Nonalcoholic fatty liver disease (NAFLD) has gradually become one of the most serious liver diseases threatening human health in the world. Currently, Chinese herbal medicine is a potentially important treatment option for NAFLD, and the development of effective Chinese herbal medicine has a good prospect. Previous studies have suggested that Ficus hirta Vahl. (FV) has various protective effects on the liver. In this study, we investigated the therapeutic outcomes of FV treatment for the liver disease and its underlying mechanism using HepG2 cell lines induced by palmitate (PA) and mouse model fed with high‐fat diet (HFD). FV mainly exerts pharmacological effects by mediating lipid metabolism and inflammation. During the lipid metabolism regulation process, CD36, SREBP‐1, SCD1, PPAR γ, ACOX1, and CPT1α are the key factors related to the healing effects of FV on NAFLD. During the inflammation process, the downregulation of IL‐6, IL‐1β, and TNF‐α is involved in alleviation of NAFLD. Furthermore, CD36 overexpression promotes lipid abnormal metabolism and inflammation in PA‐induced HepG2 cells, while CD36 knockdown and FV supplementation reverse these responses. In addition, FV also modulates gut microbiota composition, such as Allobaculum, Faecalibaculum, and Butyricicoccus in HFD‐fed mice. In summary, our findings demonstrated that FV exerted a beneficial preventive and therapeutic effect on NAFLD by improving lipid metabolism and inflammation as well as regulating the structure of gut microbiota, and therefore, FV may be a candidate for the treatment of NAFLD.

Ficus hirta Vahl., a traditional Chinese medicine commonly used in the Lingnan region, has been extensively used for liver disease treatment in China. Its notable antioxidant and anti-inflammatory properties have been reported in previous studies. However, its potential effect and underlying mechanism on liver fibrosis remains unclear. This study was aimed to investigate the effect and its underlying mechanism of Ficus hirta Vahl on liver fibrosis in vitro and in vivo. The main components of Ficus hirta Vahl in blood were investigated by using UPLC-Q/TOF-MS/MS. Two animal models of liver fibrosis, the CCl₄ and MCD induced mice, were used to assess the efficacy of Ficus hirta Vahl on liver fibrosis. Metabolomics was used to detect the level of metabolites in the serum of liver fibrosis mice after Ficus hirta Vahl treatment. Furthermore, the mechanism was validated in vitro using the human liver stellate cell line LX-2. The binding affinities of the active ingredients of Ficus hirta Vahl to the main targets of liver fibrosis were also determined. Finally, we identified the key active ingredients responsible for the treatment of liver fibrosis in vivo. Fibrosis and inflammatory markers were significant down-regulation in both CCl₄ and MCD induced liver fibrosis mice after Ficus hirta Vahl administration in a dose-dependent manner. We found that Ficus hirta Vahl may primarily exert its effect on liver fibrosis through the glutathione metabolic pathway. Importantly, the glutathione metabolic pathway is closely associated with ferroptosis, and our subsequent in vitro experiments provided evidence supporting this association. Ficus hirta Vahl was found to modulate the GSH/GPX4 pathway, ultimately leading to the amelioration of liver fibrosis. Moreover, using serum pharmacochemistry and molecular docking, we successfully identified apigenin as a probable efficacious monomer for the management of liver fibrosis and subsequently validated its efficacy in mice with CCl₄-induced hepatic fibrosis. Ficus hirta Vahl triggered the ferroptosis of hepatic stellate cell by regulating the GSH/GPX4 pathway, thereby alleviating liver fibrosis in mice. Moreover, apigenin is a key compound in Ficus hirta Vahl responsible for the effective treatment of liver fibrosis.

Objective: Investigate the high risk factors contributed to voriconazole-induced liver injury and develop a predictive nomogram for voriconazole-induced liver injury risk, thereby optimizing the clinical medication safety. Methods: This observational study retrospectively analyzed the electronic health records of hospitalized patients who received voriconazole treatment or prophylaxis at a tertiary hospital. Patients who met the inclusion and exclusion criteria were enrolled between June 2020 and June 2024, and their general biological data were collected. The diagnosis and severity grading of voriconazole-associated liver injury were determined according to the diagnostic and treatment guidelines for drug-induced liver injury. Patients were categorized into liver injury and non-injury groups based on the results of post-treatment liver function tests. Associations between baseline characteristics and liver injury were analyzed using non-parametric and chi-squared tests. To avoid omitting potentially significant factors, variables demonstrating P ≤ 0.1 in univariate screening and retained through least absolute shrinkage and selection operator (LASSO) regression underwent multivariate logistic regression to identify independent predictors. The nomogram was developed and internally validated through receiver operating characteristic (ROC) analysis, calibration curves, and decision curve analysis (DCA). Results: Among the 1,964 patients screened, 1,196 were excluded, leaving 768 patients included in the statistical analysis. Liver injury occurred in 95 patients, resulting in an incidence rate of 12.4%. Multivariable logistic regression analysis demonstrated that total cholesterol (TC) (OR = 1.893, P < 0.01), concomitant use of glucocorticoids (OR = 1.861, P = 0.041), ezetimibe (OR = 7.453, P = 0.047), and caspofungin (OR = 2.485, P = 0.032). Patients with TC levels exceeding 4.485 mmol/L exhibited a significantly elevated risk of liver injury. ROC analysis revealed an area under the curve (AUC) of 0.728 (95% CI: 0.66–0.797), with a sensitivity of 0.661 and specificity of 0.722. Internal validation indicated good discrimination and calibration, with predicted probabilities closely aligned with actual outcomes. The decision curve analysis suggested a substantial net clinical benefit. These findings were subsequently validated in a test cohort. Conclusion: Concomitant use of ezetimibe, caspofungin, glucocorticoids, and TC levels exceeding 4.485 mmol/L are independent risk factors for voriconazole-induced liver injury. The developed nomogram model offers clinically meaningful predictions for drug-induced liver injury risk, facilitating the optimization of voriconazole therapy safety.

