PMID: 

Phytother Res. 2012 Aug ;26(8):1133-41. Epub 2011 Dec 14. PMID: 22170854

Abstract Title: 

Liquiritigenin inhibits serum-induced HIF-1α and VEGF expression via the AKT/mTOR-p70S6K signalling pathway in HeLa cells.

Abstract: 

Liquiritigenin (LQ) is a non-toxic dietary flavonoid with chemopreventive and anticancer properties. However, the mechanism of its antiangiogenesis remains unclear. Hypoxia-inducible factor-1α (HIF-1α) and its downstream target, vascular endothelial growth factor (VEGF), play a critical role in tumour angiogenesis and represent an attractive chemotherapeutic target. In this study, we investigated the effect of LQ on the molecular mechanism of angiogenesis. We found that LQ inhibited VEGF expression at both mRNA and protein levels. Liquiritigenin did not affect HIF-1α expression at the mRNA level, but it dramatically inhibited both serum- and mimicked hypoxic-induced HIF-1α protein accumulation in HeLa cells. Furthermore, we showed that LQ inhibited serum-induced expression ofHIF-1α by reducing its stability and decreased the synthesis in a dose-dependent manner. Mechanistically, we demonstrated that LQ inhibited HIF-1α and VEGF expression involved in blocking the protein kinase B (PKB/Akt) signalling pathway, and the mechanisms correlated with dephosphorylation of themammalian target of rapamycin (mTOR) and its effector ribosomal protein S6 kinase (p70S6K). In addition, LQ inhibited VEGF-induced formation of capillary-like structures in human umbilical vein endothelial cells (HUVEC). Taken together, our study provided valuable insights into the mechanism of antiangiogenic effect of LQ.

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PMID: 

Nutr Cancer. 2012 ;64(4):627-34. Epub 2012 Apr 20. PMID: 22519916

Abstract Title: 

Inhibitory effect of liquiritigenin on migration via downregulation proMMP-2 and PI3K/Akt signaling pathway in human lung adenocarcinoma A549 cells.

Abstract: 

Liquiritigenin (LQ) is a flavanone extracted from Glycyrrhizae, which has multiple biological effects, such as antiinflammation and anticancer. This study is the first to investigate the effect of LQ on the migration of human lung adenocarcinoma A549 cells in vitro. First, LQ exhibited inhibitory effects on the adhesion and migration of A549 cells in the absence of cytotoxicity. Gelatin zymography and Western blot analysis showed that LQ significantly reduced the expression of promatrix metalloproteinase-2 (proMMP-2) in A549 cells in terms of both activity and protein level. Second, LQ inhibited the phosphorylation of Akt and activated the phosphorylation of extracellular signal-regulated kinase 1 and 2 (ERK1/2). Furthermore, the treatment of inhibitors specific for Akt (LY294002) and ERK1/2 (U0126) to A549 cells resulted in reduced activity of proMMP-2. These results suggested that the inhibition on proMMP-2 expression by LQ may be through suppression on PI3K/Akt signaling pathway, which in turn led to the inhibition of lung adenocarcinoma A549 cells migration. However, activation of ERK might not be involved in the regulation of proMMP-2. Taken together, LQ may be considered as a potential interfering agent of cancer progression.

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PMID: 

Molecules. 2012 Jun 12 ;17(6):7206-16. Epub 2012 Jun 12. PMID: 22692244

Abstract Title: 

Liquiritigenin inhibits tumor growth and vascularization in a mouse model of HeLa cells.

