour). (M) Immunohistochemistry images showing the expression of kidney injury markers in kidney cortex region; magnification 20x, scale bar 100 µm. Each group contained three animals (n = 3). CTL = NRK52E cells treated with conditioned media from control NRK52E cells, CTL + DMA = NRK52E cells treated with conditioned media from DMA-exposed NRK52E cells, HD = NRK52E cells treated with conditioned media from four months OTA-exposed NRK52E cells, HD + DMA = NRK52E cells treated with conditioned media from four months OTA-exposed NRK52E cells treated with DMA, V-control = vehicle-treated rats, OTA = OTA-exposed rats, OTA + DMA = both DMA and OTA-exposed rats, and DMA = only DMA-exposed rats