scholarly journals Lignans from Opuntia ficus-indica seeds protect rat primary hepatocytes and HepG2 cells against ethanol-induced oxidative stress

2016 ◽  
Vol 81 (1) ◽  
pp. 181-183 ◽  
Author(s):  
Jung Wha Kim ◽  
Heejung Yang ◽  
Hyeon Woo Kim ◽  
Hong Pyo Kim ◽  
Sang Hyun Sung
1997 ◽  
Vol 35 (12) ◽  
pp. 1159-1164 ◽  
Author(s):  
T.-H. Tseng ◽  
E.-S. Kao ◽  
C.-Y. Chu ◽  
F.-P. Chou ◽  
H.-W. Lin Wu ◽  
...  

Molecules ◽  
2020 ◽  
Vol 25 (20) ◽  
pp. 4849
Author(s):  
Acharya Balkrishna ◽  
Vivek Gohel ◽  
Rani Singh ◽  
Monali Joshi ◽  
Yash Varshney ◽  
...  

Steatosis is characterized by excessive triglycerides accumulation in liver cells. Recently, application of herbal formulations has gained importance in treating complex diseases. Therefore, this study explores the efficacy of tri-herbal medicine Divya Sarva-Kalp-Kwath (SKK; brand name, Livogrit) in treating free fatty acid (FFA)-induced steatosis in human liver (HepG2) cells and rat primary hepatocytes. Previously, we demonstrated that cytosafe SKK ameliorated CCl4-induced hepatotoxicity. In this study, we evaluated the role of SKK in reducing FFA-induced cell-death, and steatosis in HepG2 through analysis of cell viability, intracellular lipid and triglyceride accumulation, extracellular free glycerol levels, and mRNA expression changes. Plant metabolic components fingerprinting in SKK was performed via High Performance Thin Layer Chromatography (HPTLC). Treatment with SKK significantly reduced the loss of cell viability induced by 2 mM-FFA in a dose-dependent manner. SKK also reduced intracellular lipid, triglyceride accumulation, secreted AST levels, and increased extracellular free glycerol presence in the FFA-exposed cells. SKK normalized the FFA-stimulated overexpression of SREBP1c, FAS, C/EBPα, and CPT1A genes associated with the induction of steatosis. In addition, treatment of rat primary hepatocytes with FFA and SKK concurrently, reduced intracellular lipid accumulation. Thus, SKK showed efficacy in reducing intracellular triglyceride accumulation and increasing extracellular glycerol release, along with downregulation of related key genetic factors for FFA-associated steatosis.


2012 ◽  
Vol 261 (3) ◽  
pp. 280-291 ◽  
Author(s):  
Tao Xue ◽  
Peihua Luo ◽  
Hong Zhu ◽  
Yuqin Zhao ◽  
Honghai Wu ◽  
...  

2007 ◽  
Vol 468 (1) ◽  
pp. 44-48 ◽  
Author(s):  
Yoshinori Sugimoto ◽  
Yoshimitsu Naniwa ◽  
Takayuki Nakamura ◽  
Hirotsugu Kato ◽  
Masanori Yamamoto ◽  
...  

2019 ◽  
Vol 67 (4) ◽  
pp. 578-587
Author(s):  
Réka Fanni Barna ◽  
Judit Mercédesz Pomothy ◽  
Zsuzsanna Paréj ◽  
Erzsébet Pásztiné Gere

Sphingosine-1-phosphate (S1P) has been reported as a matriptase activator. The aim of this study was to reveal if S1P can influence hepcidin production. Furthermore, we investigated how S1P can affect the viability and the redox status of primary hepatocytes. Rat primary hepatocytes were cultivated for 72 h and were treated with 50, 200, 1000 ng/ml S1P. Cell-free supernatants were collected every 24 h. Cell viability was tested by a colorimetric method using tetrazolium compound (MTS). The hepcidin levels in the cell-free supernatants were examined with hepcidin sandwich ELISA to determine the effect of S1P on the hepcidin-modulating ability of matriptase. In order to estimate the extent of S1P-generated oxidative stress, extracellular H2O2 measurements were performed by the use of fluorescent dye. Based on the findings, S1P treatment did not cause cell death for 72 h at concentrations up to 1000 ng/ml. S1P did not influence the extracellular H2O2 production for 72 h. The hepcidin levels were significantly suppressed in hepatocytes exposed to S1P treatment. Further studies would be needed to explore the exact mechanism of action of S1P.


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