• Modeling Mechanism：

  Alloxan monohydrate damages pancreatic islet β cells through oxidative stress, leading to β cell necrosis or loss of function, significantly reducing insulin secretion, and thus causing persistent hyperglycemia, which is consistent with the core pathological features of type 1 diabetes or type 2 diabetes with pancreatic islet failure. High-dose administration may cause fatal hypoglycemia in the early stages due to the release of a large amount of insulin.

• Related Products：

  Alloxan monohydrate (T7814)

• Modeling Method：

  Experimental Subject：

  Rats, Wistar albino, Males and females equally, 180-240g, 12-14 weeks old

  Dosage and Administration Route：

  150 mg/kg alloxan, dissolved in fresh distilled water, intraperitoneal injection (i.p.)
  Post-administration management: 6 hours post-dose, administer 10 mL of 20% (w/v) glucose solution orally; subsequently provide 5% (w/v) glucose solution continuously for 24 hours to prevent hypoglycaemic mortality

  Dosing Frequency and Duration Model：

  Single dose

• Validation：

  1. Blood glucose indicators: After modeling, rats with fasting blood glucose >250 mg/dL (approximately 13.9 mmol/L) were selected to confirm the successful establishment of the diabetic model; the oral glucose tolerance test (OGTT) showed that blood glucose significantly increased 0.5-1 hours after glucose loading and failed to effectively decrease after 2 hours; 2. Pathological indicators: HE staining of pancreatic tissue showed severe damage and reduced number of pancreatic β cells, and disordered pancreatic islet structure (significantly different from normal rat pancreatic tissue); 3. Functional indicators: decreased insulin secretion capacity and weakened insulin response to exogenous glucose stimulation.

*Precautions：

*References：Agwaya MS,et,al. Hypoglycemic Activity of Aqueous Root Bark Extract Zanthoxylum chalybeum in Alloxan-Induced Diabetic Rats. J Diabetes Res. 2016;2016:8727590.