Rutin ameliorates calcium oxalate crystal-induced kidney injury through anti-oxidative stress and modulation of intestinal flora.

Abstract

Kidney stones are a common urological disease. Although there are many ways to treat them, their high recurrence rate remains unresolved. Research has demonstrated that Lysimachia christinae Hance influences kidney stone development; however, the exact mechanism remains unclear. In this experiment, we investigated the protective effect of Lysimachia christinae Hance extract, rutin, on renal injury and its mechanism of action in a mouse model of glyoxalate-induced renal calculi. A kidney stone model was established in Balb/c mice by continuous intraperitoneal injection of glyoxalate (80 mg/kg) for 6 days. Simultaneous gavage of 30, and 60 mg/kg of rutin was administered for 6 days. Samples were collected for determination of index coefficients. Mouse kidney tissue was collected for RNA-seq, and segments of mouse colon were analyzed with 16 S RNA sequencing. We found that rutin significantly reduced renal calcium oxalate deposition and renal tissue injury in the glyoxylate-induced kidney stone model of mice. Rutin also significantly inhibited calcium oxalate deposition-induced apoptosis. In addition, rutin attenuates oxidative stress damage and inhibits the expression of signaling pathways associated with inflammation. 16 S RNA sequencing revealed that rutin regulated intestinal flora composition, significantly increasing the relative abundance of short-chain fatty acid-producing flora and promoting short-chain fatty acid production. In summary, rutin ameliorated renal tubular damage and apoptosis caused by renal stone deposition and reduced oxidative stress. It also regulates the intestinal flora, increases the enrichment of intestinal probiotics, and promotes the production of short-chain fatty acids, thereby inhibiting the formation of kidney stones.