High mobility group box chromosomal protein 1 in acute-on-chronic liver failure patients and mice with ConA-induced acute liver injury

2012 ◽  
Vol 93 (2) ◽  
pp. 213-219 ◽  
Author(s):  
Rong-Rong Zhou ◽  
Hong-Bo Liu ◽  
Jian-Ping Peng ◽  
Yan Huang ◽  
Ning Li ◽  
...  
2019 ◽  
Vol 18 (3) ◽  
pp. 514-516
Author(s):  
Magdalena Arłukowicz-Grabowska ◽  
Maciej Wójcicki ◽  
Joanna Raszeja-Wyszomirska ◽  
Monika Szydłowska-Jakimiuk ◽  
Bernard Piotuch ◽  
...  

2013 ◽  
Vol 62 (7) ◽  
pp. 703-709 ◽  
Author(s):  
Xun Li ◽  
Li-Kun Wang ◽  
Lu-Wen Wang ◽  
Xiao-Qun Han ◽  
Fan Yang ◽  
...  

2014 ◽  
Vol 8 (4) ◽  
pp. 1178-1184 ◽  
Author(s):  
HENG XU ◽  
HONGXIA LI ◽  
YACHAO QU ◽  
JUNFU ZHENG ◽  
JUN LU

2020 ◽  
pp. 3089-3100
Author(s):  
Jane Macnaughtan ◽  
Rajiv Jalan

Liver failure occurs when loss of hepatic parenchymal function exceeds the capacity of hepatocytes to regenerate or repair liver injury. Acute liver failure is characterized by jaundice and prolongation of the prothrombin time in the context of recent acute liver injury, with hepatic encephalopathy occurring within 8 weeks of the first onset of liver disease. Acute-on-chronic liver failure is characterized by hepatic and/or extrahepatic organ failure in patients with cirrhosis associated with an identified or unidentified precipitating event. The commonest causes of acute liver failure are acute viral hepatitis and drugs. Acute-on-chronic liver failure is most commonly precipitated by infection, alcohol abuse, and superimposed viral infection. The main clinical manifestations are hepatic encephalopathy, coagulopathy, jaundice, renal dysfunction, and haemodynamic instability. Infection and systemic inflammation contribute to pathogenesis and critically contribute to prognosis. Specific therapy for the underlying liver disease is administered when available, but this is not possible for most causes of liver failure. Treatment is predominantly supportive, with particular emphasis on (1) correction or removal of precipitating factors; (2) if encephalopathy is present, using phosphate enemata, nonhydrolysed disaccharide laxatives, and/or rifaximin; (3) early detection and prompt treatment of complications such as hypoglycaemia, hypokalaemia, cerebral oedema, infection, and bleeding. The onset of organ failure should prompt discussion with a liver transplantation centre. The mortality of acute liver failure (without liver transplantation) is about 40%. Patients with acute liver failure who do not develop encephalopathy can be expected to recover completely. Those who recover from an episode of acute-on-chronic liver failure should be considered for liver transplantation because otherwise their subsequent mortality remains high.


2018 ◽  
Vol 113 (Supplement) ◽  
pp. S1350-S1351
Author(s):  
Majd Khasawneh ◽  
Zaid Imam ◽  
Fadi Odish ◽  
Mohamad Rasm Al Sibae

2020 ◽  
Author(s):  
Li Tang ◽  
Feixia Wang ◽  
Lingyan Xiao ◽  
Min Shen ◽  
Siwei Xia ◽  
...  

Abstract BackgroundAcute-on-chronic liver failure (ACLF) is a severe complication of cirrhosis, which seriously endanger human life and health. Yiqijianpi decoction (YQJPF) is a Traditional Chinese Medicine (TCM) formula that has been widely used in the treatment of liver failure with significant effect. The purpose of this study was to investigate the active components and mechanism to ameliorate acute on chronic liver failure(ACLF).MethodsLPS combined with D-Gal was used to establish the rat model of ACLF, pathological examination was detected by H&E staining, liver function test was assayed by ELISA. LPS was used to induce hepatocytes injury in vitro. Cell proliferation assay, TUNEL assay were used in human hepatic L02 cells. The active components and putative targets of YQJPF were predicted by network pharmacology approach and GEO analysis. Functional and pathway enrichment analysis were presented by using String, Cytoscape and Metascape. Further, experimental validation was done to verify the effect of YQJPF on PI3K/AKT-HIF-1ɑ and apoptosis-related signaling pathways by using Immunohistochemistry and Western blotting.ResultsAfter being treated with YQJPF, the rat liver injury and fibrosis were alleviated, and Cell Counting Kit-8 assay, TUNEL assay indicated YQJPF also inhibited the apoptosis in hepatic L02 cells. Through network pharmacologic analysis, 135 active components in YQJPF decoction, 573 known therapeutic targets and 2940 liver failure-related human genes were identified. 163 gene symbols maybe the key for liver failure treatment by YQJPF decoction. VEGF-A was hub gene in PPI network. The KEGG pathway and GO enrichment analyses indicated that the PI3K/AKT, HIF-1 signaling pathways were the prominently enriched signaling pathways. In vivo, YQJPF upregulated the expression of PI3K/AKT-HIF1-ɑ and VEGF-A. Moreover apoptosis pathway were verified by up-regulating Bcl2 expression and down-regulating Bax expression in vivo and in vitro.ConclusionYQJPF is beneficial for alleviating liver failure, may regulate hypoxic liver injury through PI3K/AKT-HIF1α dependent apoptosis pathway.


2013 ◽  
Vol 146 (3) ◽  
pp. 207-216 ◽  
Author(s):  
Tao Chen ◽  
Lin Zhu ◽  
Yaoyong Zhou ◽  
Bin Pi ◽  
Xiaojuan Liu ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document