Background. Radix Fici Hirtae (RFH), known as Cantonese ginseng, is an alternative folk medicine that is widely used to treat various diseases in southern China. The aim of this study was to investigate the effect and metabolic mechanisms of pretreatment with RFH on the serum metabolic profiles of carbon tetrachloride (CCl₄) induced acute liver injury in mice. Methods. Mice fed with the water extract of RFH at a dose of 1.5g/kg and 0.75g/kg for consecutive 7 days, and then serum samples were taken for the metabolomic analysis. Furthermore, the bioinformatics and pathways analysis were measured. Results. The UHPLC-Orbitrap/MS based-metabolomic analysis identified 20 differential metabolic markers in serum of CCl₄-induced liver injury mice compared to that of the normal controls, which were mainly related to the metabolism of amino acids and fatty acids. Furthermore, most of these biomarkers contributing to CCl₄ induction were ameliorated by RFH, and the bioinformatics and pathways analysis revealed that therapeutic actions of RFH were mainly involved in the regulation of the oxidative stress responses and energy homeostasis. Conclusion. These findings provide potential metabolic mechanism for future study and allow for hypothesis generation about the hepatoprotective effects of Radix Fici Hirtae.

Genetic factors may have a significant influence on the likelihood of liver fibrosis in individuals with nonalcoholic fatty liver disease (NAFLD). The present study was conducted to explore how single-nucleotide polymorphism (SNP) impacts the development of fibrosis in those suffering from NAFLD. Utilizing the UK Biobank dataset, we conducted a nested case-control analysis among NAFLD participants, defining the case group as those with liver fibrosis and cirrhosis during follow-up. For our in vitro investigations, we employed the LX-2 human hepatic stellate cell line. Our procedures included cultivating these cells, employing SAMM50-rs2073080 plasmid techniques to enhance the expression of recently discovered SNPs, and conducting biochemical assays. To quantify gene expression, we used real-time PCR with fluorescence detection. The study analyzed data from 5467 participants (1094 cases and 4373 controls). Genome-wide association analysis identified nine significant loci, including the novel rs2073080 variant, strongly associated with NAFLD-associated hepatic fibrosis. In vitro TGF-β modeling revealed significant upregulation of α-SMA and COL1A1, confirming model effectiveness. Oxidative stress markers like elevated malondialdehyde (MDA) and reduced catalase (CAT) and superoxide dismutase (SOD) levels indicated liver damage in the TGF-β group. SAMM50-rs2073080 was upregulated in the NAFLD-associated fibrosis model. In vitro experiments on LX-2 cells showed that SAMM50-rs2073080 overexpression led to increased fibrosis, as indicated by higher cellular MDA levels and lower CAT and SOD levels, compared to the vector group. Our research highlights a significant association of SAMM50-rs2073080 with the progression of NAFLD to hepatic fibrosis, and the in vitro experiments further corroborated these findings.

AIMS: Patients with liver disease are more prone to thrombosis and bleeding events than healthy people. The decision to use anticoagulation in patients with pulmonary embolism and liver disease requires a cautious evaluation of the risks of bleeding and the benefits of anticoagulation. In order to make a recommendation for patient with fatty liver that developed pulmonary embolism, we reported this case. METHODS: In this paper, we reported a case of a patient with fatty liver that developed pulmonary embolism. The low molecular weight heparin sodium injection and different anticoagulants were evaluated for this patient.RESULTS: After evaluating the efficacy and safety of different anticoagulants in patients with pulmonary embolism and liver dysfunction, rivaroxaban is more suitable for this patient to be treated by sequential therapy. After three weeks of treatment with rivaroxaban, the patient’s blood routine test results were normal, and no side effect was found. CONCLUSIONS: For patients with pulmonary embolism and fatty liver, maybe NOAC is more suitable.