Objective:
The study aimed to evaluate the preventive effects of hydroxycitric
acid（HCA） for stone formation in the glyoxylate-induced mouse model.
Materials and methods:
Male C57BL/6J mice were divided into a control group,
glyoxylate(GOX) 100 mg/kg group, a GOX+HCA 100 mg/kg group, and a GOX+HCA
200 mg/kg group. Blood samples and kidney samples were collected on the eighth day
of the experiment. We used Pizzolato staining and a polarized light microscope to
examine crystal formation and evaluated oxidative stress via the levels of
malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase
(GSH-Px). Quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) was
used to detect the expression of monocyte chemotactic protein-1(MCP-1), nuclear
factor-kappa B (NF κ B), interleukin-1 β (IL-1 β) and interleukin-6 (IL-6) messenger RNA
(mRNA). The expression of osteopontin (OPN) and a cluster of differentiation-44(CD44)
were detected by immunohistochemistry and qRT-PCR. In addition, periodic acid Schiff
(PAS) staining and TUNEL assay were used to evaluate renal tubular injury and
apoptosis.
Results:
HCA treatment could reduce markers of renal impairment (Blood Urea
Nitrogen and serum creatinine). There was significantly less calcium oxalate crystal
deposition in mice treated with HCA. Calcium oxalate crystals induced the production of
reactive oxygen species and reduced the activity of antioxidant defense enzymes. HCA
attenuated oxidative stress induced by calcium oxalate crystallization. HCA had
inhibitory effects on calcium oxalate-induced inflammatory cytokines, such as MCP-1, IL-
1 β, and IL-6. In addition, HCA alleviated tubular injury and apoptosis caused by calcium
oxalate crystals.
Conclusion:
HCA inhibits renal injury and calcium oxalate crystal deposition in the
glyoxylate-induced mouse model through antioxidation and anti-inflammation.
Case Report of a Fatal Antifreeze Ingestion with a Record High Level and Impressive Renal Crystal Deposition
