Cytotoxic constituents from <i>Vicia monantha</i> subsp. <i>monantha</i> seeds

<p>Chemical investigation of <i>Vicia monantha</i> subsp. <i>monantha</i> Retz. revealed isolation of one new hydroxy- fatty acid (<b>6</b>) identified as (6-<i>Z</i>, 10-<i>E</i>)-9-hydroxy henicosa-6,10-dienoic acid in addition to six known metabolites; hexadecanoic acid (<b>1</b>), β-sitosterol (<b>2</b>), β-amyrin (<b>3</b>), β-sitosterol-glucoside (<b>4</b>), 2,3-dihydroxypropyl tetradecanoate (<b>5</b>) and (Z)-9-hydroxypentadec-6-enoic acid (<b>7</b>). The cytotoxic effect of the isolated compounds was assessed by MTT assay using lung cancer A-549, prostate cancer PC3, breast cancer MCF-7, colon cancer HCT-116 and liver cancer HepG2 cell lines. Only compounds <b>1</b>, <b>2</b>, and <b>4</b> showed cytotoxic effect on HCT-116 cells where compound <b>2</b> was the most active with IC₅₀ value of 22.61 μg/mL. In addition, compounds <b>1</b>, <b>2</b>, <b>3</b>, and <b>4</b> showed promising cytotoxic effect on MCF-7 cells with IC₅₀ values of 21.03, 15.42, 10.089, and 11.34 μg/mL, respectively.</p

Mangostanaxanthone VIII, a new xanthone from <i>Garcinia mangostana</i> and its cytotoxic activity

<p>A new prenylated xanthone, mangostanaxanthone VIII (<b>7</b>) and six known metabolites: gartanin (<b>1</b>), 1,3,8-trihydroxy-2-(3-methyl-2-butenyl)-4-(3-hydroxy-3-methylbutanoyl)-xanthone (<b>2</b>), rubraxanthone (<b>3</b>), 1,3,6,7-tetrahydroxy-8-prenylxanthone (<b>4</b>), garcinone C (<b>5</b>), and xanthone I (9-hydroxycalabaxanthone) (<b>6</b>) were separated from the EtOAc-soluble fraction of the air-dried pericarps of <i>Garcinia mangostana</i> (Clusiaceae). Their structures have been verified on the basis of spectroscopic data analysis as well as comparison with the literature. The cytotoxic activity of <b>7</b> was assessed against MCF7, A549, and HCT116 cell lines using sulforhodamine B (SRB) assay. Compound <b>7</b> showed significant cytotoxic potential against MCF7 and A549 cell lines with IC₅₀s 3.01 and 1.96 μM, respectively compared to doxorubicin (0.06 and 0.44 μM, respectively). However, it exhibited moderate activity towards HCT116 cell line.</p

Isolation of Antiosteoporotic Compounds from Seeds of <i>Sophora japonica</i>

<div><p>Chemical investigation of <i>Sophora japonica</i> seeds resulted in the isolation of seven metabolites identified as: genistin (<b>1</b>), sophoricoside (<b>2</b>), sophorabioside (<b>3</b>), sophoraflavonoloside (<b>4</b>), genistein 7,4’-di-<i>O</i>-<i>β</i>-D-glucopyransoide (<b>5</b>), kaempferol 3-<i>O</i>-<i>α</i>–L-rhamnopyranosyl(1→6)<i>β</i>-D-glucopyranosyl(1→2)<i>β</i>-D-glucopyranoside (<b>6</b>) and rutin (<b>7</b>). Compounds <b>1</b>, <b>2</b> and <b>5</b> showed significant estrogenic proliferative effect in MCF-7 cell in sub-cytotoxic concentration range. Compounds <b>1</b> and <b>2</b> showed minimal cell membrane damaging effect using LDH leakage assay. Accordingly, compound <b>2</b> (sophoricoside, (SPH)) was selected for further <i>in-vivo</i> studies as a potential anti-osteoporosis agent. The anti-osteoporotic effect of SPH was assessed in ovarectomized (OVX) rats after oral administration (15 mg/kg and 30 mg/kg) for 45 days compared to estradiol (10 µg/kg) as a positive control. Only in a dose of 30 mg/kg, SPH regained the original mechanical bone hardness compared to normal non-osteoporotic group. However, SPH (15 mg/kg) significantly increased the level of alkaline phosphatase (ALP) to normal level. Treatment with SPH (30 mg/kg) increased the level of ALP to be higher than normal group. SPH (15 mg/kg) did not significantly increase the serum level of osteocalcin (OC) compared to OVX group. On the other hand, treatment with SPH (30 mg/kg) significantly increased the level of OC to 78% higher than normal non-ovarectomized animals group. In addition, SPH (15 mg/kg) decreased the bone resorption marker, acid phosphatase (ACP) to normal level and SPH (30 mg/kg) further diminished the level of serum ACP. Histopathologically, sophoricoside ameliorated the ovarectomy induced osteoporosis in a dose dependent manner. The drug showed thicker bony trabeculae, more osteoid, and more osteoblastic rimming compared to OVX group.</p></div

Cytotoxicity assessment of compounds isolated from <i>S. Japonica</i> using trypan blue exclusion assay.

<p>Cytotoxicity assessment of compounds isolated from <i>S. Japonica</i> using trypan blue exclusion assay.</p

Chemical structure for compounds isolated from <i>Sophora japonica</i> seeds.

<p>Chemical structure for compounds isolated from <i>Sophora japonica</i> seeds.</p

Histopathological assessment of the anti-osteoporosis effect of sophoricoside.

<p>Normal group (A) shows normal bony tissue with intact well-formed dense trabeculae (star in the inner panel) with osteoblastic rimming (arrow) and average intervening bone marrow. OVX group (B) showed scant, disconnected (arrow in inner panel), thin (arrow in the outer panel), and widely separated trabeculae (double-headed arrow in the outer panel) with eroded surface (star in the outer panel). Estrogen treated group (C) showed widely distributed osteoid and osteoblastic rimming (arrow). SPH-15 group (D) showed thick trabeculae (double-headed arrow), more osteoid, and osteoblastic activity (arrow). SPH-30 group (E) showed thick trabeculae (double-headed arrow), more osteoid and osteoblastic activity (arrow).</p

Mechanical and biochemical assessment for anti-osteoporosis effect of sophoricoside <i>in-vivo.</i>

<p>Ovariectomized rats were treated with SPH (15 mg/kg and 30 mg/kg) for 6 weeks and compared to E₂ treated animals (10 µg/kg) and sham-operation group. Mechanical hardness was evaluated using hardness tester along (A) and perpendicular (B) to femur bone shaft. Biochemical assessment of osteoporosis was evaluated by measuring serum alkaline phosphatase (C) and osteocalcin (D) at the end of treatment period.</p

Assessing the estrogenic properties of compounds isolated from <i>S. japonica</i> in estrogen dependent MCF-7 cell line.

<p>Sub-cytotoxic concentrations of the isolated compounds were determined using LDH leakage assay (A); and proliferative effect was determined using SRB assay (B).</p