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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 mitigated CCl4-induced ROS. The cellular ROS in rat livers treated with CCl4 and/or liquiritigenin was stained with dihydroethidium followed by fluorescence microscopy or flow cytometry. ∗P < 0.05 compared to control rats; ∧P < 0.05 compared to CCl4 treated rats.
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fig4: Liquiritigenin mitigated CCl4-induced ROS. The cellular ROS in rat livers treated with CCl4 and/or liquiritigenin was stained with dihydroethidium followed by fluorescence microscopy or flow cytometry. ∗P < 0.05 compared to control rats; ∧P < 0.05 compared to CCl4 treated rats.

Mentions: Meantime, the reactive oxygen species level of hepatocytes from CCl4 treated rats was more than 8-fold higher than that of control rat hepatocytes. Liquiritigenin alone did not have effects on the ROS level of rat hepatocytes, but it reduced ROS levels by more than 53% compared to hepatocytes from rats exposed to CCl4 only (Figure 4).


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 mitigated CCl4-induced ROS. The cellular ROS in rat livers treated with CCl4 and/or liquiritigenin was stained with dihydroethidium followed by fluorescence microscopy or flow cytometry. ∗P < 0.05 compared to control rats; ∧P < 0.05 compared to CCl4 treated rats.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig4: Liquiritigenin mitigated CCl4-induced ROS. The cellular ROS in rat livers treated with CCl4 and/or liquiritigenin was stained with dihydroethidium followed by fluorescence microscopy or flow cytometry. ∗P < 0.05 compared to control rats; ∧P < 0.05 compared to CCl4 treated rats.
Mentions: Meantime, the reactive oxygen species level of hepatocytes from CCl4 treated rats was more than 8-fold higher than that of control rat hepatocytes. Liquiritigenin alone did not have effects on the ROS level of rat hepatocytes, but it reduced ROS levels by more than 53% compared to hepatocytes from rats exposed to CCl4 only (Figure 4).

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