| Description: |
Puerarin is a 5-HT2C receptor and benzodiazepine site antagonist, it exerts a regulatory effect on lipid accumulation by decreasing lipogenesis in hepatocytes, it may have therapeutic benefits in the treatment of fatty liver and lipid-related metabolic disorders, it also may act as an intracellular ROS scavenger, and its antioxidant properties may protect against Abeta25-35-induced cell injury,and apoptosis and could also promote the survival of PC12 cells. |
| Targets: |
PPAR | AMPK | IL Receptor | NOS | PI3K | Akt | ROS | Bcl-2/Bax | Beta Amyloid | P450 (e.g. CYP17) |
| In vitro: |
| Int J Mol Med. 2015 Mar;35(3):803-9. | | Puerarin ameliorates hepatic steatosis by activating the PPARα and AMPK signaling pathways in hepatocytes.[Pubmed: 25605057] | Non-alcoholic fatty liver disease (NAFLD) is characterized by the hepatic manifestation of metabolic syndrome and is the leading cause of chronic liver disease. Steatohepatitis plays a critical role in the process resulting in liver fibrosis and cirrhosis. Puerarin is a herbal product widely used in Asia, and is believed to have therapeutic benefits for alleviating the symptoms of steatohepatitis.
METHODS AND RESULTS:
The present study was designed to investigate the effects and mechanisms of action of puerarin in reducing lipid accumulation in oleic acid (OA)-treated HepG2 cells. Hepatocytes were treated with OA with or without puerarin to observe lipid accumulation by Oil Red O staining. We also examined hepatic lipid contents (e.g., triacylglycerol and cholesterol) following treatment with puerarin. Western blot analysis and reverse transcription-polymerase chain reaction (RT-PCR) were used to measure sterol regulatory element binding protein (SREBP)-1, fatty acid synthase (FAS), peroxisome proliferator-activated receptor α (PPARα) and adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) protein and mRNA expression, respectively. Our results revealed that puerarin suppressed OA-induced lipid accumulation, and reduced the triacylglycerol and cholesterol levels. Furthermore, puerarin decreased the expression levels of lipogenic enzymes, such as FAS and SREBPs, and increased the expression levels of PPARα, which are critical regulators of hepatic lipid metabolism through the AMPK signaling pathway. These results indicate that puerarin has the same ability to activate AMPK, and reduce SREBP-1 and FAS expression, thus inhibiting hepatic lipogenesis and increasing hepatic antioxidant activity.
CONCLUSIONS:
We found that puerarin exerted a regulatory effect on lipid accumulation by decreasing lipogenesis in hepatocytes. Therefore, puerarin extract may have therapeutic benefits in the treatment of fatty liver and lipid-related metabolic disorders.
| | 2016 Sep 28;64(38):7291-7. | | Protective Effects of Genistein and Puerarin against Chronic Alcohol-Induced Liver Injury in Mice via Antioxidant, Anti-inflammatory, and Anti-apoptotic Mechanisms[Pubmed: 27609057] | | This study aimed to investigate the protective effect of genistein or puerarin on chronic alcohol-induced liver injury in vivo and to explore the underlying mechanisms of hepatoprotective effects. Mice were administered genistein or puerarin (0.3 mmol kg(-1) body weight) and gastrically infused with 50% alcohol once per day for 5 weeks. Levels of serum transaminases, serum and hepatic lipids, hepatic antioxidant capacities, inflammation, apoptosis, and histopathological sections were analyzed. Results showed that genistein and puerarin exhibited similar effects in ameliorating alcohol-induced liver injury. However, genistein is more effective than puerarin in decreasing levels of malondialdehyde (1.05 ± 0.0947 vs 1.28 ± 0.213 nmol/mg pro, p < 0.05), tumor necrosis factor α (3.12 ± 0.498 vs 3.82 ± 0.277 pg/mg pro, p < 0.05), interleukin-6 (1.46 ± 0.223 vs 1.88 ± 0.309 pg/mg pro, p < 0.05), whereas puerarin is more effective than genistein in ameliorating serum activities or levels of alanine transaminase (35.8 ± 3.95 vs 42.6 ± 6.56 U/L, p < 0.05) and low-density lipoprotein cholesterol (1.12 ± 0.160 vs 1.55 ± 0.150 mmol/L, p < 0.05). In conclusion, both genistein and puerarin effectively alleviate hepatic damage induced by chronic alcohol administration through potential antioxidant, anti-inflammatory, or anti-apoptotic mechanisms. |
|
| In vivo: |
| Life Sci. 2006 Jun 20;79(4):324-30. | | Puerarin decreases serum total cholesterol and enhances thoracic aorta endothelial nitric oxide synthase expression in diet-induced hypercholesterolemic rats.[Pubmed: 16472823 ] | Hypercholesterolemia is a dominant risk factor for the development and progression of atherosclerosis and cardiovascular diseases. Natural compounds have been proved to be useful in lowering serum cholesterol to slow down the progression of cardiovascular diseases. Pueraria lobata is employed clinically to treat cardiovascular diseases in China.