Abstract: 

Angiogenesis is one of the crucial steps in the transition of a tumor from a small, harmless cluster of mutated cells to a large, malignant growth, capable of spreading to other organs throughout the body. Vascular endothelial growth factor (VEGF) that stimulates vasculogenesis and angiogenesis is thought to be as an anti-angiogenic target for cancer therapy. Liquiritigenin (LQ), a flavanone existing in Radix glycyrrhiza, shows extensive biological activities, such as anti-inflammatory and anti-cancer properties. In our studies, liquiritigenin effectively inhibited the growth of tumors xenografted in nude mice from human cervical cancer cell line HeLa cells, and microvascular density (MVD) of the tumor exposed to liquiritigenin was reduced in a dose dependent manner, especially in the high dose group. Moreover, the expression and secretion of VEGF were down-regulated by the drug in vivo and in vitro. Therefore, liquiritigenin can be further studied on cancer and other diseases associated with VEGF up-regulation.

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PMID: 

Chem Biol Interact. 2006 Jun 10 ;161(2):125-38. Epub 2006 Mar 27. PMID: 16647697

Abstract Title: 

Liquiritigenin, an aglycone of liquiritin in Glycyrrhizae radix, prevents acute liver injuries in rats induced by acetaminophen with or without buthionine sulfoximine.

Abstract: 

Glycyrrhizae radix has been used as one of the oldest and most frequently employed botanicals in both western and oriental countries. Previously, we showed that liquiritigenin (LQ), an aglycone of liquiritin in G. radix, exerts cytoprotective effects against heavy metal-induced toxicity in vitro. This study investigated in vivo protective effects of LQ against acute liver injuries induced by acetaminophen (APAP) or APAP plus buthionine sulfoximine (BSO). Liver injuries were assessed by blood biochemistry and histopathology in rats administered with LQ purified from the acid hydrolyates of liquiritin singly (p.o. or i.v., 2-4 days) or in combination with dimethyl-4,4'-dimethoxy-5,6,5',6'-dimethylenedioxybiphenyl-2,2'-dicarboxylate (DDB), a synthetic derivative of Schisandrin C in Fructus shizandrae, and exposed to APAP or APAP + BSO. LQ treatments (oral) effectively decreased liver injuries induced by a single dose of APAP, as evidenced by decreases in hepatic necrosis and inflammation as well as plasma alanine aminotransferase and lactate dehydrogenase activities. LQ, when intravenously applied, enhanced hepatoprotective effect with a greater potency. APAP + BSO led to severe liver injuries, resulting in lethality. LQ pretreatments significantly reduced the potentiated liver necrosis, decreasing mortality. In spite of the improvement in blood biochemistry, DDB failed to protect the liver from injuries induced by APAP or APAP + BSO. Combined treatments of rats with LQ and DDB showed some additive protective effect. The present study demonstrates that LQ efficaciously protects the liver from acute injuries induced by APAP or from APAP-induced severe injuries during GSH deficiency, indicating that LQ is one of the principal cytoprotective components comprised in G. radix.

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Hyperbole can be rampant in health news, particularly with respect to cannabis. One recent headline declared: “CBD is effective in treating heroin addiction.” Another proclaimed: “New study finds CBD could curb heroin addiction.”

These stories were referring to a recent study in the American Journal of Psychiatry that found a short-term course of cannabidiol (CBD) reduced cue-induced cravings and anxiety in drug-abstinent individuals who were recovering from opioid use disorder, specifically heroin addiction.

This study is undoubtedly exciting and a welcome contribution to the scientific literature demonstrating the potentially helpful role of cannabinoids in the treatment of opioid use disorder.

That said, there is a mismatch between these headlines and the accurate interpretation of the findings from the study. And this mismatch is not trivial.

Read more…

Credits: 
Source: https://medicalxpress.com/

News Link: https://medicalxpress.com/news/2019-07-cannabis-misinformation-cbd-life-threatening.html

The post Cannabis: Misinformation about CBD can be life-threatening appeared first on AlternativeWellness.

PMID: 

J Asian Nat Prod Res. 2013 ;15(4):390-9. Epub 2013 Mar 6. PMID: 23464667

Abstract Title: 

Liquiritigenin prevents Staphylococcus aureus-mediated lung cell injury via inhibiting the production ofα-hemolysin.

