• Modeling Mechanism：

  Lipopolysaccharides (LPS) activate innate immune cells in the lungs (macrophages, epithelial cells), induce the release of pro-inflammatory factors such as TNF-α and IL-6, recruit a large number of neutrophils to infiltrate lung tissue, disrupt the integrity of the alveolar-capillary barrier, causing plasma components such as albumin and total protein to extravasate into the alveolar cavity, induce inflammatory damage to lung tissue, increase lung elastic resistance, reduce inspiratory volume, and mimic the core pathological process of human ARDS.

• Related Products：

  Lipopolysaccharides (T11855)

• Modeling Method：

  Experimental Subject：

  Mice, C57BL/6J, Female, 11 weeks old

  Dosage and Administration Route：

  3 mg/kg LPS, Dissolved in physiological saline (3 µg/µL), Intranasal administration (1 µL/g body weight instilled into one nostril during inspiration) or intratracheal administration (instilled via laryngoscope-assisted intubation, followed by injection of 200 µL air to push the solution)

  Dosing Frequency and Duration Model：

  Single dose

• Validation：

  The total cell count and neutrophil ratio in bronchoalveolar lavage fluid (BALF) were significantly increased, while the macrophage ratio was decreased; the total protein and albumin concentrations in BALF were also increased; lung tissue pathology showed inflammatory cell infiltration and an elevated inflammation score; respiratory mechanics testing showed an increase in quasi-static elastic resistance (Est) and a decrease in inspiratory volume-related parameters (A).

*Precautions： All mice were anesthetized and sacrificed 24 hours after modeling, and lung function tests, bronchoalveolar lavage, and separation of lung tissue and trachea were performed sequentially.

*References：Khadangi F,et,al. Intranasal versus intratracheal exposure to lipopolysaccharides in a murine model of acute respiratory distress syndrome. Sci Rep. 2021 Apr 8;11(1):7777.

• Modeling Mechanism：

  Lipopolysaccharides (LPS), when injected intra-articularly, activate the inflammatory response in synovial tissue, induce leukocyte infiltration and synovial edema; directly inhibit the synthesis of chondroitin proteoglycans, while stimulating proteoglycan degradation, leading to loss of cartilage matrix.

• Related Products：

  Lipopolysaccharides (T11855)

• Modeling Method：

  Experimental Subject：

  Hamster, Mesocricetus auratus, LAK.LVG (SYR), Female, Body weight 100–110 g, Single-caged with running wheel for 3 days of acclimatisation

  Dosage and Administration Route：

  0.1–100 μg/knee joint LPS , Dissolved in physiological saline (20 μL/knee), Intra-articular injection with 30-gauge needle

  Dosing Frequency and Duration Model：

  Single dose

• Validation：

  Exercise capacity: Daily running distance decreased in a dose-dependent manner (normal 9-14 km/day), recovering after 4 days in the 0.1 μg/knee group, while still significantly inhibiting it after 7 days in the 100 μg/knee group; Histology: Synovial edema, leukocyte infiltration, loss of chondroitin (decreased Safranin O staining intensity), femoral condyle cartilage erosion and empty chondrocyte lacunae appeared in the high-dose group; Biochemical indicators: Chondroitin synthesis was initially inhibited and then increased (inhibited by 55% on day 2, exceeding normal levels on day 6), plasma keratin sulfate increased rapidly after 18 hours and recovered rapidly, without a sustained correlation with cartilage damage.

*Precautions： The rats need to be adapted to being kept in captivity for one week (with a 10-14 hour light-dark cycle and free access to food and water).

*References：Otterness IG,et,al. Comparison of mobility changes with histological and biochemical changes during lipopolysaccharide-induced arthritis in the hamster. Am J Pathol. 1994 May;144(5):1098-108.