Purified anthocyanins from Zea mays L. cob ameliorates chronic liver injury in mice via modulating of oxidative stress and apoptosis

2021 ◽  
Author(s):  
Hong‐Xin Cui ◽  
Yang Luo ◽  
Yue‐Yue Mao ◽  
Ke Yuan ◽  
Song‐Heng Jin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Zea Mays ◽  
Liver Injury ◽  
Zea Mays L ◽  
Chronic Liver ◽  
Chronic Liver Injury

Aspirin induces autophagy and alleviates liver fibrosis by reducing oxidative stress and inflammation in mice model of chronic liver injury

2020 ◽  
Vol 73 ◽  
pp. S527
Author(s):  
Adil Bhat ◽  
Sudrishti Chaudhary ◽  
Gaurav Yadav ◽  
Anupama Parasar ◽  
Chhagan Bihari ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Fibrosis ◽  
Liver Injury ◽  
Chronic Liver ◽  
Mice Model ◽  
Chronic Liver Injury

β-Sitosterol attenuates carbon tetrachloride–induced oxidative stress and chronic liver injury in rats

2020 ◽  
Vol 393 (6) ◽  
pp. 1067-1075 ◽  
Author(s):  
Ezhilarasan Devaraj ◽  
Anitha Roy ◽  
Geetha Royapuram Veeraragavan ◽  
Anitha Magesh ◽  
Aneymol Varikalam Sleeba ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Chronic Liver ◽  
Chronic Liver Injury

scholarly journals Naturally Occurring Nrf2 Activators: Potential in Treatment of Liver Injury

2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
Ravirajsinh N. Jadeja ◽  
Kapil K. Upadhyay ◽  
Ranjitsinh V. Devkar ◽  
Sandeep Khurana
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Antioxidant Response ◽  
Chronic Liver ◽  
Related Factor ◽  
Chronic Liver Injury ◽  
Potential Therapeutic Target ◽  
Naturally Occurring ◽  
Liver Injuries ◽  
Nrf2 Signaling Pathway

Oxidative stress plays a major role in acute and chronic liver injury. In hepatocytes, oxidative stress frequently triggers antioxidant response by activating nuclear erythroid 2-related factor 2 (Nrf2), a transcription factor, which upregulates various cytoprotective genes. Thus, Nrf2 is considered a potential therapeutic target to halt liver injury. Several studies indicate that activation of Nrf2 signaling pathway ameliorates liver injury. The hepatoprotective potential of naturally occurring compounds has been investigated in various models of liver injuries. In this review, we comprehensively appraise various phytochemicals that have been assessed for their potential to halt acute and chronic liver injury by enhancing the activation of Nrf2 and have the potential for use in humans.

Ductular reactions provide a structural biliary network to preserve bile drainage in the CDE-model of hepatocellular chronic liver injury

2017 ◽  
Vol 66 (1) ◽  
pp. S6
Author(s):  
L.-A. Clerbaux ◽  
R. Manco ◽  
N. Van Hul ◽  
R. Español-Suñer ◽  
C. Bouzin ◽  
...  
Keyword(s):  
Liver Injury ◽  
Chronic Liver ◽  
Chronic Liver Injury ◽  
Bile Drainage

Gab1 in livers with persistent hepatocyte apoptosis has an antiapoptotic effect and reduces chronic liver injury, fibrosis and tumorigenesis

2021 ◽  
Author(s):  
Tetsuo Takehara ◽  
Naoki Mizutani ◽  
Hayato Hikita ◽  
Yoshinobu Saito ◽  
Yuta Myojin ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Liver Injury ◽  
Cell Viability ◽  
Liver Regeneration ◽  
Adaptor Protein ◽  
Chronic Liver ◽  
Hepatocyte Apoptosis ◽  
Chronic Liver Injury ◽  
The Impact

Grb2-associated binder 1 (Gab1) is an adaptor protein that is important for intracellular signal transduction by receptor tyrosine kinases that are receptors for various growth factors and plays an important role in rapid liver regeneration after partial hepatectomy and during acute hepatitis. On the other hand, mild liver regeneration is induced in livers of individuals with chronic hepatitis, where hepatocyte apoptosis is persistent; however, the impact of Gab1 on such livers remains unclear. We examined the role of Gab1 in chronic hepatitis. Gab1 knockdown enhanced the decrease in cell viability and apoptosis induced by ABT-737, a Bcl-2/-xL/-w inhibitor, in BNL.CL2 cells, while cell viability and caspase activity were unchanged in the absence of ABT-737. ABT-737 treatment induced Gab1 cleavage to form p35-Gab1. p35-Gab1 was also detected in the livers of mice with hepatocyte-specific Mcl-1 knockout (KO), which causes persistent hepatocyte apoptosis. Gab1 deficiency exacerbated hepatocyte apoptosis in Mcl-1 KO mice with posttranscriptional downregulation of Bcl-XL. In BNL.CL2 cells treated with ABT-737, Gab1 knockdown posttranscriptionally suppressed Bcl-xL expression, and p35-Gab1 overexpression enhanced Bcl-xL expression. Gab1 deficiency in Mcl-1 KO mice activated STAT3 signaling in hepatocytes, increased hepatocyte proliferation, and increased the incidence of liver cancer with the exacerbation of liver fibrosis. In conclusion, Gab1 is cleaved in the presence of apoptotic stimuli and forms p35-Gab1 in hepatocytes. In chronic liver injury, the role of Gab1 in suppressing apoptosis and reducing liver damage, fibrosis, and tumorigenesis is more important than its role in liver regeneration.

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