Zvast Biotechnology
via a single high-dose intragastric administration of 56° Chinese liquor
The ethanol-induced acute alcoholism model in rats is a SCI gold-standard standardized animal model based on single high-dose ethanol impact exposure to accurately simulate clinical acute alcoholism caused by binge drinking and one-time excessive alcohol intake. It focuses on the core pathological mechanisms of acute ethanol metabolic disturbance, oxidative stress outbreak, inflammatory cascade activation and multi-organ acute injury, and highly recapitulates acute hepatic lipid metabolism disorder, acute gastric mucosal congestion and erosion, systemic oxidative inflammatory damage and neurobehavioral abnormalities induced by clinical acute alcoholism. After rapid gastrointestinal absorption of high-concentration ethanol, the metabolic threshold of alcohol dehydrogenase is exceeded, resulting in instantaneous accumulation of a large amount of ethanol and toxic metabolite acetaldehyde in the body. It sharply consumes endogenous antioxidants such as SOD and GSH-Px, triggers massive ROS outbreak and abnormal accumulation of lipid peroxidation product MDA, and completely breaks the redox homeostasis of the body. Meanwhile, acute ethanol impact rapidly activates the NF-κB inflammatory signaling pathway, promotes the massive release of pro-inflammatory factors such as TNF-α, IL-6 and IL-1β, and induces systemic acute low-grade inflammatory infiltration in the liver, gastric mucosa and serum. In addition, ethanol rapidly penetrates the blood-brain barrier to inhibit central nervous system excitability, causing acute neurotoxic symptoms such as drowsiness, ataxia and decreased activity. SD rats have stable metabolic responses and high sensitivity to acute ethanol stimulation, with rapid modeling phenotype outbreak, typical pathological features and excellent intra-group uniformity without individual tolerance differences. It is an internationally recognized standard model for researching acute alcoholism pathogenesis, hangover-relieving and liver-protective drug screening, acute oxidative inflammatory injury intervention and acute alcoholic neurotoxicity, and is widely applicable to basic mechanism research and preclinical efficacy evaluation of first-aid drugs for alcohol intoxication.
Rats in the blank control group were mentally active, flexible in movement, sensitive in response and normal in posture. Six hours after administration, rats in the model group presented typical acute alcoholism signs: listlessness, drowsiness, significantly reduced activity, slow response, unsteady gait, ataxia and messy fur, and partial individuals showed curled static state. The behavioral phenotypes were extremely significantly different from those of the blank group, confirming the preliminary formation of the acute intoxication model.
The activities of serum liver function indexes ALT and AST in the model group were significantly increased, indicating that acute ethanol impact induced acute hepatocyte injury and cell membrane permeability damage. Meanwhile, serum TG and TC lipid levels were abnormally elevated, presenting characteristics of acute lipid metabolism disorder, which fully conforms to the biochemical characteristics of liver injury in clinical acute alcoholism and serves as the core quantitative criterion for successful modeling.
HE staining of liver tissues showed characteristics of acute alcoholic liver injury: mild hepatocyte edema, loose cytoplasm, a small number of fat vacuoles, slightly disordered hepatic cord arrangement and a small amount of inflammatory cell infiltration in the portal area. Gastric mucosal tissues showed mucosal congestion and edema, mild epithelial damage and slight inflammatory infiltration without deep mucosal necrosis, which accurately corresponds to the pathological phenotypes of transient acute liver and gastric injury caused by clinical acute alcohol intake with stable and typical modeling characteristics.
The contents of ROS and MDA in serum and liver tissues of the model group were significantly upregulated, while the activities of antioxidant enzymes SOD and GSH-Px were significantly decreased, presenting a typical acute oxidative stress outbreak state. The expression of core pro-inflammatory factors (TNF-α, IL-6, IL-1β) was greatly increased, forming an acute inflammatory cascade reaction, which fully conforms to the core mechanism of oxidative stress-inflammation interactive injury in acute ethanol intoxication and serves as the core academic criterion for successful model construction.
As a SCI-certified exclusive gold-standard model for acute ethanol intoxication, it adopts single high-concentration ethanol impact modeling to perfectly simulate the real intoxication course of human binge drinking and acute alcohol intake with a pure modeling mechanism and no complex intervention interference. It features an extremely short modeling cycle (completed within 6 hours), extremely simple operation, low cost and high timeliness. The intoxication phenotype breaks out rapidly with typical pathological injury, small data fluctuation and excellent reproducibility, and the intra-group consistency is far better than that of chronic alcohol models. It accurately focuses on the core mechanisms of acute oxidative stress outbreak, transient inflammatory activation and acute liver and gastric injury, and is specially suitable for rapid pharmacodynamic evaluation of hangover-relieving, liver-protective, acute antioxidant and acute anti-inflammatory drugs. With strong project innovation, short experimental cycle and highly recognized data, it is fully applicable for project declaration, rapid mechanism verification, master and doctoral theses and high-score SCI publication.
The ethanol-induced acute alcoholism model in rats is corely applied to the research of oxidative stress outbreak mechanism, transient inflammatory activation mechanism and acute liver and gastric injury pharmacological mechanism in acute alcoholism. It is specially used for rapid screening and evaluation of traditional Chinese medicine compounds, natural active ingredients, small chemical molecules and functional food preparations with effects of relieving hangover, protecting liver and stomach, anti-oxidation and inhibiting acute inflammation. It is widely used in the elucidation of acute alcoholism pathogenesis, target exploration of acute alcoholic visceral injury and rapid preclinical pharmacodynamic evaluation of hangover-relieving first-aid drugs, serving as an essential core standardized model in the fields of hangover pharmacology, acute toxicology and digestive emergency pharmacology.
We're here to help! Whether you have questions about our products, need support, or want to share feedback, we'd love to hear from you. Please reach out through any of the methods below, and our team will get back to you as soon as possible.
