Salvianolic acid B ameliorates vascular calcification in rats with chronic kidney disease combined with arteriovenous fistula by inhibiting BMP2/Smads signaling.

Salvianolic acid B (Sal B) can reduce the symptoms of uremia in rats and has a good protective effect on the kidney, but its effect on vascular calcification in chronic kidney disease (CKD) combined with arteriovenous fistula (AVF) is unclear. This study aimed to investigate the effects and mechanisms of Sal B on CKD-AVF. The rat model of CKD-AVF was established and rats were treated with different doses of Sal B. The levels of creatinine (Cr) and urea nitrogen (BUN) in serum were analyzed biochemically; the levels of ALP in serum were measured by ELISA, the pathological damage of kidney and AVF venous segments tissues was observed by HE staining, Masson staining to detect renal fibrosis, and the calcium salt deposition in AVF venous segments tissue was examined by Von Kossa staining, and the protein expression of BMP-2, p-Smad1, Smad1, p-Smad5, Smad5, Osterix, and Runx2 in AVF venous segments tissue was analyzed by Western blot. Sal B attenuated the pathological damage of kidney and AVF venous segments tissues, improved calcium salt deposition, reduced the levels of Cr, BUN, and ALP, and inhibited the expression of BMP-2, p-Smad1, p-Smad5, Osterix, and Runx2 in AVF venous segments tissue ( < 0.05). The mechanism of Sal B inhibition of calcium salt deposition in rats of CKD-AVF may be related to the inhibition of the BMP2/Smads signaling pathway.