• Modeling Mechanism：

  Ethambutol dihydrochloride inhibits renal uric acid excretion, exacerbates uric acid accumulation in the body, and further aggravates kidney damage; ③ The two work together to activate inflammatory pathways, leading to upregulation of pro-inflammatory factors such as IL-6 and TNF, triggering renal tissue inflammation, glomerular sclerosis and interstitial fibrosis, mimicking the core pathological process of human hyperuricemic nephropathy.

• Related Products：

  Ethambutol dihydrochloride (T0810)

• Modeling Method：

  Experimental Subject：

  Rats, Wistar, Male, 7–8 weeks old, Body weight 200–220 g

  Dosage and Administration Route：

  ① Core modelling: Adenine (100 mg/kg)+Ethambutol hydrochloride (250 mg/kg), Dissolved in deionised water to prepare a 1% adenine+2.5% ethambutol hydrochloride suspension, Administered via gastric lavage;
  ② Control treatment: Equal volume of deionised water administered via gastric lavage using the same method;
  ③ Intervention Verification (Optional):
  - Allopurinol (50 mg/kg), 0.5% solution administered via gastric lavage, commencing from week 2 of modelling, for 2 consecutive weeks;
  - Chicory formula (CF): high dose 8.64 g/kg, low dose 2.16 g/kg; administered via gastric lavage as a decoction; commencing from week 2 of modelling, for 2 consecutive weeks.

  Dosing Frequency and Duration Model：

  Once daily, for 3 consecutive weeks

• Validation：

  Key indicators (serum biochemistry): - Serum uric acid (UA): The model group reached 2.40 μMol/L, significantly higher than the control group (2.25 μMol/L). After intervention with allopurinol and high-dose CF, it decreased to 1.57 μMol/L (p<0.05); - Renal function indicators: Serum urea (UREA) increased from 6.75 mMol/L to 15.87 mMol/L, and serum creatinine (CREA) increased from 38.5 μmol/L to 64.83 μMol/L (p<0.001), both significantly decreasing after intervention; Pathological indicators: - HE staining showed disordered kidney structure in the model group, with glomerular sclerosis, renal tubular epithelial cell damage, renal interstitial inflammation, and uric acid crystal deposition. Pathological damage was significantly reduced in the intervention group; Molecular indicators: - Significantly upregulated expression of IL-6, TP53, and TNF mRNA in renal tissue (p<0.05), and VEGFA and CASP3 mRNA expression... The expression was downgraded, and the trend could be reversed after intervention.

*Precautions： To alleviate pain, rats were euthanized by intraperitoneal injection of sodium pentobarbital.

*References：Li N,et,al. Integration of network pharmacology and intestinal flora to investigate the mechanism of action of Chinese herbal Cichorium intybus formula in attenuating adenine and ethambutol hydrochloride-induced hyperuricemic nephropathy in rats. Pharm Biol. 2022 Dec;60(1):2338-2354.