Thymoquinone attenuates liver fibrosis via PI3K and TLR4 signaling pathways in activated hepatic stellate cells

2013 ◽  
Vol 15 (2) ◽  
pp. 275-281 ◽  
Author(s):  
Ting Bai ◽  
Li-Hua Lian ◽  
Yan-Ling Wu ◽  
Ying Wan ◽  
Ji-Xing Nan
APOPTOSIS ◽  
2020 ◽  
Vol 25 (1-2) ◽  
pp. 105-119
Author(s):  
Rui Li ◽  
Zhao Li ◽  
Yanru Feng ◽  
Hao Yang ◽  
Qiuxiao Shi ◽  
...  

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Dan Li ◽  
Li He ◽  
Huizhuang Guo ◽  
Hanwei Chen ◽  
Hong Shan

1998 ◽  
Vol 33 (5) ◽  
pp. 751-754 ◽  
Author(s):  
Yoshinori Harada ◽  
Masaki Iwai ◽  
Masamichi Kakusui ◽  
Takahiro Mori ◽  
Kazunobu Tada ◽  
...  

2016 ◽  
Vol 150 (4) ◽  
pp. S1025
Author(s):  
Tianhao Zhou ◽  
Heather L. Francis ◽  
Ying Wan ◽  
Julie Venter ◽  
Nan Wu ◽  
...  

2017 ◽  
Vol 95 (2) ◽  
pp. 263-272 ◽  
Author(s):  
Palanivel Gajalakshmi ◽  
Syamantak Majumder ◽  
Cornelia S. Viebahn ◽  
Akila Swaminathan ◽  
George C. Yeoh ◽  
...  

Liver fibrosis is now well recognized as the causative factor for increased mortality from complications associated with liver pathologies. Activated hepatic stellate cells (HSCs) play a critical role in the progression of liver fibrosis. Therefore, targeting these activated HSCs to prevent and (or) treat liver disease is a worthwhile approach to explore. In the present in vitro study, we investigated the use of bipotential murine oval liver cells (BMOL) in regulating the functions of activated HSCs to prevent progression of liver fibrosis. We used a conditioned medium-based approach to study the effect of BMOL cells on activated HSC survival and function. Our data showed that BMOL cells block the contraction of activated HSCs by inducing apoptosis of these cells. We demonstrated that BMOL cells secrete soluble factors, such as interleukin-6 (IL-6), which induced apoptosis of activated HSCs. Using both pharmacological and molecular inhibitor approaches, we further identified that IL-6-mediated activation of NF-κB–iNOS–NO–ROS signaling in activated HSCs plays a critical role in BMOL-cell-mediated apoptosis of activated HSCs. Thus, the present study provides an alternative cell-based therapeutic approach to treat liver fibrosis.


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