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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

CCl4-illicited oxidative stress was effectively inhibited by liquiritigenin. The enzymatic activities of liver SOD (a) and GSH-Px (b) were analyzed with commercially available assay kits. (c) The mRNA levels of SOD2 and GPx in livers of CCl4 and/or liquiritigenin treated rats were assessed by quantitative real-time PCR. (d) The MDA (lipid peroxidation) level was analyzed using an assay kit. ∗P < 0.05 compared to control rats; ∧P < 0.05 compared to CCl4 treated rats.
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fig3: CCl4-illicited oxidative stress was effectively inhibited by liquiritigenin. The enzymatic activities of liver SOD (a) and GSH-Px (b) were analyzed with commercially available assay kits. (c) The mRNA levels of SOD2 and GPx in livers of CCl4 and/or liquiritigenin treated rats were assessed by quantitative real-time PCR. (d) The MDA (lipid peroxidation) level was analyzed using an assay kit. ∗P < 0.05 compared to control rats; ∧P < 0.05 compared to CCl4 treated rats.

Mentions: Chronic CCl4 exposure significantly decreased the activities of superoxide dismutase (Figure 3(a)) and glutathione peroxidase (Figure 3(b)) as well as their mRNA levels (Figure 3(c)) in rat liver. The SOD and GSH-Px activities in the livers of rats exposed to chronic CCl4 were reduced by 23.5% and 16.3% compared to control rats, respectively (Figures 3(a) and 3(b)). Liquiritigenin treatment abolished CCl4-induced reduction of SOD (Figure 3(a)) and GSH-Px (Figure 3(b)) activities and their expression levels (Figure 3(c)). The SOD activity of rat livers treated with both liquiritigenin and CCl4 recovered from 34.6 μmol/mg protein in CCl4-treated rats to 42.9 μmol/mg protein (P < 0.05), which was similar to that of control rats (45.2 μmol/mg protein) (Figure 3(a)). The activity of GSH-Px of liquiritigenin/CCl4 rat livers was 17.9% higher than that of CCl4 rat livers (P < 0.05, Figure 3(b)). The liver mRNA levels of SOD2 and GSH-Px of CCl4 treated rats were 57.3% and 65.8% of those of the control, which were improved to 97.1% and 102.3% of the control in rats that received liquiritigenin while being exposed to CCl4 (Figure 3(c)).


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)

CCl4-illicited oxidative stress was effectively inhibited by liquiritigenin. The enzymatic activities of liver SOD (a) and GSH-Px (b) were analyzed with commercially available assay kits. (c) The mRNA levels of SOD2 and GPx in livers of CCl4 and/or liquiritigenin treated rats were assessed by quantitative real-time PCR. (d) The MDA (lipid peroxidation) level was analyzed using an assay kit. ∗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

fig3: CCl4-illicited oxidative stress was effectively inhibited by liquiritigenin. The enzymatic activities of liver SOD (a) and GSH-Px (b) were analyzed with commercially available assay kits. (c) The mRNA levels of SOD2 and GPx in livers of CCl4 and/or liquiritigenin treated rats were assessed by quantitative real-time PCR. (d) The MDA (lipid peroxidation) level was analyzed using an assay kit. ∗P < 0.05 compared to control rats; ∧P < 0.05 compared to CCl4 treated rats.
Mentions: Chronic CCl4 exposure significantly decreased the activities of superoxide dismutase (Figure 3(a)) and glutathione peroxidase (Figure 3(b)) as well as their mRNA levels (Figure 3(c)) in rat liver. The SOD and GSH-Px activities in the livers of rats exposed to chronic CCl4 were reduced by 23.5% and 16.3% compared to control rats, respectively (Figures 3(a) and 3(b)). Liquiritigenin treatment abolished CCl4-induced reduction of SOD (Figure 3(a)) and GSH-Px (Figure 3(b)) activities and their expression levels (Figure 3(c)). The SOD activity of rat livers treated with both liquiritigenin and CCl4 recovered from 34.6 μmol/mg protein in CCl4-treated rats to 42.9 μmol/mg protein (P < 0.05), which was similar to that of control rats (45.2 μmol/mg protein) (Figure 3(a)). The activity of GSH-Px of liquiritigenin/CCl4 rat livers was 17.9% higher than that of CCl4 rat livers (P < 0.05, Figure 3(b)). The liver mRNA levels of SOD2 and GSH-Px of CCl4 treated rats were 57.3% and 65.8% of those of the control, which were improved to 97.1% and 102.3% of the control in rats that received liquiritigenin while being exposed to CCl4 (Figure 3(c)).

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