METHODS AND RESULTS:
In the present study, the atheroscleroprotective potential of the herb's major active compound, puerarin, was investigated by monitoring serum lipid profile and major enzyme expressions on cholesterol homeostasis in Sprague-Dawley rats fed with control diet, hypercholesterolmic diet or hypercholesterolmic diet plus administration of puerarin (300 mg/kg/day, p.o.) for 4 weeks. Puerarin markedly attenuated the increased total cholesterol induced by hypercholesterolmic diet in both serum and liver. It caused a significant reduction in the atherogenic index. Expression of mRNA for hepatic 7alpha-hydroxylase (CYP7A1) was significantly enhanced but not for those of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR) and lanosterol 14alpha-demethylase (CYP51). To further explore the atheroscleroprotective potential of puerarin, acetylcholine induced endothelium-dependent vasorelaxation and endothelial nitric oxide synthase (eNOS) expression on isolated thoracic aortas were analyzed. Animals administered with puerarin suppressed the hypercholesterolemic diet induced impairment of eNOS expression, whereas there was no significant difference in the endothelium-dependent vasorelaxation among various groups of animals.
CONCLUSIONS:
These data indicated that puerarin reduced the atherogenic properties of dietary cholesterol in rats. Its hypocholesterolemic function may be due to the promotion of cholesterol and bile acids excretion in liver. Whether puerarin targets directly on cholesterol homeostasis or both cholesterol homeostasis and endothelial function remains to be determined. | | 2016 Sep 28;64(38):7291-7. | | Protective Effects of Genistein and Puerarin against Chronic Alcohol-Induced Liver Injury in Mice via Antioxidant, Anti-inflammatory, and Anti-apoptotic Mechanisms[Pubmed: 27609057] | | Abstract
This study aimed to investigate the protective effect of genistein or puerarin on chronic alcohol-induced liver injury in vivo and to explore the underlying mechanisms of hepatoprotective effects. Mice were administered genistein or puerarin (0.3 mmol kg(-1) body weight) and gastrically infused with 50% alcohol once per day for 5 weeks. Levels of serum transaminases, serum and hepatic lipids, hepatic antioxidant capacities, inflammation, apoptosis, and histopathological sections were analyzed. Results showed that genistein and puerarin exhibited similar effects in ameliorating alcohol-induced liver injury. However, genistein is more effective than puerarin in decreasing levels of malondialdehyde (1.05 ± 0.0947 vs 1.28 ± 0.213 nmol/mg pro, p < 0.05), tumor necrosis factor α (3.12 ± 0.498 vs 3.82 ± 0.277 pg/mg pro, p < 0.05), interleukin-6 (1.46 ± 0.223 vs 1.88 ± 0.309 pg/mg pro, p < 0.05), whereas puerarin is more effective than genistein in ameliorating serum activities or levels of alanine transaminase (35.8 ± 3.95 vs 42.6 ± 6.56 U/L, p < 0.05) and low-density lipoprotein cholesterol (1.12 ± 0.160 vs 1.55 ± 0.150 mmol/L, p < 0.05). In conclusion, both genistein and puerarin effectively alleviate hepatic damage induced by chronic alcohol administration through potential antioxidant, anti-inflammatory, or anti-apoptotic mechanisms.
Keywords: alcohol; inflammation; isoflavones; liver damage; oxidative stress. |
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