Abstract: 

Staphylococcus aureus is a significant Gram-positive bacterium that is associated with a broad spectrum of diseases ranging from minor skin infections to lethal pneumonia, endocarditis, and toxinoses.α-Hemolysin is one of the most important exotoxins that contribute to the pathogenesis of S. aureus infections. Liquiritigenin is one of the most significant active components in licorice. In this study, hemolysis, western blot, and real-time reverse transcription-PCR assays were performed to investigate the impact of liquiritigenin on the production of S. aureus α-hemolysin. The results showed that low concentrations of liquiritigenin remarkably decreased S. aureus α-hemolysin production in a dose-dependent manner. Using live/dead cell staining and lactate dehydrogenase assays, we found that liquiritigenin could protect human lung cells (A549) from α-hemolysin-mediated injury. The data indicated that this compound could potentially be useful in developing drugs aiming at staphylococcal α-hemolysin.

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PMID: 

Neurotoxicology. 2013 Dec ;39:114-23. Epub 2013 Sep 5. PMID: 24012889

Abstract Title: 

Neuroprotective effects of liquiritigenin isolated from licorice roots on glutamate-induced apoptosis in hippocampal neuronal cells.

Abstract: 

The progressive death of neurons following exposure to high concentrations of glutamate leads to loss of learning and memory and pathogenesis of neurodegenerative disorders. Therefore, identification of drugs that protect against glutamate-mediated neuronal cell death is a good strategy for prevention and treatment of neurodegenerative diseases. In this study, we isolated liquiritigenin, an active compound found in licorice roots, by column chromatography and examined its protective effects against glutamate-mediated apoptotic stimuli in a mouse hippocampus-derived neuronal cell line (HT22 cells). Cell viability was significantly recovered following treatment with 50μM liquiritigenin up to 77.50±1.93% over the control (100.00±5.62%), whereas cell viability following 5mM glutamate treatment was decreased to 52.52±4.82%. Liquiritigenin effectively reduced glutamate-induced early apoptosis through inhibition of Ca(2+) influx, intracellular reactive oxygen species (ROS) production, and lipid peroxidation. In addition, the levels of Bcl-2 and full-length Bid were protected, and that of mitochondrial Bax was reduced by liquiritigenin. Liquiritigenin suppressed not only the release of apoptosis-inducing factor (AIF), but also activation of mitogen-activatedprotein kinases (MAPKs) such as p38, extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase (JNK). Therefore, the active component in licorice roots, liquiritigenin, might facilitate development of drug leads for neurodegenerative disorders.

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PMID: 

Phytother Res. 2014 Jun ;28(6):880-6. Epub 2013 Oct 3. PMID: 24123597

Abstract Title: 

Liquiritigenin restores osteoblast damage through regulating oxidative stress and mitochondrial dysfunction.

Abstract: 

We investigated the protective effect of liquiritigenin, one of the flavonoids present in Glycyrrhizae radix, against antimycin A-induced mitochondrial dysfunction in MC3T3-E1 osteoblast cells. Osteoblastic MC3T3-E1 cells were pre-incubated with liquiritigenin before treatment with antimycin A, and markers of mitochondrial function and oxidative damage were examined. In addition, the effects of liquiritigenin on the activation of phosphoinositide 3-kinase (PI3K) were examined in MC3T3-E1 cells. Liquiritigenin protected MC3T3-E1 cells from antimycin A-induced cell death. However, the PI3K inhibitor, LY294002, significantly attenuated liquiritigenin-mediated cell survival, indicating the involvement of PI3K in the cytoprotective effect of liquiritigenin. Pretreatment with liquiritigenin prior to antimycin A exposure significantly reduced antimycin A-induced PI3K inactivation, mitochondrial membrane potential dissipation, complex IV inactivation, and ATP loss. Liquiritigenin also reduced mitochondrial superoxide generation, nitrotyrosine production, and cardiolipin peroxidation during mitochondrial complex inhibition with antimycin A. Taken together, the results of this study show that modulation of PI3K, antioxidant effects, and the attenuation of mitochondrial dysfunction by liquiritigenin represent an important mechanism for its protection of osteoblasts against cytotoxicity resulting from mitochondrial oxidative stress.

