scholarly journals Protective Effects of Taraxacum officinale L. (Dandelion) Root Extract in Experimental Acute on Chronic Liver Failure

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 504
Author(s):  
Iulia Olimpia Pfingstgraf ◽  
Marian Taulescu ◽  
Raluca Maria Pop ◽  
Remus Orăsan ◽  
Laurian Vlase ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Failure ◽  
Tissue Injury ◽  
Taraxacum Officinale ◽  
Chronic Liver ◽  
Root Extract ◽  
Protective Effects ◽  
Stress Tests ◽  
Chronic Liver Failure

Background: Taraxacum officinale (TO) or dandelion has been frequently used to prevent or treat different liver diseases because of its rich composition in phytochemicals with demonstrated effect against hepatic injuries. This study aimed to investigate the possible preventing effect of ethanolic TO root extract (TOERE) on a rat experimental acute on chronic liver failure (ACLF) model. Methods: Chronic liver failure (CLF) was induced by human serum albumin, and ACLF was induced in CLF by D-galactosamine and lipopolysaccharide (D-Gal-LPS). Five groups (n = 5) of male Wistar rats (200–250 g) were used: ACLF, ACLF-silymarin (200 mg/kg b.w./day), three ACLF-TO administered in three doses (200 mg, 100 mg, 50 mg/kg b.w./day). Results: The in vivo results showed that treatment with TOERE administered in three chosen doses before ACLF induction reduced serum liver injury markers (AST, ALT, ALP, GGT, total bilirubin), renal tests (creatinine, urea), and oxidative stress tests (TOS, OSI, MDA, NO, 3NT). Histopathologically, TOERE diminished the level of liver tissue injury and 3NT immunoexpression. Conclusions: This paper indicated oxidative stress reduction as possible mechanisms for the hepatoprotective effect of TOERE in ACLF and provided evidence for the preventive treatment.

scholarly journals Hepatoprotective Effect of Yiqijianpi Formula (YQJPF) on Liver Failure Through Modulation of Hypoxic and Apoptosis Pathways

2020 ◽  
Author(s):  
Li Tang ◽  
Feixia Wang ◽  
Lingyan Xiao ◽  
Min Shen ◽  
Siwei Xia ◽  
...  
Keyword(s):  
Liver Injury ◽  
Liver Failure ◽  
Signaling Pathways ◽  
Tunel Assay ◽  
Chronic Liver ◽  
Active Components ◽  
Chronic Liver Failure ◽  
Apoptosis Pathway ◽  
L02 Cells

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.

scholarly journals Protective Effects of Rhodiola Crenulata Extract on Hypoxia-Induced Endothelial Damage via Regulation of AMPK and ERK Pathways

2018 ◽  
Vol 19 (8) ◽  
pp. 2286 ◽  
Author(s):  
Pi-Kai Chang ◽  
I-Chuan Yen ◽  
Wei-Cheng Tsai ◽  
Tsu-Chung Chang ◽  
Shih-Yu Lee
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Umbilical Vein ◽  
Hypoxic Exposure ◽  
No Production ◽  
Root Extract ◽  
Protective Effects ◽  
Rhodiola Crenulata

Rhodiola crenulata root extract (RCE) has been shown to possess protective activities against hypoxia both in vitro and in vivo. However, the effects of RCE on response to hypoxia in the endothelium remain unclear. In this study, we aimed to examine the effects of RCE in endothelial cells challenged with hypoxic exposure and to elucidate the underlying mechanisms. Human umbilical vein endothelial cells were pretreated with or without RCE and then exposed to hypoxia (1% O2) for 24 h. Cell viability, nitric oxide (NO) production, oxidative stress markers, as well as mechanistic readouts were studied. We found that hypoxia-induced cell death, impaired NO production, and oxidative stress. These responses were significantly attenuated by RCE treatment and were associated with the activation of AMP-activated kinase and extracellular signal-regulated kinase 1/2 signaling pathways. In summary, we showed that RCE protected endothelial cells from hypoxic insult and suggested that R. crenulata might be useful for the prevention of hypoxia-associated vascular dysfunction.

