Acute-on-chronic liver failure （ACLF） is a complex clinical syndrome， and early identification and accurate prognostic evaluation are of great importance for patient treatment and management. In recent years， with in-depth research on the pathogenesis of ACLF， multiple prognostic biomarkers have been proposed and used in clinical practice. This article systematically reviews the research advances in prognostic biomarkers for ACLF from the aspects of clinical predictive models， immunological biomarkers， metabolic biomarkers， genetic and epigenetic biomarkers， microbiome-related biomarkers， and emerging technologies such as artificial intelligence and multi-omics， and it also discusses the value and application prospects of these biomarkers in the prognostic evaluation of ACLF and proposes future research directions， in order to provide a scientific and comprehensive reference for clinicians， guide individualized treatment and management of ACLF patients， and finally improve the clinical outcomes of patients.

Hepatitis B virus（HBV）infection poses a significant global health burden，with chronic infection driving progression to cirrhosis，hepatic failure，and hepatocellular carcinoma（HCC）. Mounting evidence implicates immune dysfunction and microbiota dysbiosis as core drivers of disease progression across all HBV infection stages. Gut and tissue-specific microbiota alterations disrupt innate/adaptive immunity，fueling inflammation，immunosuppression，and tumor immune evasion in chronic and end-stage disease. This review synthesizes mechanisms of immune-microbiota interplay in HBV pathogenesis and explores their translational potential for diagnostics and targeted interventions，including microbiota modulation and microbial biomarker applications.

Hepatitis B virus（HBV）infection poses a significant global health burden，with chronic infection driving progression to cirrhosis，hepatic failure，and hepatocellular carcinoma（HCC）. Mounting evidence implicates immune dysfunction and microbiota dysbiosis as core drivers of disease progression across all HBV infection stages. Gut and tissue-specific microbiota alterations disrupt innate/adaptive immunity，fueling inflammation，immunosuppression，and tumor immune evasion in chronic and end-stage disease. This review synthesizes mechanisms of immune-microbiota interplay in HBV pathogenesis and explores their translational potential for diagnostics and targeted interventions，including microbiota modulation and microbial biomarker applications.

Objective:To study the preventive effect of Sanguisorba officinalis on renal fibrosis by observing the influence of San-guisorba officinalis tannins extract (STE) on the proliferation of human renal epithelia (HK-2) induced by transforming growth factor-β1 ( TGF-β1 ) . Methods:HK-2 cells were cultured in DMEM medium with high glucose containing 10% fetal bovine serum. The cul-tured cells were divided into 5 groups, including the blank control group, TGF-β1 group (5 ng· ml-1 TGF-β1), intervention group 1 (5 ng·ml-1 TGF-β1 +12. 5μg·ml-1 STE), intervention group 2 (5 ng·ml-1 TGF-β1 +25μg·ml-1 STE) and intervention group 3(5 ng·ml-1 TGF-β1 +50 μg·ml-1 STE). The changes of cell morphology were observed under an inverted microscope and the in-fluence of SET on the cell proliferation was detected by CCK8 assay. Results: TGF-β1 could significantly induce the proliferation of HK-2 and promote the cell fibrosis with significant difference when compared with the control group (P<0. 05). However, after trea-ted with STE, the cell proliferation was inhibited obviously (P<0. 05) and the cells morphology tended to be normal in a dose-depend-ent manner. Conclusion:STE can inhibit the proliferation of HK-2 and prevent renal fibrosis to some extent.