STUDY ON THE EXPRESSION OF HMGB1 AND ITS RECEPTOR IN PATIENTS WITH ACLF

Objective: Acute-on-chronic liver failure (ACLF) is a complex group of acute-on-chronic liver failure caused by a variety of acute precipitating factors on the basis of chronic liver disease. Patients and methods: Select patients diagnosed with ACLF related to hepatitis B in our hospital from November 2018 to September 2019 as the experimental group, and select chronic hepatitis B patients and health examinations in the hospital who match the general condition of ACLF patients at the same time period Those are the experimental control group. On the 1st, 5th, and 10th days after hospitalization, 4ml of venous blood was drawn on an empty stomach in the morning of the confirmed patient, centrifuged at 3000r/min for 5min, and the serum was collected for testing of related indicators. If the specimen cannot be tested in time, the serum should be collected and stored in the refrigerator at -80 degrees C for later use. Biochemical index detection uses Siemens biochemical assembly line equipment to detect ALT, AST, TBIL, DBIL, creatinine, urea, glomerular filtration rate and other indicators after hospitalization; coagulation phase uses ACL TOP/TOP700 instrument PT, APTT, PTA, FIB, etc. Indicators, ELISA method was used to detect the expression levels of serum HMGB1, TLR4, RAGE in each group of patients. Results: In this study, it was found that the level of HMGB1 and its receptor TLR4 in the serum of ACLF patients was higher than that in patients with chronic hepatitis B and healthy subjects. After HMGB1 binds to its receptor, it stimulates the release of inflammatory factors and further stimulates the inflammatory response. HMGB1 may be in ACLF Play a key role in related systemic inflammation. The HMGB1/TLR pathway is the central link of chronic inflammatory response. Conclusions: ACLF is a multi-factor, multi-link, and multi-path evolution process. Its pathogenesis is still unclear. At present, there are two theories about the pathogenesis of ACLF. The first is that the immune system-related factors mediate damage, and the acute cause or pathogen is directly or directly or Indirectly activates immune cells and inflammatory cytokine pathways, leading to tissue damage.