scholarly journals Protective effects of hydrogen sulfide on oxidative stress and fibrosis in hepatic stellate cells

2012 ◽  
Vol 7 (1) ◽  
pp. 247-253 ◽  
Author(s):  
HAI-NING FAN ◽  
HAI-JIU WANG ◽  
CAI-RANG YANG-DAN ◽  
LI REN ◽  
CONG WANG ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Sulfide ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Protective Effects

scholarly journals Diallyl Trisulfide Suppresses Oxidative Stress-Induced Activation of Hepatic Stellate Cells through Production of Hydrogen Sulfide

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Feng Zhang ◽  
Huanhuan Jin ◽  
Li Wu ◽  
Jiangjuan Shao ◽  
Xiaojing Zhu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Sulfide ◽  
Hepatic Stellate Cells ◽  
Lipid Peroxide ◽  
Stellate Cells ◽  
Cyclin B1 ◽  
Diallyl Trisulfide ◽  
Fibrotic Liver ◽  
Production Of Hydrogen ◽  
And Oxidative Stress

Accumulating data reveal that garlic has beneficial effects against chronic liver disease. We previously reported that diallyl trisulfide (DATS), the primary organosulfur compound in garlic, reduced fibrosis and attenuated oxidative stress in rat fibrotic liver. The present study was aimed at elucidating the underlying mechanisms. The primary rat hepatic stellate cells (HSCs) were cultured and stimulated with hydrogen peroxide (H2O2) for inducing HSC activation under oxidative stress. We examined the effects of DATS on the profibrogenic properties and oxidative stress in H2O2-treated HSCs. The results showed that DATS suppressed and reduced fibrotic marker expression in HSCs. DATS arrested cell cycle at G2/M checkpoint associated with downregulating cyclin B1 and cyclin-dependent kinase 1, induced caspase-dependent apoptosis, and reduced migration in HSCs. Moreover, intracellular levels of reactive oxygen species and lipid peroxide were decreased by DATS, but intracellular levels of glutathione were increased in HSCs. Furthermore, DATS significantly elevated hydrogen sulfide (H2S) levels within HSCs, but iodoacetamide (IAM) reduced H2S levels and significantly abrogated DATS production of H2S within HSCs. IAM also abolished all the inhibitory effects of DATS on the profibrogenic properties and oxidative stress in HSCs. Altogether, we demonstrated an H2S-associated mechanism underlying DATS inhibition of profibrogenic properties and alleviation of oxidative stress in HSCs. Modulation of H2S production may represent a therapeutic remedy for liver fibrosis.

scholarly journals Oxidative stress effect on the activation of hepatic stellate cells

2001 ◽  
Vol 42 (1) ◽  
pp. 1 ◽  
Author(s):  
Kwan Sik Lee ◽  
Se Joon Lee ◽  
Hyo Jin Park ◽  
Jun Pyo Chung ◽  
Kwang Hyub Han ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Stress Effect

scholarly journals Role of mitophagy regulation by ROS in hepatic stellate cells during acute liver failure

2018 ◽  
Vol 315 (3) ◽  
pp. G374-G384 ◽  
Author(s):  
Zhen Tian ◽  
Yi Chen ◽  
Naijuan Yao ◽  
Chunhua Hu ◽  
Yuchao Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Liver Failure ◽  
Acute Liver Failure ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Oxygen Species ◽  
End Stage Liver Disease ◽  
End Stage

Liver sinusoids serve as the first line of defense against extrahepatic stimuli from the intestinal tract. Hepatic stellate cells (HSCs) are pericytes residing in the perisinusoidal space that integrate cytokine-mediated inflammatory responses in the sinusoids and relay these signals to the liver parenchyma. Oxidative stress has been shown to promote inflammation during acute liver failure (ALF). Whether and how oxidative stress is involved in HSC inflammation during ALF remains unclear. Level of systemic oxidative stress is reflected by superoxide dismutase (SOD). Thus, ALF patients were recruited to investigate the correlation between plasma SOD levels and clinical features. Liver tissues were collected from chronic hepatitis patients by biopsy and from ALF patients who had undergone liver transplantation. SOD2 expression and HSCs activation were investigated by immunohistochemistry. Inflammation, mitophagy, and apoptosis were investigated by immunoblot analysis and flow cytometry in HSCs treated with lipopolysaccharide (LPS) and reactive oxygen species (ROS) donors. The plasma SOD level was significantly increased in patients with ALF compared with those with cirrhosis (444.4 ± 23.58 vs. 170.07 ± 3.52 U/ml, P < 0.01) and was positively correlated with the Model for End-Stage Liver Disease-Na score ( R2 = 0.4720, P < 0.01). In vivo observations revealed that SOD2 immunostaining was increased in ALF patients and mice models, and in vitro experiments demonstrated that LPS/ROS promoted inflammation via inhibiting mitophagy. Moreover, the regulation of inflammation was apoptosis independent in HSCs. LPS-induced increases in oxidative stress promote inflammation through inhibiting mitophagy in HSCs during the process of ALF, providing a novel strategy for the treatment of patients with ALF. NEW & NOTEWORTHY Here we demonstrate that the serum superoxide dismutase (SOD) level is significantly increased in patients with acute liver failure (ALF), and, correlated with the Model for End-Stage Liver Disease-Na score, SOD level dropped in the remission stage of ALF. We identify that, in liver tissue from ALF patients and mice models, manganese-dependent SOD was overexpressed, and show lipopolysaccharide/H2O2 inhibits mitophagy via reactive oxygen species in hepatic stellate cells (HSCs). We show that inhibited mitophagy promotes inflammation in HSCs, whereas mitophagy inducer rescues HSCs from lipopolysaccharide-induced inflammation.

The Na+/H+ exchanger modulates the fibrogenic effect of oxidative stress in rat hepatic stellate cells

1999 ◽  
Vol 30 (5) ◽  
pp. 868-875 ◽  
Author(s):  
Gianluca Svegliati-Baroni ◽  
Antonio Di Sario ◽  
Alessandro Casini ◽  
Gianna Ferretti ◽  
Letizia D'Ambrosio ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatic Stellate Cells ◽  
Stellate Cells
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