Table 2.

Bidirectional effects of IL-6 in Calcium Oxalate Nephrolithiasis formation (23, 24).

Contents	Anti-calculative effect of IL-6	The lithophilic effect of IL-6
Model	Mice	Rats
Inducing medications	Glyoxylate (GA)	Ethylene glycol(EG)and ammonium chloride(AC)
Mode of intervention	Mice were administered 75 mg/kg body weight of glyoxonic acid by intraperitoneal injection for 6 consecutive days.	EG is provided as drinking water for 3 weeks. AC is given by gavage for the first three days of the first and third weeks at 2 mL/animal per day.
Signaling pathways	IL-6/JAK/STAT3 activates → inhibits DAO expression → reduces endogenous oxalate synthesis	IL-6 mediates oxidative stress (e.g., 8-OHdG↑) → promotes the inflammatory microenvironment → crystal adhesion
Core mechanics	Metabolic regulation: Reduces oxalic acid production	Inflammatory damage: oxidative stress exacerbates tubular epithelial damage
Biomarkers	DAO expression ↓, serum/urine oxalate level ↓	8-OHdG↑, MDA↑, SOD activity↓
Functional positioning	Inhibition of upstream oxalic acid synthesis	Downstream crystal deposition facilitation

In the formation of calcium oxalate kidney stones, IL-6 shows a dual regulation of “early protection - late injury”: In the early stage, it induces methylation of the DAO gene through the JAK/STAT3 pathway and inhibits oxalate synthesis; In the late stage, the ROS/NF-κB pathway is activated under the drive of chronic inflammation, and the increased oxidative stress promotes crystal deposition.