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BACKGROUND The fibrosis virus, which is common among people's health worldwide, is a major disease that threatens people's wellbeing. Hypothesis/purpose In the process of liver fibrosis and the relationship between Cav-1 and ferroptosis, it is interesting to investigate the regulatory mechanism of isoliquigitin. Using several ROS probes to quickly determine ROS content and distribution in live zebrafish and cells. To demonstrate the crucial role of Cav-1 in vitro, Lentivirus and siRNA-mediated transfection methods were used for the production of Cav-1 overexpression and knockdown cell lines. Results We first explained that ISL fibrosis by inducing hepatic stellate cells ferroptosis by reducing GPX4 expression and increasing the number of TFR and DMT1, thus generating a large number of ROS, but we also found that Cav-1 exacerbated its anti-hepatic fibrosis by promoting HSCs ferroptosis. Conclusion The results have shown that Cav-1-mediated HSCs ferroptosis is required for ISL to have an anti-fibrotic effect in vitro and in vivo.
Source link: https://europepmc.org/article/MED/35489326
Boys with Barth syndrome have a lean phenotype. Body weight, liver fat, and fat pad weights were determined after the animals were on a high fat diet for eight weeks. In comparison to the control or the single tafazzin knockout mice, the liver- and beta cell-specific double tafazzin knockout mice had a reduced rate of weight gain by 8 weeks. In addition, the liver, the gonadal, inguinal, and perirenal white adipose tissue, and the brown adipose tissue were all reduced in tissues known to accumulate fat, including the liver, the gonadal, inguinal and perirenal white adipose tissue and the brown adipose tissue at 8 weeks. Male mice are thus shielded from high fat diet-induced weight gain and fat accumulation, as shown by liver- and pancreatic beta cell-specific double tafazzin. These findings may help explain why some Barth Syndrome boys have a lean phenotype.
Source link: https://europepmc.org/article/PPR/PPR484752
In an animal model of thioacetamide, this study sought to investigate the effect of EE on liver fibrosis. In C57BL6J mice, Intraperitoneal administration of TAA was carried out twice a week for four weeks. Tissue-resident NK cells from mice livers were tested for activating receptors and cytotoxicity. The TAA-induced liver injury caused attenuation in the histopathology result after EE treatment compared to vehicle-treated mice. In addition, EE-treated mice resulted in lower serum ALT, AST, and ALP levels, which were related to a decrease in IL-20, TGF-, IL-22, and MCP-1 concentrations. The TAA-mice's EE regimentie maintained GSH, GPX, and CAT liver antioxidant production, as well as elevated numbers of tissue-resident NK cells. In an in vitro assay, trNK revealed an increase in CD107a and IFN-- with improved potentials to kill activated hepatic-stellate cells. This plant extract could be a targeted therapy for patients with advanced liver disease.
Source link: https://europepmc.org/article/MED/35429743
Liver fibrosis and its end-stage disease cirrhosis are two common global health problems resulting from persistent liver injury. HSC apoptosis and cell death have sparked new concerns in recent years. In the new analysis, we investigated the effects of cholesterol and bile acids on HSC apoptosis and liver fibrosis. Female Mdr2 mice were also treated with ND with ND and without 1% cholesterol. The effect of cholesterol on liver fibrosis and HSC clearance was investigated. In a model of non-alcoholic steatohepatitis, cholesterol may cause HSC lipid peroxidation and death in the liver. These findings show that cholesterol may be a cause of HSC lipid peroxidation and death in the liver. A high cholesterol-to-bile acid ratio can determine the course of the liver disease's path toward fibrosis relief.
Source link: https://europepmc.org/article/MED/35326188
The deletion of the Hhex gene can cause the liver and polycystic liver disease, which can be characterized by its timing. The present study was conducted to determine the role of the Hhex gene in not only causing cascades to cyst and abnormal bile duct formation, but also the liver progenitor role in cystic formation. The growth of bile ducts and cysts of cKO livers was higher than that of wild-type livers, according to Ki67 immunohistochemistry, which was also elevated. Compared to placebo veins of cKO livers or bile ductule cells around portal veins of cKO livers with fewer liver progenitor cells or bile ductule cells than in wild-type livers. Several liver-enriched transcription factors, including Foxa1 and Foxa2, were heterogeneously expressed in bile ducts and cysts of cKO livers, whereas expression in wild-type bile ducts was relatively homogeneous. Cystic cysts may develop in liver progenitor cells. Hhex cKO mice may be a good animal model for hepatic cystic disease.
Source link: https://europepmc.org/article/MED/35248949
Hepatic Stem/progenitor cells have piqued a lot of attention in treating acute liver disease. Both CD49f + and Sca-1 + cells were found to have clonogenic activity and clonogenic activity, according to colony-forming experiments and cell cycle studies. CD49f + cells were detected ALB and CK-19, while Sca-1 + cells were limited to ALB and cholangiocyte, indicating that CD49f + cells were bipotent and capable of differentiated into hepatocyte and cholangiocyte. As a result, PAS stain demonstrated that differentiated CD49f+ and Sca-1+ cells synthesised glycogen, indicating that they could be distinguished into functional hepatocytes. Both CD49f + and Sca-1 + cells, as well as liver progenitor function, such as Sox9 and EpCam, were found to have differing expression of genes associated with liver progenitor function, according to a mRNA expression report. In summary, we hypothesized that CD49f + cells were a form of HSPCs and could be used for clinical stem cell therapy.
Source link: https://europepmc.org/article/MED/35166962
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