Abstract
Abstract Urolithin B, gut microbiota metabolite of ellagitannins, contributes toward multiple health benefits attributed to ellagitannin-rich foods. The influence of urolithin B on unilateral ureteral obstruction (UUO) induced renal fibrosis and TGF-β1 induced HK-2 cells and the underlying mechanism was investigated. The results showed UUO-induced kidney injury was significantly ameliorated as shown by the improvement of renal function (BUN and Cr), kidney morphology and the suppression of renal tubular injury markers of TGF-β1, Ang II, alpha-SMA and Col IV mRNA levels. Meanwhile, the renal inflammatory induced by UUO were also strikingly attenuated in urolithin B-treated rats (TNF-α, IL-6 and MCP-1). In vitro, urolithin B treatment markedly inhibited TGF-β1-induced HK-2 cells fibrosis and proliferation, suppressed TGF-β1 and NF-κB activation. This works indicated that urolithin B contributes critically to renal inflammation in vivo and in vitro, involving the inhibition on TGF-β/Smad and TLR4/NF-кB signaling activation.
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