The antibacterial effect produced by ethanolic licorice root extract on S. mutans was comparable to chlorhexidine mouthwash.

PMID: 

J Contemp Dent Pract. 2019 Dec 1 ;20(12):1389-1394. Epub 2019 Dec 1. PMID: 32381838

Abstract Title: 

Analysis of Licorice () Root Extract Activity onin Comparison to Chlorhexidine and Fluoride Mouthwash.

Abstract: 

AIM: The present study was done to determine the activity of licorice root extract on() in comparison to chlorhexidine and fluoride mouthwash.MATERIALS AND METHODS: In the current study, the different concentrations of aqueous and ethanolic licorice root extract were subjected to microbiological assay and zone of inhibition was determined againstby agar ditch method. Minimum inhibitory concentration (MIC) of aqueous and ethanolic solution was obtained by using broth dilution method and agar dilution method. Chlorhexidine and fluoride mouthwash were kept as a positive control in the present study. One-way ANOVA along with Tukeytest were used at 5% level of significance to analyze data.RESULTS: Mean zone of inhibition of chlorhexidine mouthwash, fluoride mouthwash, aqueous and ethanolic licorice root extracts againstat 24 hours were 23 mm, 14.2 mm, 15.8 mm and 22.4 mm, respectively. Minimum inhibitory concentration of aqueous and ethanolic licorice root extract onwas 20 mg/mL and 12.5 mg/mL, respectively by both broth dilution method and agar dilution method.CONCLUSION: The antibacterial effect produced by ethanolic licorice root extract onwas comparable to chlorhexidine mouthwash while significantly higher in comparison with aqueous form and fluoride mouthwash.CLINICAL SIGNIFICANCE: The interest in the plants with antibacterial and anti-inflammatory activity has increased now days to treat various dental diseases as consequences of current problems associated with the conventional agents. Licorice root is easily available, economically feasible and culturally acceptable and may possess minimal side effects as compared to conventional means of chemicotherapeutic agents used for reduction ofin oral cavity and hence can be recommended for prevention of dental caries.

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Effect of hot water extract of a glycyrrhizin-deficient strain of Glycyrrhiza uralensis on contact hypersensitivity.

PMID: 

J Nat Med. 2020 Mar ;74(2):415-420. Epub 2020 Jan 8. PMID: 31916003

Abstract Title: 

Effect of hot water extract of a glycyrrhizin-deficient strain of Glycyrrhiza uralensis on contact hypersensitivity in mice.

Abstract: 

To evaluate the medicinal properties of a glycyrrhizin (GL)-deficient strain of Glycyrrhiza uralensis, we investigated the anti-allergic effect of the hot water extract obtained from its roots on contact hypersensitivity in mice, and compared it with that of the hot water extract of a commercial crude drug, Glycyrrhiza Radix. The hot water root extract of the GL-deficient strain contained glucoglycyrrhizin (GGL) and rhaoglucoglycyrrhizin (RGL) instead of GL, and it showed anti-allergic activity against contact hypersensitivity in a fashion similar to that of the crude drug extract. We further confirmed the presence of glycyrrhetinic acid (GA), a major metabolite of GL, in mice serum after oral administration of the hot water root extract of a GL-deficient strain. We demonstrated that GGL underwent hydrolysis by intestinal microflora of mice to form GA. These results suggest that a GL-deficient strain of G. uralensis is a useful medicinal resource since the glycosides of GA work in a fashion similar to that of GL when orally administered.

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Paeoniflorin exerts neuroprotective effects in a transgenic mouse model of Alzheimer’s disease via activation of adenosine A1 receptor.

PMID: 

Neurosci Lett. 2020 May 1:135016. Epub 2020 May 1. PMID: 32371159

Abstract Title: 

Paeoniflorin exerts neuroprotective effects in a transgenic mouse model of Alzheimer's disease via activation of adenosine Areceptor.

