Catecholic alkaloid sulfonates and aromatic nitro compounds from Portulaca oleracea and screening of their anti-inflammatory and anti-microbial activities.

Acidic compounds were enriched from a water decoction of Portulaca oleracea using 717 anion exchange resin column chromatography. A total of 22 compounds including 9 catecholamine derivatives, of which six were rare sulfonic acid derivatives, and 9 nitro derivatives, were further isolated through various column chromatographic methods, and their structures were elucidated by interpreting their spectroscopic data and ECD calculations. Among them, 16 compounds were isolated from P. oleracea for the first time, 8 of which were undescribed compounds and four compounds were natural products. Pharmacological screening indicated that cis-3-(3-nitro-4-hydroxyphenyl)-methyl acrylate exhibited anti-inflammatory activity, measured as inhibition of nitric oxide production in LPS-stimulated RAW264.7 macrophage cells, with an EC50 value of 18.0 µM, The compounds showed only weak anti-microbial activity with (2R)-(+)-2-chloro-3-(3-nitro-4-hydroxyphenyl)-propionic acid methyl ester inhibiting Candida albicans with a MIC of 256 µg/mL, and 3-methoxy-4,5-dinitrophenol inhibiting Shigella sonnei with a MIC of 512 µg/mL.

Catecholic Isoquinolines from Portulaca oleracea and Their Anti-inflammatory and ß2-Adrenergic Receptor Agonist Activity.

Isoquinoline alkaloids possess a wide range of structural features and pharmaceutical activities and are promising drug candidates. Ten water-soluble catecholic isoquinolines were isolated from the medicinal plant Portulaca oleracea, including three new (1-3) and seven known compounds (4-10), along with the known catecholamines 11 and 12 and four other known compounds (13-16). A method of polyamide column chromatography using EtOAc-MeOH as the mobile phase was developed for the isolation of catecholic isoquinolines. Alkaloids 1-12 exhibited anti-inflammatory activities (EC50 = 18.0-497.7 µM) through inhibition of NO production in lipopolysaccharide-induced murine macrophage RAW 264.7 cells. Among these compounds, 11, 2, 5, 4, and 8 were more potent than was the positive control, 3,4-dihydroxybenzohydroxamic acid (EC50 = 82.4 µM), with EC50 values of 18.0, 18.1, 35.4, 36.3, and 58.7 µM, respectively. Additionally, at 100 µM, compounds 1-12 showed different degrees of ß2-adrenergic receptor (ß2-AR) agonist activity in the CHO-K1/GA15 cell line which stably expressed ß2-AR as detected by a calcium assay. The EC50 values of 2 and 10 were 5.1 µM and 87.9 nM, respectively.

Phenolic alkaloid oleracein E attenuates oxidative stress and neurotoxicity in AlCl3-treated mice.

AIMS: Chelation therapy and antioxidant supplements have been demonstrated to be useful in ameliorating aluminum (Al) induced neurotoxicity. Oleracein E (OE) is a phenolic antioxidant alkaloid which possesses a rare tetrahydroisoquinoline/pyrrolidone tricyclic skeleton and a catechol moiety. The aim of this study was to investigate whether OE can chelate with Al and alleviate AlCl3-induced oxidative stress and neurotoxicity. MAIN METHODS: Kunming mice were administered AlCl3 (40mg/kg/d, i.p., 28days), with co-administration of OE (3mg/kg/d, 15mg/kg/d, i.g.) and the positive control piracetam (PA, 400mg/kg/d, i.g.). The Al contents in the brain and plasma were determined using ICP-MS. Al chelating ability of OE was assayed using UV spectroscopy. MDA, GSH, SOD or CAT, in the brain or plasma were determined. HE staining was used to examine hippocampal morphology alterations. IHC staining was employed to measure the expression of apoptotic-related proteins Bax, Bcl-2 and Caspase-3. KEY FINDINGS: AlCl3 remarkably increased the brain and plasma Al contents, increased lipid peroxidation and induced hippocampal neuronal damage. OE chelated with Al to form a stable complex. An increase in brain Al content by OE (15mg/kg) likely occurred through chelating with Al, which reduced the toxicity of free Al ion in the brain. OE significantly decreased MDA by regulating some antioxidant biomarkers. Furthermore, OE significantly ameliorated the protein expression changes in some apoptotic indices induced by AlCl3. SIGNIFICANCE: The phenolic alkaloid OE, as an antioxidant, Al chelator and apoptosis inhibitor, alleviates oxidative stress and neurotoxicity induced by AlCl3.