In hepatic fibrosis, hepatic stellate cells (HSCs) are activated and change into myofibroblast-like cells which are characterized by increased proliferation and extracellular matrix (ECM) synthesis. In this study, we investigated the regulatory effects of hydrogen sulfide (H2S) on hepatic fibrosis. We detected the proliferation, cell cycle progression, apoptosis, intracellular reactive oxygen species (ROS) and free calcium levels in ferric nitrilotriacetate (Fe-NTA)-activated HSCs treated with sodium hydrogen sulphide (NaHS), an H2S-releasing molecule. We also evaluated the effects of NaHS on fibrosis and ECM synthesis in rats with hepatic fibrosis induced by carbon tetrachloride (CCl4). MTT assay revealed that NaHS (500 µmol/l) suppressed the Fe-NTA-induced proliferation of HSC-T6 cells in a dose-dependent manner. NaHS induced G1 phase cell cycle arrest and apoptosis in the Fe-NTA-treated HSC-T6 cells. Furthermore, in the Fe-NTA-treated HSC-T6 cells, NaHS reduced intracellular levels of ROS at 1, 3 and 6 h and reduced intracellular free calcium levels at 3 and 6 h. H2S administration attenuated hepatic fibrosis and collagen Ⅰ protein expression in the rats with CCl4-induced hepatic fibrosis. In conclusion, exogenous H2S inhibits proliferation and induces cell cycle arrest and apoptosis in activated HSCs and attenuates CCl4-induced hepatic fibrosis and ECM expression.

Rationale:Hepatic alveolar echinococcosis (HAE) is a potentially fatal and chronically progressive infestation that is caused by the multivesicular metacestode of Echinococcus multilocularis (EM). HAE behaves like a malignant tumor and has been referred to as “worm cancer.” The main treatment method for HAE is surgical resection.Patient concerns:We present a 41-year-old Tibetan alveolar echinococcosis (AE) patient with AE lesions invading the right liver lobe and retrohepatic inferior vena cava (RHIVC).Diagnoses:The patient was diagnosed with HAE based on results obtained from ultrasound examination, computed tomography, liver 3-dimensional reconstruction, serology tests, clinical presentation, and surgical exploration. The final pathology report confirmed the diagnosis as HAE.Interventions:A radical surgery that combined resection of the liver and RHIVC was performed successfully.Outcomes:The patient had an uneventful postoperative recovery and a good prognosis.Lessons:When lesions of the liver significantly violate the RHIVC, resecting the RHIVC without reconstruction may be considered if possible.

Background. To analyze the expression of vascular endothelial growth factor (VEGF) in hepatocellular carcinoma (HCC) and cognitive impairment, explore the relationship between the expression of VEGF family genes and prognosis of patients with HCC, and evaluate the predictive ability of VEGF in cognitive impairment using computerized methods. Methods. VEGF expression in liver cancer tissues and normal tissues was analyzed using bioinformatics methods. The Kaplan-Meier survival analysis method was also used to analyze the relationship between VEGF expression and the prognosis of patients with HCC. Furthermore, immune infiltration assessment and gene set enrichment analysis were performed. Meanwhile, the differential expression of VEGF family genes between patients with Alzheimer’s disease (AD) and healthy controls was also checked. Results. Based on The Cancer Genome Atlas (TCGA) database, the VEGF family genes (VEFGA, VEGFB, VEGFC, and VEGFD) were highly expressed in cancer tissues and were significantly associated with poor prognosis in HCC. In HCC, the VEGF family genes showed significant heterogeneity in their functional and immune infiltration characteristics. Finally, VEGF family genes were identified as prognostic biomarkers in AD and risk prediction markers in HCC. Conclusions. VEGF is highly expressed in patients with HCC and lowly expressed in patients with AD. VEGF has opposite opposing roles in the treatment of tumors and cognitive impairment.

Introduction Alveolar echinococcosis (AE) is a zoonotic disease caused by the parasitism of Echinococcus multilocularis larvae in the intermediate host or the final host. This study aims to identify and analyze the B-cell and T-cell (Th1, Th2 and Th17) epitopes of E. multilocularis antigen Emy162. Methods (1) The secondary structural characteristics of the Emy162 protein were predicted by bioinformatics software to further predict the potential T-and B-cell epitopes. (2) The dominant antigen epitopes were detected by ELISA through the reaction of patient serum with small B-cell antigen peptide and assessing the proliferation of splenic lymphocytes of mice immunized with Emy162. (3) The expression of cytokines in splenic lymphocytes of mice stimulated by small T-cell antigen peptides was detected by ELISA, ELISpot and flow cytometry to enable the identification of the T-cell epitopes. Results (1) The high-scored T-cell epitopes were located at positions E7-13, E36-41, E80-89, E87-96, E97-106 and E129-139, while B-cell epitopes were located at positions E7-13, E19-27, E28-36, E37-48, E78-83, E101-109, E112-121 and E129-139. (2) The three advanced antigen epitopes of Emy162 were E19-27, E112-121 and E129-139. (3) The four Th1 advanced antigen epitopes of Emy162 were E7-13, E36-41, E80-89 and E129-139. The three Th2 advanced antigen epitopes were E36-41, E87-96 and E97-106. The three Th17 advanced antigen epitopes were E36-41, E87-96 and E97-106. Conclusion (1) The Emy162 protein has advanced antigenicity and numerous potential epitopes. Six T-cell and eight B-cell dominant epitopes were revealed using bioinformatics methods. (2) There are three dominant B-cell epitopes, four dominant Th1 epitopes, three dominant Th2 epitopes, and three dominant Th17 epitopes in the Emy162 antigen.