Monitoring oxidative stress in acute-on-chronic liver failure by advanced oxidation protein products

2011 ◽  
Vol 42 (2) ◽  
pp. 171-180 ◽  
Author(s):  
Hua Liu ◽  
Tao Han ◽  
Jie Tian ◽  
Zheng-Yan Zhu ◽  
Ying Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Failure ◽  
Advanced Oxidation ◽  
Chronic Liver ◽  
Chronic Liver Failure ◽  
Advanced Oxidation Protein Products

scholarly journals Systemic oxidative stress is implicated in the pathogenesis of brain edema in rats with chronic liver failure

2012 ◽  
Vol 52 (7) ◽  
pp. 1228-1235 ◽  
Author(s):  
Cristina R. Bosoi ◽  
Xiaoling Yang ◽  
Jimmy Huynh ◽  
Christian Parent-Robitaille ◽  
Wenlei Jiang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Failure ◽  
Brain Edema ◽  
Chronic Liver ◽  
Chronic Liver Failure ◽  
Systemic Oxidative Stress

573 ATTENUATION OF OXIDATIVE STRESS PROTECTS THE BRAIN IN RATS WITH “ACUTE-ON-CHRONIC” LIVER FAILURE

2013 ◽  
Vol 58 ◽  
pp. S235
Author(s):  
C.R. Bosoi ◽  
C. Bemeur ◽  
B. Nguyen ◽  
M. Tremblay ◽  
C.F. Rose
Keyword(s):  
Oxidative Stress ◽  
Liver Failure ◽  
Chronic Liver ◽  
Chronic Liver Failure ◽  
The Brain

scholarly journals M2-like macrophages exert hepatoprotection in acute-on-chronic liver failure through inhibiting necroptosis-S100A9-necroinflammation axis

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Li Bai ◽  
Ming Kong ◽  
Zhongping Duan ◽  
Shuang Liu ◽  
Sujun Zheng ◽  
...  
Keyword(s):  
Liver Failure ◽  
Macrophage Activation ◽  
Chronic Liver ◽  
Inflammasome Activation ◽  
M2 Macrophage ◽  
Chronic Liver Failure ◽  
Lps Challenge ◽  
S100a9 Expression

AbstractNecroptosis has emerged as a novel and crucial player in acute and chronic liver diseases. Necroptotic cells lead to the release of DAMPs including S100A9, followed by the development of necroinflammation. We previously have documented the beneficial hepatoprotection conferred by M2-like macrophages in acute-on-chronic liver failure (ACLF) in vitro and in vivo, namely, M2-like macrophages protect hepatocytes against apoptosis. Herein, we integrated necroptosis, S100A9, and necroinflammation into this hepatoprotection, and hypothesized M2-like macrophages exert a hepatoprotective effect through inhibiting necroptosis-S100A9-necroinflammation axis. To testify this hypothesis, control mice were pre-treated with necroptosis or S100A9 inhibitors followed by D-GalN/LPS challenge. The extent of liver injury and M1/M2 macrophage activation was assessed. Necroptosis signaling and S100A9 expression were analysed and compared in control and fibrotic mice with or without acute insult. To document the pivotal role of M2-like macrophages in necroptosis and S100A9 inhibition, loss-of-function and gain-of-function experiments were performed. In addition, necroinflammation and its dependence on necroptosis and S100A9 were analysed. Moreover, the inhibitory effects of M2-like macrophages on necroinflammation were investigated in vivo and in vitro. We found that: firstly, the inhibition of necroptosis signaling and S100A9 expression alleviated D-GalN/LPS-induced hepatic damage, which was accompanied by M2-like macrophage activation; secondly, fibrosis inhibited necroptosis signaling and S100A9 expression, which could be attributed to M2-like macrophage activation; thirdly, S100A9 may function as a downstream player of necroptosis signaling; fourthly, fibrosis suppressed necroptosis- and S100A9-dependent necroinflammation; and finally, M2-like macrophages inhibited NLRP3 inflammasome activation and resultant necroinflammation via IL-10. Therefore, M2-like macrophages exert a beneficial hepatoprotection by inhibiting necroptosis-S100A9-necroinflammation axis in ACLF. Our findings provide novel insight for treating ACLF patients by specially targeting this signaling axis.

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