The aminonaphthoquinone, spinamine E (5), was isolated for the first time from the sea urchins Strongylocentrotus pallidus (Sars G.O., 1872) and Mesocentrotus nudus (A. Agassiz, 1864). The structure of 5 was elucidated as 2-amino-3,5,6,7,8-pentahydroxy-1,4-naphthoquinone using 1D 1 H-, 13 C-and 2D NMR procedures, and HR-ESI mass-spectrometric data of 5 and its trimethyl ether. Spinamine E, as well as two other aminonaphthoquinones of sea urchins, echinamines A (2) and B (3), along with their hydroxylated analogues, spinochrome E (4) and echinochrome A (1), were tested for their ability to scavenge the stable DPPH radical and to inhibit lipid peroxidation. All investigated naphthoquinones obtained from the sea urchins showed a high antiradical activity, which was up to 1.5 times higher than that of α-tocopherol. Echinamine B showed the highest scavenging effect (EC 50 = 6.5•10-6 M); this effect decreases in the series 35124α-tocopherol. In a lipid peroxidation inhibition testing model, echinamine B and spinamine E showed the highest inhibitory effect. The stability of compounds 1-5 in weakly alkaline solutions was evaluated.

Echinochrome A (Ech A), a natural pigment extracted from sea urchins, is the active ingredient of a marine-derived pharmaceutical called ‘histochrome’. Since it exhibits several biological activities including anti-oxidative and anti-inflammatory effects, it has been applied to the management of cardiac injury and ocular degenerative disorders in Russia and its protective role has been studied for other pathologic conditions. In the present study, we sought to investigate the therapeutic potential of Ech A for inflammatory bowel disease (IBD) using a murine model of experimental colitis. We found that intravenous injection of Ech A significantly prevented body weight loss and subsequent lethality in colitis-induced mice. Interestingly, T cell proliferation was significantly inhibited upon Ech A treatment in vitro. During the helper T (Th) cell differentiation process, Ech A stimulated the generation regulatory T (Treg) cells that modulate the inflammatory response and immune homeostasis. Moreover, Ech A treatment suppressed the in vitro activation of pro-inflammatory M1 type macrophages, while inducing the production of M2 type macrophages that promote the resolution of inflammation and initiate tissue repair. Based on these results, we suggest that Ech A could provide a beneficial impact on IBD by correcting the imbalance in the intestinal immune system.

On long-term introduction to rats in dosage 100 mg/kg polyphenol complexes from heartwood and callus culture of Maackia amurensis Rupr. et Maxim. had a marked influence on the activity of free radical oxidation. Under conditions of induced oxidant stress both polyphenol complexes inhibited prooxidant activity directly affecting the products of free radical oxidation. Inhibiting influence on the production of oxygen active forms that is characteristic for both phytocomplexes is determined by inhibition of mechanisms both enzymatic and non-enzymatic defense.

Seven isoflavonoids, including a new glycoside, (6aR,11aR)-medicarpin-3-O-gentiobioside (6), were isolated from the roots of Maackia amurensis using repeated column chromatography on a Toyopearl HW-50F sorbent and identified by HPLC-PDA-MS, 1 H NMR, 13 C, 1 H-1 H COSY, HSQC NMR and HMBC NMR analyses as daidzin (1), genistein-7-O-gentiobioside (2), pseudobaptigenin-7-O-gentiobioside (3), formononetin-7-O-gentiobioside (4), (6aR,11aR)maackiain-3-O-gentiobioside (5), and 5-O-methylgenistein-7-O-gentiobioside (7). In the model of oxidative stress induced by formalin injection, the isolated isoflavone and pterocarpan glucosides 1-7 were shown to reduce the formation of malondialdehyde (MDA) and other thiobarbituric acid reactive substances (TBARS), as well as glutathione peroxidase (GPO) activity in rats.

