ABSTRACT
@#Abstract: Objective To investigate the changes in expression of Toll-like receptor 3 (TLR3) and interferon-α (IFN-α) in patients with different clinical outcomes of hepatitis C virus (HCV) infection treated with direct-acting antiviral agents (DAAs), and to explore the relationship between the expression of TLR3 and IFN-α with the clinical outcomes of HCV infection. Methods A total of 149 HCV infected patients who received initial treatment were selected from Hainan General Hospital between September 2020 and August 2022. The patients were divided into two groups: chronic hepatitis C (CHC) group (n=129) and liver cirrhosis (LC) group (n=20). Additionally, 28 volunteers were selected as the control group during the same period. All patients with HCV infection were first treated with Sofosbuvir/Vipatavir tablets for 12 weeks. Blood samples were collected at 0, 4, 12, 24 and 48 weeks after treatment. Liver function indicators were detected by enzyme-linked immunosorbent assay (ELISA), while TLR3 mRNA were detected by real-time fluorescence quantitative polymerase chain reaction (qRCR), IFN-α was detected by Luminex multiplex cytokine assays. Measurement data subject to normal distribution were represented by x±s, and t test was used between groups. Compare differences between groups. Results TLR3 mRNA in CHC group was higher than that in LC group and control group at baseline (P<0.05). After 4 weeks of DAAs treatment, TLR3 mRNA in CHC and LC groups was significantly up-regulated (P<0.05). TLR3 mRNA in the CHC group was gradually down-regulated to the level of the control group at 12, 24, and 48 weeks. In addition, IFN-α expression gradually increased with prolonged treatment, while it decreased in the LC group. The liver inflammation indicators in both the CHC and LC groups partially recovered after treatment with DAAs. Conclusions TLR3 is involved in viral clearance and chronic inflammatory response. The expression difference of TLR3 in patients with different clinical outcomes of HCV infection after DAAs treatment may be related to the severity of the disease.
ABSTRACT
@#Abstract:Alcoholic liver disease (ALD) is one of the most common liver diseases in the world. Long-term alcoholism causes a series of pathological changes in the liver, which eventually leads to the occurrence of liver diseases with an increasing incidence. At present, significant progress has been made in the pathogenesis and pathological development of alcoholic liver disease, but the relevant mechanism of ALD has not been thoroughly studied. It is necessary to improve the existing animal model or establish a new, more comprehensive animal ALD model to simulate human ALD. Experimental animal models of ALD, especially rodents, are often used to simulate human ALD, and the ideal rodent ALD model can effectively simulate all aspects of alcohol in human liver. But so far, the commonly used animal models all have certain defects, and there is no complete animal model that can simulate human ALD. This paper reviewed the pathogenesis of ALD, related methods and influencing factors of ALD model, and provided a theoretical basis for relevant researchers to establish the ALD rodent model.