Abstract: 

Alzheimer's disease (AD) is the most common cause of dementia, characterised by advanced cognitive and memory deterioration with no effective treatments available. Previous in vitro and in vivo studies suggest that paeoniflorin (PF), a major bioactive constituent of Radix Paeoniae, might possess anti-dementia properties; however, the underlying mechanism remains unclear. The aim of the current study was to determine the therapeutic effects of PF in a transgenic mouse model of AD and to identify its mechanism. Transgenic mice with five familial AD mutations (5XFAD) were used in this study. We showed that 28 days of PF (5 mg/kg, ip) treatment significantly decreased the escape latency and path length in the Morris water maze test and increased the alternation rate in the T-maze test, compared to the vehicle treatment group. In addition, PF treatment significantly alleviated amyloid β plaque burden, inhibited astrocyte activation, and decreased IL-1β and TNF-α expression in the brain of 5XFAD mice. However, the anti-cognitive deficits, anti-amyloidogenic, and anti-inflammatory effects of PF were abolished by 1,3-dipropyl-8-cyclopentylxanthine (DPCPX, 0.3 mg/kg), an adenosine Areceptor (AR) antagonist. In conclusion, our results suggest that PF might act as a potential therapeutic agent for AD via activation of adenosine AR.

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Antifungal effect of tea extracts on Candida albicans.

PMID: 

Dent Mater J. 2020 Apr 3. Epub 2020 Apr 3. PMID: 32249233

Abstract Title: 

Antifungal effect of tea extracts on Candida albicans.

Abstract: 

Determining whether tea extracts are effective in removing Candida albicans (C. albicans) from dentures is of interest. This study aimed to investigate the antifungal effect of tea extracts on C. albicans. One green tea (Anji white tea, AGW) and 2 oolong teas (Tie Guan Yin, TGY; Da Hong Pao, DHP) of different concentrations were tested. C. albicans suspensions were inoculated on the plates and the numbers of colony-forming units (CFU) in the culture medium were used to screen for the optimum tea extracts. Polymethyl methacrylate (PMMA) specimens that contained C. albicans biofilms were then treated with the tea extracts and the numbers of CFU were counted. The antifungal activities of the tea extracts were not significantly correlated with their catechin concentrations. Although AGW at 10.0 mg/mL and DHP at 2.5 mg/mL significantly inhibited C. albicans in the culture medium, the extracts failed to exert inhibitory effects against C. albicans biofilms on the PMMA surfaces.

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Jiaogulan tea potentiates the antidiabetic effect of white tea.

PMID: 

Food Funct. 2020 May 5. Epub 2020 May 5. PMID: 32369096

Abstract Title: 

Jiaogulan tea (Gpostemma pentaphyllum) potentiates the antidiabetic effect of white tea via the AMPK and PI3K pathways in C57BL/6 mice.

Abstract: 

The use of plant-based beverages to interfere with the onset of diabetes may be a promising approach towards type 2 diabetes mellitus (T2DM). The present study investigated the antidiabetic effects of the oral consumption of white tea and G. pentaphyllum (Jiaogulan), especially their combination on HFD/STZ-induced T2DM in C57BL/6 mice. White tea and Jiaogulan administration could mitigate glycolipid metabolic disorders in the diabetic mice by different degrees. White tea administration markedly reduced the blood glucose and ameliorated the glucose intolerance compared to the T2DM mice. Moreover, white tea consumption could protect the isletβ-cells against oxidative and inflammatory damage, related to the Nrf-2 signaling pathway. Jiaogulan prominently attenuated liver lipid accumulation by downregulation of SREBP levels. However, interestingly, when white tea was used in combination with Jiaogulan, these effects were enhanced to a certain extent. In particular, the combination significantly suppressed the hepatic G6Pase expressions by activating the AMPK pathway, thus inhibiting gluconeogenesis and improving insulin resistance. On the other hand, the combined formula could regulate the PPAR expressions and ameliorate the hepaticinflammation, further activating the IRS/PI3K/AKT pathway and exerting the antidiabetic potential. Therefore, it was speculated that the antidiabetic effect of this combination may be associated with the AMPK/PI3K pathways. Our findings might provide insight into the combined use of white tea withJiaogulan tea as a potential functional beverage or food for preventing T2DM.

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White tea plays important roles in ameliorating abnormal lipid metabolism in vitro.