No abstract

From a root bark of Lespedeza bicolor Turch we isolated two new (7 and 8) and six previously known compounds (1-6) belonging to the group of prenylated polyphenols. Their structures were elucidated using mass spectrometry, nuclear magnetic resonance and circular dichroism spectroscopy. These natural compounds selectively inhibited human drug-resistant prostate cancer in vitro. Prenylated pterocarpans 1-3 prevented the cell cycle progression of human cancer cells in S-phase. This was accompanied by a reduced expression of mRNA corresponding to several human cyclin-dependent kinases (CDKs). In contrast, compounds 4-8 induced a G1-phase cell cycle arrest without any pronounced effect on CDKs mRNA expression. Interestingly, a non-substituted hydroxy group at C-8 of ring D of the pterocarpan skeleton of compounds 1-3 seems to be important for the CDKs inhibitory activity.

Echinochrome A (Ech A, 1) is one of the main pigments of several sea urchin species and is registered in the Russian pharmacopeia as an active drug substance (Histochrome®), used in the fields of cardiology and ophthalmology. In this study, Ech A degradation products formed during oxidation by O2 in air-equilibrated aqueous solutions were identified, isolated, and structurally characterized. An HPLC method coupled with diode-array detection (DAD) and mass spectrometry (MS) was developed and validated to monitor the Ech A degradation process and identify the appearing compounds. Five primary oxidation products were detected and their structures were proposed on the basis of high-resolution electrospray ionization mass spectrometry (HR-ESI-MS) as 7-ethyl-2,2,3,3,5,7,8-heptahydroxy-2,3-dihydro-1,4-naphthoquinone (2), 6-ethyl-5,7,8-trihydroxy-1,2,3,4-tetrahydronaphthalene-1,2,3,4-tetraone (3), 2,3-epoxy-7-ethyl-2,3-dihydro-2,3,5,6,8-pentahydroxy-1,4-naphthoquinone (4), 2,3,4,5,7-pentahydroxy-6-ethylinden-1-one (5), and 2,2,4,5,7-pentahydroxy-6-ethylindane-1,3-dione (6). Three novel oxidation products were isolated, and NMR and HR-ESI-MS methods were used to establish their structures as 4-ethyl-3,5,6-trihydroxy-2-oxalobenzoic acid (7), 4-ethyl-2-formyl-3,5,6-trihydroxybenzoic acid (8), and 4-ethyl-2,3,5-trihydroxybenzoic acid (9). The known compound 3-ethyl-2,5-dihydroxy-1,4-benzoquinone (10) was isolated along with products 7–9. Compound 7 turned out to be unstable; its anhydro derivative 11 was obtained in two crystal forms, the structure of which was elucidated using X-ray crystallography as 7-ethyl-5,6-dihydroxy-2,3-dioxo-2,3-dihydrobenzofuran-4-carboxylic acid and named echinolactone. The chemical mechanism of Ech A oxidative degradation is proposed. The in silico toxicity of Ech A and its degradation products 2 and 7–10 were predicted using the ProTox-II webserver. The predicted median lethal dose (LD50) value for product 2 was 221 mg/kg, and, for products 7–10, it appeared to be much lower (≥2000 mg/kg). For Ech A, the predicted toxicity and mutagenicity differed from our experimental data.

Annot For finding-out of a role of separate groups of polyphenols in realization hepatoprotective properties of maksar we investigate activity of polyphenolic complexes (PPC) from duramen and cellular culture of maakia amur. Experiments are carried out on 40 not purebred white rats with an experimental СCl4-hepatites. Therapeutic efficiency of researched objects estimated on their influence on survival rate of animals, morphological and biochemical parameters of a liver and wheys of blood. In rat's CCl4-hepatitis PPC from duramen and cellular culture of maakia amur reduce the acute toxity of tetrachloromethane, decrease the necrosis of hepatocytes and cellural infiltration of liver's parenchyma, prevent from development of fatty and protein dystrophy of a liver, normalize the activity of amino transferase, ƒ-glutamyltransferase in blood, the concentration of proteins and lipids, stimulate conjugation of bilirubin. The therapeutic effect of PPC of cellular culture is more evident. The hepatoprotective action is caused by a presence of isoflavonoids daidzein, retuzin, genistein, afromozin, formononetin, orobol, tektorigenin, maakiain and medicarpin. PPC from a culture of cells doesn't influence on a level of cholesterol in blood, that apparently is caused by an absence of mono- and dimeric stilbenes in its structure.