PMID: 

Environ Sci Pollut Res Int. 2020 Feb 8. Epub 2020 Feb 8. PMID: 32036533

Abstract Title: 

Therapeutic role of garlic and vitamins C and E against toxicity induced by lead on various organs.

Abstract: 

Due to industrial and urban sewage, the metal contaminations in aquatic and terrestrial environments are increasing day by day, especially in developing countries. Despite the study of several years, we are inert far away from an actual medication for prolonged toxicity of heavy metals such as mercury, lead, cadmium etc. Lead is one of the most common heavy metals that possess toxicological effects on numerous tissues of animals as well as humans. Several toxic effects of lead on reproductive organs, renal system, central nervous system, liver, lungs, blood parameters, and bones have been reported. On the other hand, several reports depicted that garlic is operative in declining the absorption of lead in bones as well as soft tissues. A combination of vitamin C and vitamin E enhances the biological recovery induced by lead and mobilize the heavy metal such as lead from intra-cellular positions. This review provides therapeutic approaches such as vitamin C, vitamin E, and extract of garlic to treat the detrimental effects caused after the exposure of lead. These therapeutic strategies are beneficial for both the prevention and alleviation of lead noxiousness.

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PMID: 

J Trauma Acute Care Surg. 2020 Feb 7. Epub 2020 Feb 7. PMID: 32039973

Abstract Title: 

Vitamin C and Thiamine Are Associated with Lower Mortality in Sepsis.

Abstract: 

INTRODUCTION: The efficacy of vitamin C (VitC) and thiamine (THMN) in patients admitted to the intensive care unit (ICU) with sepsis is unclear. The purpose of this study was to evaluate the effect of VitC and THMN on mortality and lactate clearance in ICU patients. We hypothesized that survival and lactate clearance would be improved when treated with thiamine and/or vitamin C.METHODS: The Philips eICU database version 2.0 was queried for patients admitted to the ICU in 2014-2015 for≥48 hours and patients with sepsis and an elevated lactate≥2.0 mmol/L. Subjects were categorized according to the receipt of VitC, THMN, both, or neither. The primary outcome was in-hospital mortality. Secondary outcome was lactate clearance defined as lactate

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PMID: 

Biomed Pharmacother. 2018 Jul ;103:1592-1601. Epub 2018 May 7. PMID: 29864947

Abstract Title: 

Atomic force microscopy technique used for assessment of the anti-arthritic effect of licochalcone A via suppressing NF-κB activation.

Abstract: 

Atomic force microscopy (AFM) is appropriately applied to the examination of hard surfaces and soft samples with extremely high resolution and ultrasensitive force, which cannot be obtained by other imaging techniques, including optical and electron microscopy. In the current study, AFM was employed to evaluate the anti-arthritic effect of licochalcone A (LCA), a flavonoid isolated from the root of Chinese medicinal herb Glycyrrhiza inflate, on rheumatoid arthritis synovial fibroblasts (RASFs) at the nanoscale for the first time. The morphology, ultrastructure and stiffness of RASFs was modified by LCA as determined by AFM, suggesting that LCA most likely exerts an anti-arthritic effect based on the key role of RASFs in the progression of RA. Further studies showed that the inhibitory effect of LCA on IκBα phosphorylation and degradation as well as on p65 nuclear translocation and phosphorylation contributed to altering the morphology, ultrastructure and stiffness of the RASF membrane. Interestingly, IKKβ phosphorylation was not detectable in RASFs, indicating that LCA altered the morphology, ultrastructure and stiffness of the RASF membrane by inhibiting NF-κB activation independent of IKKβ phosphorylation. Antigen-induced arthritis (AIA) was established in Sprague Dawley (SD) rats to validate the anti-arthritic effect of LCA, and LCA significantly decreased both the arthritis scores and paw swelling in the AIA rats, suggesting that LCA inhibits the progression and development of arthritis in vivo. Collectively, AFM provides evidence at the nanoscale to predict the anti-arthritic effect of drugs on RASFs, and LCA should be further investigated as a candidate agent for the treatment of arthritis.

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PMID: 

Phytomedicine. 2020 Jan ;66:153108. Epub 2019 Oct 4. PMID: 31790896

Abstract Title: 

Liquiritigenin suppresses the activation of hepatic stellate cells via targeting miR-181b/PTEN axis.

