Abstract
Obcordata A (OA) is a polyoxypregnane glycoside derived from the Dai medicine Aspidopterys obcordata vines. This study aims to investigate the efficacy of OA on renal tubular epithelial cells exposed to calcium oxalate crystals. We incubated renal tubular cells with 28 μg·cm2 calcium oxalate crystals for 24 h with and without OA, GKT137831, phorbol-12-myristate-13-acetate (PMA), and tocopherol. The MTT [3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay, microscopic examination, flow cytometry, and immunofluorescence staining revealed that calcium oxalate crystals decreased cell viability and elevated reactive oxygen species (ROS) levels. OA, GKT137831, and tocopherol protected cells and decreased ROS levels. However, OA did not exhibit direct DPPH scavenging ability. In addition, immunoblotting illustrated that OA inhibited the NOX4 (nicotinamide adenine dinucleotide phosphate oxidases 4) expression and downregulated the protein expression in the NOX4/ROS/p38 MAPK (p38 mitogen-activated protein kinase) pathway. The findings suggest that the cytoprotective and antioxidant effects of OA can be blocked by the NOX4 agonist PMA. In conclusion, OA could be used as a NOX4 inhibitor to prevent kidney stones.
Highlights
Nephrolithiasis, which is caused by the pathological mineralization of crystals and organic substrate in the kidneys [1,2], is a common urological disease worldwide with a lifetime incidence of10–15% [3,4]
Considering the potential cytotoxicity of Obcordata A (OA) in mammalian cells, human kidney 2 (HK-2) cells were treated with various doses of OA for 24 h, and cell viability was determined using the MTT assay
The incidence of kidney stones is increasing year by year, and one-quarter of patients are hospitalized for surgical treatment of renal colic or hematuria [18]
Summary
Nephrolithiasis, which is caused by the pathological mineralization of crystals and organic substrate in the kidneys [1,2], is a common urological disease worldwide with a lifetime incidence of10–15% [3,4]. Nephrolithiasis, which is caused by the pathological mineralization of crystals and organic substrate in the kidneys [1,2], is a common urological disease worldwide with a lifetime incidence of. 70–80% of nephrolithiasis is composed of calcium oxalate [5,6]. The primary treatment for kidney stones comprises of surgery, including extracorporeal shockwave lithotripsy, ureterorenoscopic lithotripsy, nephrolithotomy, and open surgery; these surgeries are complicated and expensive and do not affect the recurrence of stones. The 2012 estimates of the Urologic Diseases in America project reported that the cost is up to $10 billion, rendering stone disease one of the most expensive urological conditions [7]. The recurrence rate of nephrolithiasis is approximately. Patients with nephrolithiasis bear a massive economic burden and face an additional risk of urinary tract obstruction, infection, kidney seeper, and renal insufficiency
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