Background  As a common disease of the urinary system, the incidence and recurrence of kidney stones are increasing year by year, and there are still few effective drugs for the early treatment of renal salt crystals.

Objective To preliminarily investigate the effects and possible mechanisms of action of rhodopsin on renal function in calcium oxalate (CaOx) kidney stone model rats based on the NF-κB/NLRP3/Caspase-1 signaling pathway.

Methods  Forty SPF-grade Wistar male rats were randomly divided into control group, model group, intervention group, positive control group, with 10 rats in each group. The CaOx kidney stone rat model was induced by drinking 0.75% ethylene glycol solution and gavage with 2% ammonium chloride solution every other day in all groups except the control group, while the intervention group and the positive control group were gavaged with emodin and shenshitong granules, respectively. After 4 weeks of continuous drug administration, urine levels of oxalate, citrate, Ca^{2 +} , and Mg^{2 +} were measured; serum markers of renal impairment and serum markers of renal injury were measured; HE staining and Vonkossa staining were used to observe the histopathological changes and calcium salt deposition in rat kidney, respectively; Enzyme-linked immunosorbent assay (ELISA) for the determination of markers of oxidative stress injury in renal tissues; NLRP3, IL-1β, and IL-18 mRNA levels in kidney tissues were measured by real-time fluorescence quantitative polymerase chain reaction (real-time PCR).Protein immunoblotting (Western-blotting) was used to detect kidney tissue NLRP3, NF-κB p56, Caspase-1, IL-1β, and IL-18 protein levels.

Results Compared with the control group, body mass, urinary Mg^{2 +} , and citrate decreased (P < 0.01), and renal index, urinary Ca^{2 +} , and urinary oxalate with serum creatinine, urea nitrogen, and uric acid increased (P < 0.01) in rats of the model group; Significant pathological damage and calcium salt deposits could be seen in the renal tissue; MDA and ROS content and NLRP3, IL-1β, and IL-18 mRNA levels and NLRP3, IL-1β, IL-18, NF-κB p56, and Caspase-1 protein levels were elevated in renal tissues, whereas SOD content was decreased (P < 0.01). Compared with the model group, body mass, urinary Mg^{2 +} , and citrate were elevated (P < 0.01 or P < 0.05), while renal index, urinary Ca^{2 +} , and urinary oxalate with serum creatinine, urea nitrogen, and uric acid were lowered (P < 0.01 or P < 0.05) in rats from the intervention group and the positive control group; Renal histopathologic damage and calcium salt deposition were significantly reduced; MDA, ROS content and NLRP3, IL-1β, IL-18 mRNA levels and NLRP3, IL-1β, IL-18, NF-κB p56, and Caspase-1 protein expression levels were also decreased in renal tissues, whereas SOD levels were increased (P < 0.01 or P < 0.05).

Conclusion Emodin may improve renal oxidative stress injury and calcium salt deposition in CaOx kidney stone model rats by regulating the NF-κB/NLRP3/Caspase-1 signaling pathway, thereby inhibiting CaOx stone formation and consequently protecting renal function.