Abstract: 

BACKGROUND: Liquiritigenin (LQ), an aglycone of liquiritin in licorice, has demonstrated antioxidant, anti-inflammatory and anti-tumor activities. Previously, LQ was found to inhibit liver fibrosis progression.PURPOSE: Phosphatase and tensin homolog (PTEN) has been reported to act as a negative regulator of hepatic stellate cell (HSC) activation. However, the roles of PTEN in the effects of LQ on liver fibrosis have not been identified to date.METHODS: The effects of LQ on liver fibrosis in carbon tetrachloride (CCl) mice as well as primary HSCs were examined. Moreover, the roles of PTEN and microRNA-181b (miR-181b) in the effects of LQ on liver fibrosis were examined.RESULTS: LQ markedly ameliorated CCl-induced liver fibrosis, with a reduction in collagen deposition as well asα-SMA level. Moreover, LQ induced an increase in PTEN and effectively inhibited HSC activation including cell proliferation, α-SMA and collagen expression, which was similar with curcumin (a positive control). Notably, loss of PTEN blocked down the effects of LQ on HSC activation. PTEN was confirmed as a target of miR-181b and miR-181b-mediated PTEN was involved in the effects of LQ on liver fibrosis. LQ led to a significant reduction in miR-181b expression. LQ-inhibited HSC activation could be restored by over-expression of miR-181b. Further studies demonstrated that LQ down-regulated miR-181b level via Sp1. Collectively, we demonstrate that LQ inhibits liver fibrosis, at least in part, via regulation of miR-181b and PTEN.CONCLUSION: LQ down-regulates miR-181b level, leading to the restoration of PTEN expression, which contributes to the suppression of HSC activation. LQ may be a potential candidate drug against liver fibrosis.

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PMID: 

Biochem Biophys Res Commun. 2018 11 17 ;506(1):161-168. Epub 2018 Oct 16. PMID: 30340829

Abstract Title: 

Isoliquiritigenin alleviated the Ang II-induced hypertensive renal injury through suppressing inflammation cytokines and oxidative stress-induced apoptosis via Nrf2 and NF-κB pathways.

Abstract: 

PURPOSE: Hypertensive renal injury plays important role in the pathogenesis of end-stage nephropathy and the need for dialysis. Isoliquiritigenin (ISL) is a natural compound with antioxidant and anti-inflammatory activities. In this study, the protective effects of ISL on Angiotensin II (Ang II)- induced apoptosis, inflammation and extracellular matrix production in HK-2 cells were observed and its mechanisms were elucidated.METHODS: Cell survival was determined with MTT assay. Cell cycle and apoptosis was assessed with flow cytometric analysis. The production of cytokines including IL-1β and TNF-α were evaluated with Elisa. Western blotting assay was used to determine protein levels of apoptosis related signaling, oxidative stress, NF-κB and ECM related molecules. mRNA levels of fibronectin and collagen Ⅳ were detected by RT-qPCR.RESULTS: Ang II significantly inhibited cell survival, induced cell cycle arrest and enhanced cell apoptosis. However, the above effects were markedly alleviated by ISL treatment in a dose-dependent manner. In addition, Ang II significantly induced oxidative stress and NF-κB signaling activation, as well as inflammatory cytokines release. In contrast, these effects were remarkably reversed by ISL via regulation of Nrf2. Notably, Ang II also triggered generation of extracellular matrix, including fibronectin and collagen Ⅳ, which was abolished upon ISL treatment.CONCLUSIONS: Taken together, ISL alleviated the Ang II-induced hypertensive renal injury through suppressing inflammation cytokines, excessive deposition of extracellular matrix and oxidative stress-induced apoptosis via Nrf2 and NF-κB pathways. Our findings provided the evidences for exploring the possible mechanism of hypertensive renal injury pathogenesis and identifying novel therapeutic targets.

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PMID: 

Evid Based Complement Alternat Med. 2019 ;2019:4568198. Epub 2019 May 26. PMID: 31239860

Abstract Title: 

Isoliquiritigenin Attenuates Monocrotaline-Induced Pulmonary Hypertension via Inhibition of the Inflammatory Response and PASMCs Proliferation.

Abstract: 

Pulmonary hypertension (PH) is a progressive and serious disease, where exacerbated inflammatory response plays a critical role. Isoliquiritigenin (ISL), an important flavonoid isolated from Glycyrrhizae radix, exhibits a wide range of pharmacological actions including anti-inflammation. Previously we found ISL alleviated hypoxia-induced PH; in the present study, to extend this, we evaluated the effects of ISL on monocrotaline (MCT)-induced PH and the relevant mechanisms. Rats received a single intraperitoneal injection of MCT, followed by intragastric treatments with ISL (10 mg/kg/d or 30 mg/kg/d) once a day for 28 days. The MCT administration increased the right ventricular systolic pressure (RVSP) (

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PMID: 

Biosci Rep. 2020 01 31 ;40(1). PMID: 31840737

Abstract Title: 

Isoliquiritigenin inhibits the proliferation, migration and metastasis of Hep3B cells via suppressing cyclin D1 and PI3K/AKT pathway.