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PMID: 

Biomed Res Int. 2014 ;2014:965316. Epub 2014 Mar 11. PMID: 24738081

Abstract Title: 

Liquiritigenin induces tumor cell death through mitogen-activated protein kinase- (MPAKs-) mediated pathway in hepatocellular carcinoma cells.

Abstract: 

Liquiritigenin (LQ), separated from Glycyrrhiza radix, possesses anti-inflammatory, antihyperlipidemic, and antiallergic effects. Our present study aims to investigate the antihepatocellular carcinoma effects of LQ both in cell and animal models. LQ strikingly reduced cell viability, enhanced apoptotic rate, induced lactate dehydrogenase over-release, and increased intracellular reactive oxygen species (ROS) level and caspase 3 activity in both PLC/PRL/5 and HepG2 cells. The expression of cleaved PARP, the hall-marker of apoptosis, was enhanced by LQ. LQ treatment resulted in a reduction of the expressions of B-cell lymphoma 2 (Bcl-2) and B-cell lymphoma-extra large (Bcl-xL), and an increase of the phosphorylation of c-Jun N-terminal kinases (JNK) and P38. LQ-mediated cell viability reduction, mitochondrial dysfunction, apoptosis related protein abnormal expressions, and JNK and P38 activation were partially abolished by N-Acetyl-L-cysteine (a ROS inhibitor) pretreatment. Moreover, LQ suppressed the activation of extracellular signaling-regulated kinase (ERKs) and reduced the translocation of phosphor-ERKs from cytoplasm to nucleus. This antitumor activity was further confirmed in PLC/PRL/5-xenografted mice model. All these data indicate that the antihepatocellular carcinoma effects of LQ are related to its modulation of the activations of mitogen-activated protein kinase (MAPKs). The study provides experimental evidence supporting LQ as a potential therapeutic agent for hepatocellular carcinoma treatment.

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PMID: 

Nutr Cancer. 2015 ;67(5):761-70. Epub 2015 May 15. PMID: 25978595

Abstract Title: 

Liquiritigenin Potentiates the Inhibitory Effects of Cisplatin on Invasion and Metastasis Via Downregulation MMP-2/9 and PI3 K/AKT Signaling Pathway in B16F10 Melanoma Cells and Mice Model.

Abstract: 

Liquiritigenin (LQ) is a flavanone extracted from glycyrrhizae. Previous studies have demonstrated that LQ possesses antimigration properties in HELA and A549 cells. The present research, as an extension of our earlier ones, investigated whether LQ can enhance the antimigration and antiinvasion effect of cis-diamine dichloroplatinum (CDDP) in B16F10 melanoma cell. The data indicated that LQ (25, 50, 100, 200μM) combined with CDDP (2 μM) significantly reduced B16F10 cell viability compared to CDDP (2 μM)-treated only. The different doses of LQ combined with CDDP significantly suppressed cell migration (21.5%, 49.6%, 75.6%) and cell invasion (26.2%, 51.4%, 69.5%) compared with CDDP-treated alone, suggesting that LQ enhance the inhibition action of CDDP on cell migration and invasion. Moreover, LQ/CDDP combination led to the downregulation of protein expression of MMP-2/9, PI3 K, p-AKT, and upregulated PTEN protein level that play an important role in tumor metastasis progression. Further study demonstrated the enhancement effect of LQ on CDDP suppressing lung metastasis in a mice model being inoculated by the B16F10 melanoma cells. In conclusion, the results suggested that LQ plays an intensive role on CDDP suppressing invasion and metastasis through regulating the PI3 K/AKT signal pathwayand suppressing the protein expression of MMP-2/9.

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