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Application of specific excitation Mas receptor in prevention and treatment of acetaminophen-induced drug-induced liver injury

A drug-induced liver injury, acetaminophen technology, applied in the application of drug-induced liver injury, specifically stimulates the Mas receptor field, to achieve the effect of reducing inflammation and liver damage

Active Publication Date: 2022-08-02
SHANGHAI TONGJI HOSPITAL
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  • Abstract
  • Description
  • Claims
  • Application Information

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Problems solved by technology

There is no report about the application of the present invention to specifically stimulate Mas receptors in the prevention and treatment of acetaminophen-induced drug-induced liver injury

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  • Application of specific excitation Mas receptor in prevention and treatment of acetaminophen-induced drug-induced liver injury
  • Application of specific excitation Mas receptor in prevention and treatment of acetaminophen-induced drug-induced liver injury
  • Application of specific excitation Mas receptor in prevention and treatment of acetaminophen-induced drug-induced liver injury

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Embodiment 1

[0020] 1 Experimental animals and methods

[0021] 1.1a. Transgenic mice, mouse disease model construction and experimental grouping: ① Transgenic mouse Mas1 used - / - The genetic background of both (systemic Mas1 knockout) and WT mice was C57BL / 6. ②Disease model and experimental grouping: A mouse model of acute drug-induced liver injury was established by intraperitoneal injection of APAP (300 mg / kg).

[0022] b. Experimental design: ①Collect and separate serum samples, detect ALT by ELISA, and evaluate the degree of liver damage; ②Prepare paraffin sections of liver tissue, and perform HE staining and TUNEL staining to evaluate the damage degree of parenchymal cells in liver tissue; MPO and F4 / 80 Staining to evaluate the degree of infiltration of intrahepatic inflammation (neutrophils and macrophages); ③ Prepare frozen sections of liver tissue, and BODIPY and LAMP1 staining were used to label lipid droplets and lysosomes to evaluate the degree of autophagy; ④ Collect fresh li...

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Abstract

The invention relates to an application of a specific excitation Mas receptor in prevention and treatment of acetaminophen-induced drug-induced liver injury, APAP is injected into the intraperitoneal cavity of a Mas1 gene systemic knockout (Mas1- / -) mouse and the intraperitoneal cavity of a wild type (Wildtype, WT) mouse to construct a DILI in-vivo research model, and the result shows that compared with the WT mouse, the APAP and the Mas1- / -in of the same dose have the advantages that the DILI in-vivo research model is more obvious in effect; more serious liver cell injury and intrahepatic inflammatory response can be observed; and the Mas receptor is specifically activated before the WT mouse is subjected to APAP intervention, so that the liver injury caused by APAP can be obviously relieved, and the death rate of the mouse is reduced. It is proved that Mas receptor activation can induce lipid autophagy and fatty acid oxidation to play a protective role in APAP-induced DILI. Based on currently mastered in-vivo research data, the Mas receptor can be used as an intervention target with great potential for drug-induced liver injury.

Description

technical field [0001] The invention relates to the field of biotechnology, in particular, to the application of specifically stimulating Mas receptors in preventing and treating acetaminophen-induced drug-induced liver injury. Background technique [0002] Drug-induced liver injury (DILI) is the most common adverse drug reaction and an important obstacle that seriously affects the development and marketing of new drugs. APAP is one of the most widely used analgesic drugs in clinical practice, and it is also the first pathogenic drug that causes acute liver failure. APAP is currently the most extensively studied hepatotoxic drug due to the availability of mouse models that closely resemble human pathophysiology. The harmful metabolites produced by excessive APAP metabolism in the liver are the initiation link of APAP-induced liver injury, which can further induce mitochondrial damage through oxidative stress and eventually lead to hepatocyte death. In recent years, the rol...

Claims

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Application Information

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IPC IPC(8): A61K45/00A61K31/4178A61P1/16
CPCA61K45/00A61K31/4178A61P1/16
Inventor 杨长青李婧陈帅贾昊宇杨博
Owner SHANGHAI TONGJI HOSPITAL
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