• Modeling Mechanism：

  Cyclophosphamide metabolites damage bladder urothelium and bladder tissue, activating inflammatory pathways: inducing the release of growth factors such as NGF, thereby activating the PI3-K/AKT signaling pathway, promoting the upregulation of pAKT expression in urothelium and detrusor smooth muscle, and simultaneously inducing inflammatory cell infiltration and increased vascular permeability, leading to bladder inflammation; long-term inflammatory stimulation induces bladder overactivity, manifested as increased urination frequency, decreased bladder capacity, and increased non-voiding contractions.

• Related Products：

  Cyclophosphamide (T0707L)

• Modeling Method：

  Experimental Subject：

  Rats, Wistar, Female, 200-300g

  Dosage and Administration Route：

  Acute: Cyclophosphamide, 150 mg/kg, intraperitoneal injection (ip);
  Chronic: Cyclophosphamide, 75 mg/kg, intraperitoneal injection (ip)

  Dosing Frequency and Duration Model：

  Acute modelling: 1 session; Chronic modelling: 8 consecutive days (once every 3 days)

• Validation：

  Acute model: pAKT expression in bladder tissue was upregulated 5.7-fold, with urothelial damage and interstitial edema; Chronic model: pAKT expression was upregulated 2.9-fold, with CD68⁺/MAC2⁺/F4/80⁺ macrophage infiltration visible in bladder tissue;

*Precautions： Acute models were sacrificed 4 hours after model establishment, while chronic models were sacrificed on day 8.

*References：Arms L and Vizzard MA. Role for pAKT in rat urinary bladder with cyclophosphamide (CYP)-induced cystitis. Am J Physiol Renal Physiol. 2011 Aug;301(2):F252-62.