Anti-inflammatory and cytotoxic withanolides from Physalis minima.

08:00 EDT 17th August 2018 | BioPortfolio

Summary of "Anti-inflammatory and cytotoxic withanolides from Physalis minima."

Six undescribed withanolides were isolated and characterized during the investigation of anti-inflammatory and cytotoxic constituents from the whole plants of Physalis minima L. Their structures were elucidated by extensive spectroscopic analyses (IR, UV, HR-ESI-MS, 1D-NMR, and 2D-NMR), and their anti-inflammatory and cytotoxic activities were evaluated in vitro. All the compounds exhibited anti-inflammatory ability via inhibiting the production of nitric oxide (NO) in lipopolysaccharide (LPS)-stimulated murine macrophage RAW 264.7 cells. Moderate cytotoxic activities against A549 lung adenocarcinoma cells, SMMC-7721 hepatic carcinoma cells and MCF-7 breast cancer cells with IC values in the range of 40.01-82.17 μM were observed for these withanolides.


Journal Details

This article was published in the following journal.

Name: Phytochemistry
ISSN: 1873-3700
Pages: 164-170


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Medical and Biotech [MESH] Definitions

Ergostane derivatives of 28 carbons with oxygens at C1, C22, and C26 positions and the side chain cyclized. They are found in WITHANIA plant genus and have cytotoxic and other effects.

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A non-steroidal anti-inflammatory agent with analgesic, anti-inflammatory, and antipyretic properties. It is an inhibitor of cyclooxygenase.

A non-steroidal anti-inflammatory agent (ANTI-INFLAMMATORY AGENTS, NON-STEROIDAL) similar in mode of action to INDOMETHACIN.

Anti-inflammatory agents that are not steroids. In addition to anti-inflammatory actions, they have analgesic, antipyretic, and platelet-inhibitory actions. They are used primarily in the treatment of chronic arthritic conditions and certain soft tissue disorders associated with pain and inflammation. They act by blocking the synthesis of prostaglandins by inhibiting cyclooxygenase, which converts arachidonic acid to cyclic endoperoxides, precursors of prostaglandins. Inhibition of prostaglandin synthesis accounts for their analgesic, antipyretic, and platelet-inhibitory actions; other mechanisms may contribute to their anti-inflammatory effects. Certain NSAIDs also may inhibit lipoxygenase enzymes or TYPE C PHOSPHOLIPASES or may modulate T-cell function. (AMA Drug Evaluations Annual, 1994, p 1814-5)

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