phyllanthus engleri/protease

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Potent HCV NS3 Protease Inhibition by a Water-Soluble Phyllanthin Congener

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NS3/4A protease of hepatitis C virus (HCV) plays an important role in viral RNA replication. A 1,4-diphenylbutanedicarboxylic acid derivative, namely, phyllanthin, extracted from the leaf of a herbal plant, Phyllanthus amarus, inhibits HCV NS3/4A protease and replication activities. However,

Antimetastatic potentials of Phyllanthus urinaria L on A549 and Lewis lung carcinoma cells via repression of matrix-degrading proteases.

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Tumor metastasis is the most important cause of cancer death and various treatment strategies have targeted at preventing the occurrence of metastasis. Phyllanthus urinaria L is a popular folk medicine and has several proven biological properties, including antioxidant, antihypertension, and

Preparation of Lignan-Rich Extract from the Aerial Parts of Phyllanthus niruri Using Nonconventional Methods.

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Phyllanthin and related lignans were found to be responsible, at least in part, for most of the activity of Phyllanthus species. This observation encouraged the authors to develop methods for the preparation of an extract rich in phyllanthin and related lignans from the aerial parts of P.

A natural small molecule inhibitor corilagin blocks HCV replication and modulates oxidative stress to reduce liver damage.
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Hepatitis C virus (HCV) infection causes chronic liver disease, which often leads to hepatocellular carcinoma. Earlier, we have demonstrated anti-HCV property of the methanolic extract of Phyllanthus amarus, an age-old folk-medicine against viral hepatitis. Here, we report identification of a

Concerted inhibitory activities of Phyllanthus amarus on HIV replication in vitro and ex vivo.
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Phyllanthus amarus derived preparations were previously shown to inhibit RT inhibitor-resistant HIV variants as efficiently as wild-type strains. The drugs target different steps of the HIV life cycle, thereby presenting multiple antiviral activities. Here we show that a water/alcohol extract blocks

Inhibition of hepatitis C virus replication by herbal extract: Phyllanthus amarus as potent natural source.
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Hepatitis C virus infection is a major health problem worldwide. Developing effective antiviral therapy for HCV is the need of the hour. The viral enzymes NS3 protease and NS5B RNA dependent RNA polymerase are essential enzymes for polyprotein processing and viral RNA replication and thus can be

A prolyl endopeptidase-inhibiting antioxidant from Phyllanthus ussurensis.
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A prolyl endopeptidase inhibitor was isolated from the ethyl acetate soluble fraction of Phyllanthus ussurensis. The active compound was identified as an ellagitannin, corilagin. It was shown to non-competitively inhibit prolyl endopeptidase (PEP) with the IC50 value of 1.17x10(-6) microM. The Ki

Phyllanthus urinaria suppresses human osteosarcoma cell invasion and migration by transcriptionally inhibiting u-PA via ERK and Akt signaling pathways.
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Phyllanthus urinaria is widely used as anti-inflammatory, antiviral, antibacterial, and anti-hepatotoxic medicines in almost every tropical country. However, scientific evidence supporting its use in cancer metastasis is limited, particularly osteosarcoma. We investigated the effect of P. urinaria

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phyllanthus engleri/protease

Potent HCV NS3 Protease Inhibition by a Water-Soluble Phyllanthin Congener

Antimetastatic potentials of Phyllanthus urinaria L on A549 and Lewis lung carcinoma cells via repression of matrix-degrading proteases.

Preparation of Lignan-Rich Extract from the Aerial Parts of Phyllanthus niruri Using Nonconventional Methods.

A natural small molecule inhibitor corilagin blocks HCV replication and modulates oxidative stress to reduce liver damage.

Concerted inhibitory activities of Phyllanthus amarus on HIV replication in vitro and ex vivo.

Inhibition of hepatitis C virus replication by herbal extract: Phyllanthus amarus as potent natural source.

A prolyl endopeptidase-inhibiting antioxidant from Phyllanthus ussurensis.

Phyllanthus urinaria suppresses human osteosarcoma cell invasion and migration by transcriptionally inhibiting u-PA via ERK and Akt signaling pathways.

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