PMID: 

Biomed Pharmacother. 2020 Apr 22 ;127:110146. Epub 2020 Apr 22. PMID: 32334376

Abstract Title: 

White tea and its active polyphenols lower cholesterol through reduction of very-low-density lipoprotein production and induction of LDLR expression.

Abstract: 

Emerging in vivo and vitro data suggest that white tea extract (WTE) is capable of favourably modulating metabolic syndrome, especially by ameliorating abnormal lipid metabolism. Microarray-based gene expression profiling was performed in HepG2 cells to analyze the effects of WTE from a systematic perspective. Gene Ontology and pathway analysis revealed that WTE significantly affected pathways related to lipid metabolism. WTE significantly downregulated apolipoprotein B (APOB) and microsomal triglyceride transfer protein (MTTP) expression and thereby reduced the production of very-low-density lipoprotein. In the meanwhile, WTE stimulated low-density lipoprotein-cholesterol (LDL-c) uptake through targeting low-density lipoprotein receptor (LDLR), as a consequence of the activation of sterol regulatory element-binding protein 2 (SREBP2) and peroxisome proliferator-activated receptorδ (PPARδ). Furthermore, WTE significantly downregulated triglycerides synthetic genes and reduced intracellular triglycerides accumulation. Besides, we demonstrated that the tea catechins epigallocatechin-3-gallate (EGCG) and epicatechin-3-gallate (ECG) are abundant in WTE and contribute to the regulation of cholesterol metabolism related genes, including LDLR, MTTP and APOB. Our findings suggest white tea plays important roles in ameliorating abnormal lipid metabolism in vitro.

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The synergistic Antitumor effect of 5-fluorouracil combined with allicin against lung and colorectal carcinoma cells.

PMID: 

Molecules. 2020 Apr 22 ;25(8). Epub 2020 Apr 22. PMID: 32331446

Abstract Title: 

The Synergistic Antitumor Effect of 5-Fluorouracil Combined with Allicin against Lung and Colorectal Carcinoma Cells.

Abstract: 

5-fluorouracil (5-FU) is an anticancer drug used to inhibit the proliferation of many different tumor cells. Since severe events are associated with this compound, its combination with different anticancer drugs or adjuvants would allow the use of a significantly lower dose of 5-FU. In this study, we highlighted that the combination of allicin with 5-FU inhibited the cell migration and proliferation of colorectal and lung cancer cells. 5-FU inhibited cell growth with a similar inhibitory concentration for both normal and tumor cells (~200µM), while allicin showed different inhibitory concentrations. With an IC50 of 8.625 µM, lung cancer cells were the most sensitive to allicin. Compared to 5-FU and allicin single-agent treatments, the co-treatment showed a reduced viability rate, with

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Arctigenin suppresses cell proliferation via autophagy inhibition in hepatocellular carcinoma cells.

PMID: 

J Nat Med. 2020 Mar 23. Epub 2020 Mar 23. PMID: 32207025

Abstract Title: 

Arctigenin suppresses cell proliferation via autophagy inhibition in hepatocellular carcinoma cells.

Abstract: 

Autophagy is a catabolic process that degrades dysfunctional proteins and organelles and plays critical roles in cancer development. Our preliminary screening identified that extracts of the fruits of Arctium lappa and the fruits of Forsythia suspensa notably suppressed the proliferation of hepatocellular carcinoma HepG2 cells and downregulated the autophagy. In this study, we explored the effect of arctigenin (ARG), a bioactive lignan in both extracts, on cell proliferation and autophagy-related proteins in HepG2 cells. ARG inhibited the proliferation of HepG2 cells. Analysis of autophagy-related proteins demonstrated that ARG might block the autophagy that leads to sequestosome 1/p62 (p62) accumulation. The stage of inhibition in autophagy by ARG differed from those by the autophagy inhibitors 3-methyladenine (3-MA) or chloroquine (CQ). ARG could also inhibit starvation-induced autophagy. Further analysis of apoptosis-related proteins indicated that ARG did not affect caspase-3 activation and PARP cleavage, suggesting that the antiproliferative effect of ARG can occur independently of apoptosis. In summary, our study showed that ARG suppresses cell proliferation and inhibits autophagy, and might lead to the development of agents for autophagy research and cancer chemoprevention.