Abstract: 

The overall survival rate of patients with hepatocellular carcinoma (HCC) has remained unchanged over the last several decades. Therefore, novel drugs and therapies are required for HCC treatment. Isoliquiritigenin (ISL), a natural flavonoid predominantly isolated from the traditional Chinese medicine Glycyrrhizae Radix (Licorice), has a high anticancer potential and broad application value in various cancers. Here, we aimed to investigate the anticancer role of ISL in the HCC cell line Hep3B. Functional analysis revealed that ISL inhibited the proliferation of Hep3B cells by causing G1/S cell cycle arrest in vitro. Meanwhile, the inhibitory effect of ISL on proliferation was also observed in vivo. Further analysis revealed that ISL could suppress the migration and metastasis of Hep3B cells in vitro and in vivo. Mechanistic analysis revealed that ISL inhibited cyclin D1 and up-regulated the proteins P21, P27 that negatively regulate the cell cycle. Furthermore, ISL induced apoptosis while inhibiting cell cycle transition. In addition, phosphatidylinositol 3'-kinase/protein kinase B (PI3K/AKT) signal pathway was suppressed by ISL treatment, and the epithelial marker E-cadherin was up-regulated when the mesenchymal markers Vimentin and N-cadherin were down-regulated. In brief, our findings suggest that ISL could be a promising agent for preventing HCC tumorigenesis and metastasis.

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PMID: 

Curr Med Chem. 2018 Sep 30. Epub 2018 Sep 30. PMID: 30277142

Abstract Title: 

A Review: The Anti-inflammatory, Anticancer, Antibacterial Properties of Four Kinds of Licorice Flavonoids Isolated from Licorice.

Abstract: 

Plants have always been an important source of medicines for humans, and licorice is a very significant herb in the development of humans. As a traditional herb, it is widely cultivated in China, Japan, Russia, Spain, and India. With the development of organic chemistry and biochemistry, various chemical ingredients extracted from licorice have been studied and identified. Among them, many chemical components were considered to have strong pharmacological activities, such as anti-inflammatory, anti-ulcer, antibacterial, anticancer and so on. Based on those reports, licorice has attracted the attention of many researchers in recent years, and they are devoted to discovering the active ingredients and mechanism of action of active compounds. Licorice flavonoids are one of the main extracts of licorice root and stem, and has many potential biological properties. This paper aims to summarize the four kinds of licorice flavonoids, including liquiritigenin, isoliquiritigenin, licochalcone (including licochalcone A and licochalcone B) and glabridin, about their biological activities of anti-inflammatory, anticancer, antibacterial.

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PMID: 

Front Pharmacol. 2018 ;9:837. Epub 2018 Jul 31. PMID: 30108506

Abstract Title: 

Lico A Causes ER Stress and Apoptosis via Up-Regulating miR-144-3p in Human Lung Cancer Cell Line H292.

Abstract: 

During our study on the bioactivities of natural flavonoids, we found that the total flavonoids (TFs) and the main constituent of it, licochalcone A (lico A), activated unfolded protein response (UPR) and induced autophagy and thereby apoptosis in H292 cells. MicroRNAs, such as the tumor repressor miR-144-3p, were reported to be differentially expressed in lung cancer cells and were linked to ER stress, autophagy, and apoptosis. However, the underlying miRNA-based mechanism for lico A modulating proliferation, autophagy and apoptosis in lung cancer cells is elusive. In this study, we found that miR-144-3p was down-regulated in H292 cells comparing to normal embryonic lung cells WI-38, and lico A (10μM) could increase miR-144-3p level in H292 cells. Knockdown of miR-144-3p significantly abrogated the apoptosis and proliferation-inhibiting effects of lico A, and lico A could enhance the proliferation-inhibiting effect and apoptosis induced by miR-144-3p overexpression. Moreover, overexpressionmiR-144-3p could induce ER stress by down-regulating Nrf2, and lico A enhanced the Nrf2 down-regulation caused by miR-144-3p overexpression. Co-transfection experiments showed that lico A potentially increased the dicing of pre-miR-144 so as to increase the mature miR-144-3p level. Interestingly, high level of lico A (40 μM) up-regulated CHOP protein, but failed to increase the downstream genes levels of CHOP, including Bim and Bcl-2 in H292 cells. Docking studies indicated that CHOP-mediated pathway was potentially blocked by high dose of lico A. Our results suggested that lico A could causeUPR, autophagy and apoptosis, and the underlying mechanism involved up-regulation of miR-144-3p, and increased lico A level would also increase the potential for lico A inhibiting CHOP-dependent apoptosis in H292 cells.

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PMID: 

Molecules. 2018 Aug 13 ;23(8). Epub 2018 Aug 13. PMID: 30104527

Abstract Title: 

Chalcones Repressed the AURKA and MDR Proteins Involved in Metastasis and Multiple Drug Resistance in Breast Cancer Cell Lines.

Abstract: 

In the present investigation,-chalcone and licochalcone A were tested against MCF-7 and BT-20 breast cancer cell lines for anti-tumor activity. We found that both chalcones down regulated important genes associated to cancer development and inhibited cell migration of metastatic cells (BT-20). Finally, we observed that licochalcone A reduces the MDR-1 protein, while both chalcones suppress the AURKA protein in a dose-dependent manner. In conclusion, we observed the-chalcone and licochalcone A affected the cell viability of breast cancer cell lines MCF-7 and BT-20 and presents anti-metastatic and anti-resistance potential, by the repression of AUKA and MDR-1 proteins.

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