• Modeling Mechanism：

  Scopolamine, as an anticholinergic drug, inhibits acetylcholine-mediated neural signaling by blocking central cholinergic receptors. Simultaneously, it induces oxidative stress (accumulation of reactive oxygen species (ROS), inhibits endogenous antioxidant pathways (downregulation of Nrf2/HO-1 expression), activates the NF-κB inflammatory signaling pathway, promotes the release of pro-inflammatory factors (TNF-α) and inflammatory enzymes (COX-2), triggers neuroinflammation, and ultimately leads to learning and memory dysfunction, mimicking the core pathological features of Alzheimer's disease (memory decline, neuroinflammation, and oxidative stress).

• Related Products：

  Scopolamine (T3S0478)

• Modeling Method：

  Experimental Subject：

  Mice, BALB/c mice, Male, 7–8 weeks old, Body weight 25–30 g

  Dosage and Administration Route：

  ① Core modelling: Scopolamine, 1 mg/kg/day, dissolved in physiological saline, intraperitoneal injection;
  ② Control treatment: Control group administered equal volume saline solution via intraperitoneal injection; all other housing and treatment conditions identical;
  ③ Intervention validation group (optional): During weeks 2–3 of modelling (one week after scopolamine administration), concurrently administer neuroprotective agent (e.g., ranuncoside) at 10 mg/kg via intraperitoneal injection every other day for 2 weeks;

  Dosing Frequency and Duration Model：

  Once daily for 3 consecutive weeks

• Validation：

  1. Behavioral indicators: - Morris water maze (MWM): significantly prolonged escape latency (F=10.88, p<0.01), shortened time spent in the target quadrant (F=75, p<0.001), suggesting a decline in spatial learning and memory abilities; - Y maze: significantly reduced percentage of spontaneous alternation behavior (F=262.1, p<0.001), suggesting working memory impairment; 2. Biochemical indicators: - Metabolic indicators: elevated random blood glucose (F=370.4, p<0.01), elevated serum LDL, total cholesterol (TC), and triglycerides (TG), and decreased HDL (p<0.01); 3. Molecular indicators: - Oxidative stress: significantly downregulated expression of Nrf2 and HO-1 proteins in the brain (F=195.9 and 204.5, respectively, p<0.001); - Neuroinflammation: significantly upregulated expression of NF-κB, COX-2, and TNF-α proteins in the brain (F=195.9 and 204.5, respectively, p<0.001); The values were 175.0, 565.1, and 386.8 respectively (p < 0.001).

*Precautions：

*References：Sara Salahuddin H,et,al. Ranuncoside's attenuation of scopolamine-induced memory impairment in mice via Nrf2 and NF-ĸB signaling. Saudi Pharm J. 2023 Sep;31(9):101702.