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Arctigenin enhances the cytotoxic effect of doxorubicin in MDA-MB-231 breast cancer cells.

PMID: 

Int J Mol Sci. 2020 Apr 23 ;21(8). Epub 2020 Apr 23. PMID: 32340377

Abstract Title: 

Arctigenin Enhances the Cytotoxic Effect of Doxorubicin in MDA-MB-231 Breast Cancer Cells.

Abstract: 

Several reports have described the anti-cancer activity of arctigenin, a lignan extracted fromL. Here, we investigated the effect of arctigenin (ATG) on doxorubicin (DOX)-induced cell death using MDA-MB-231 human breast cancer cells. The results showed that DOX-induced cell death was enhanced by ATG/DOX co-treatment in a concentration-dependent manner and that this was associated with increased DOX uptake and the suppression of multidrug resistance-associated protein 1 (MRP1) gene expression in MDA-MB-231 cells. ATG enhanced DOX-induced DNA damage and decreased the phosphorylation of signal transducer and activator of transcription 3 (STAT3) and the expressions of RAD51 and survivin. Cell death caused by ATG/DOX co-treatment was mediated by the nuclear translocation of apoptosis inducing factor (AIF), reductions in cellular and mitochondrial Bcl-2 and Bcl-xL, and increases in mitochondrial BAX levels. However, caspase-3 and -7 did not participate in DOX/ATG-induced cell death. We also found that DOX/ATG-induced cell death was linked with activation of the p38 signaling pathway and suppressions of the phosphorylations and expressions of Akt and c-Jun N-terminal kinase. Taken together, these results show that ATG enhances the cytotoxic activity of DOX in MDA-MB-231 human breast cancer cells by inducing prolonged p21 expression and p38-mediated AIF-dependent cell death. In conclusion, our findings suggest that ATG might alleviate the side effects and improve the therapeutic efficacy of DOX.

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Arctigenin exhibits hepatoprotective activity in Toxoplasma gondii-infected host through HMGB1/TLR4/NF-κB pathway.

PMID: 

Int Immunopharmacol. 2020 Apr 28 ;84:106539. Epub 2020 Apr 28. PMID: 32361192

Abstract Title: 

Arctigenin exhibits hepatoprotective activity in Toxoplasma gondii-infected host through HMGB1/TLR4/NF-κB pathway.

Abstract: 

Toxoplasmosis is a parasitic zoonosis with the highest incidence in humans. Severe lesions due to acute toxoplasmosis have been recorded in the visceral organs including the liver, where hepatocytes and Kupffer cells are important innate immune cells. Arctigenin (AG) is a bioactive ingredient of Arctium lappa L. and increasing evidence suggests that AG exhibits anti-oxidant, anti-inflammatory and anti-Toxoplasma gondii (T. gondii) effects. However, the role of AG in acute liver damage induced by T. gondii infection remains unclear. In this study, we analyzed the effects of AG against T. gondii-induced liver damage by establishing an in vitro infection model using a murine liver cell line (NCTC-1469 cells) and an in vivo mouse model with acute T. gondii infection of virulent RH strain. In the current study, AG effectively attenuated hepatocytes apoptosis and inhibited the reproduction of T. gondii. The results of in vitro and in vivo studies showed that AG significantly reduced alanine aminotransferase/aspartate aminotransferase activities and lessened pathological damage of liver. Moreover, AG suppressed T. gondii-induced inducible nitric oxide synthase production. AG also attenuated liver inflammation by inhibiting T. gondii-induced activation of the high-mobility group box1/toll-like receptor 4/nuclear factor-kappa B (HMGB1/TLR4/NF-κB) signaling pathway. These findings demonstrated that AG exhibited prominent hepatoprotective activities in toxoplasmic liver injury with anti-inflammatory effects by inhibiting the HMGB1/TLR4/NF-κB signaling axis. Thus, this study provides the basis for the development of new drugs to treat toxoplasmic hepatitis.

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