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Liquiritigenin Protects Rats from Carbon Tetrachloride Induced Hepatic Injury through PGC-1α Pathway.

Zhang Y, He Y, Yu H, Ma F, Wu J, Zhang X - Evid Based Complement Alternat Med (2015)

Bottom Line: The lack of effective treatment for liver cirrhosis and hepatocellular carcinomas imposes serious challenges to the healthcare system.The results demonstrated that liquiritigenin is effective in protecting liver from injury or treating chronic liver diseases.The modulation of PGC-1α and its downstream genes might play a critical role in relieving CCl4-induced hepatic pathogenesis by liquiritigenin.

View Article: PubMed Central - PubMed

Affiliation: Key Laboratory of Molecular Biophysics of Ministry of Education, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, Hubei 430074, China ; School of Basic Medical Science, Jiujiang University, Jiujiang, Jianxi 332000, China.

ABSTRACT
The lack of effective treatment for liver cirrhosis and hepatocellular carcinomas imposes serious challenges to the healthcare system. Here, we investigated the efficacy and mechanism of liquiritigenin involved in preventing or retarding the progression of liver diseases in a rat model with chronic carbon tetrachloride (CCl4) exposure. Sprague Dawley rats were given CCl4 and lliquiritigenin alone or simultaneously for 8 weeks before liver was harvested to check histological changes by Hematoxylin and Eosin (H&E) staining, apoptosis by TUNEL assay, ROS by dihydroethidium staining, antioxidant enzyme activities and malondialdehyde using specific kits, and gene expression by quantitative real-time PCR and western blot. Chronic CCl4 exposure caused profound changes in liver histology with extensive hepatocyte death (necrosis and apoptosis), fat accumulation, and infiltration of inflammatory cells, accompanied by depressed activities of antioxidant enzymes, increased oxidative stress, elevated expression of inflammation and fibrotic genes, and downregulation of PGC-1α, ND1, and Bcl-x in rat liver. All these changes were abolished or alleviated by lliquiritigenin. The results demonstrated that liquiritigenin is effective in protecting liver from injury or treating chronic liver diseases. The modulation of PGC-1α and its downstream genes might play a critical role in relieving CCl4-induced hepatic pathogenesis by liquiritigenin.

No MeSH data available.


Related in: MedlinePlus

Liquiritigenin alleviated CCl4 caused the histological destruction of rat livers. Rats were treated with CCl4 and/or liquiritigenin for 8 weeks and liver sections were stained with Hematoxylin and Eosin. CCl4 treated rats had severe liver histological abnormity with widespread hepatocyte death, fatty accumulation, and immune cell infiltration, which was largely relieved by liquiritigenin.
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fig1: Liquiritigenin alleviated CCl4 caused the histological destruction of rat livers. Rats were treated with CCl4 and/or liquiritigenin for 8 weeks and liver sections were stained with Hematoxylin and Eosin. CCl4 treated rats had severe liver histological abnormity with widespread hepatocyte death, fatty accumulation, and immune cell infiltration, which was largely relieved by liquiritigenin.

Mentions: CCl4 treatment caused the loss of regular liver structure seen in control rat with widespread necrosis of hepatocytes, fatty accumulation, and significant lymphocytes infiltration. Liquiritigenin treatment significantly reduced the severity of CCl4-induced hepatic damages with much less necrosis of hepatocytes and few diffused fatty changes (Figure 1). Meanwhile, the number of apoptotic hepatocytes was markedly increased by CCl4 treatment, which was suppressed by liquiritigenin (Figure 2).


Liquiritigenin Protects Rats from Carbon Tetrachloride Induced Hepatic Injury through PGC-1α Pathway.

Zhang Y, He Y, Yu H, Ma F, Wu J, Zhang X - Evid Based Complement Alternat Med (2015)

Liquiritigenin alleviated CCl4 caused the histological destruction of rat livers. Rats were treated with CCl4 and/or liquiritigenin for 8 weeks and liver sections were stained with Hematoxylin and Eosin. CCl4 treated rats had severe liver histological abnormity with widespread hepatocyte death, fatty accumulation, and immune cell infiltration, which was largely relieved by liquiritigenin.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4496487&req=5

fig1: Liquiritigenin alleviated CCl4 caused the histological destruction of rat livers. Rats were treated with CCl4 and/or liquiritigenin for 8 weeks and liver sections were stained with Hematoxylin and Eosin. CCl4 treated rats had severe liver histological abnormity with widespread hepatocyte death, fatty accumulation, and immune cell infiltration, which was largely relieved by liquiritigenin.
Mentions: CCl4 treatment caused the loss of regular liver structure seen in control rat with widespread necrosis of hepatocytes, fatty accumulation, and significant lymphocytes infiltration. Liquiritigenin treatment significantly reduced the severity of CCl4-induced hepatic damages with much less necrosis of hepatocytes and few diffused fatty changes (Figure 1). Meanwhile, the number of apoptotic hepatocytes was markedly increased by CCl4 treatment, which was suppressed by liquiritigenin (Figure 2).

Bottom Line: The lack of effective treatment for liver cirrhosis and hepatocellular carcinomas imposes serious challenges to the healthcare system.The results demonstrated that liquiritigenin is effective in protecting liver from injury or treating chronic liver diseases.The modulation of PGC-1α and its downstream genes might play a critical role in relieving CCl4-induced hepatic pathogenesis by liquiritigenin.

View Article: PubMed Central - PubMed

Affiliation: Key Laboratory of Molecular Biophysics of Ministry of Education, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, Hubei 430074, China ; School of Basic Medical Science, Jiujiang University, Jiujiang, Jianxi 332000, China.

ABSTRACT
The lack of effective treatment for liver cirrhosis and hepatocellular carcinomas imposes serious challenges to the healthcare system. Here, we investigated the efficacy and mechanism of liquiritigenin involved in preventing or retarding the progression of liver diseases in a rat model with chronic carbon tetrachloride (CCl4) exposure. Sprague Dawley rats were given CCl4 and lliquiritigenin alone or simultaneously for 8 weeks before liver was harvested to check histological changes by Hematoxylin and Eosin (H&E) staining, apoptosis by TUNEL assay, ROS by dihydroethidium staining, antioxidant enzyme activities and malondialdehyde using specific kits, and gene expression by quantitative real-time PCR and western blot. Chronic CCl4 exposure caused profound changes in liver histology with extensive hepatocyte death (necrosis and apoptosis), fat accumulation, and infiltration of inflammatory cells, accompanied by depressed activities of antioxidant enzymes, increased oxidative stress, elevated expression of inflammation and fibrotic genes, and downregulation of PGC-1α, ND1, and Bcl-x in rat liver. All these changes were abolished or alleviated by lliquiritigenin. The results demonstrated that liquiritigenin is effective in protecting liver from injury or treating chronic liver diseases. The modulation of PGC-1α and its downstream genes might play a critical role in relieving CCl4-induced hepatic pathogenesis by liquiritigenin.

No MeSH data available.


Related in: MedlinePlus