Oleanolic acid (OA) inhibits the development of lung metastasis.

<p>Groups of mice, injected into the tail veins with B16F10 melanoma cells, were treated with saline, DMSO, OA (5 mg kg⁻¹ day⁻¹) or OA (10 mg kg⁻¹ day⁻¹), as described in the M&M section and in the upper panel; the number of lung metastasis was counted on day 18 (lower panel). Results are expressed as mean ± SD of the number of metastasis. * indicates <i>p</i><0.001 in relation to the control (DMSO).</p

Western blot analysis.

<p>A549 cells were treated with medium or with 50 µg/mL Oleanolic acid for 24 h and whole cell extracts were obtained as described in M&M. Proteins were separated by SDS-PAGE, transferred to PDF membranes, probed with antibodies to Bcl-2, Bax, Survivin, VEGF or α-tubulin and developed with ECL, as described in M&M. Numbers represent band intensity in relation to α-tubulin.</p

Non-small cell lung cancer cell lines express MRP1/ABCC1 activity.

<p>For P-gp/ABCB1 activity, A549 or H460 cells were incubated for 30 min with medium (AF) or 400 nM Rhodamine 123 in the absence (Rho) or presence of 50 µM verapamil (VP), For MRP1/ABCC1, cells were incubated with 5 µM CFDA in the absence (CF) or presence of 50 µM MK-571 (MK). After washing, cellular fluorescence was measured by flow cytometry. Histograms are representative of three independent experiments performed in duplicate.</p

Oleanolic acid (OA) decreases cell viability and induces apoptosis of non-small cell lung cancer cell lines.

<p>A549 or H460 cells were incubated with various OA concentrations (10, 25, 40 or 50 µg/mL or 21.9, 54.7, 87.6 or 109.5 µM) or cisplatin for 48 h. (<b>A</b>) Cell viability was assessed by MTT and plotted as percentage of cell viability inhibition. Results represent mean ± SD of 4 experiments performed in triplicate. (<b>B</b>) In parallel, cells were treated with a hypotonic solution containing propidium iodide (PI) and DNA-content was analyzed by flow cytometry. Upper panel: representative histogram of the cell cycle. Lower panel: percentage of apoptotic sub-G1 cells. Values represent mean ± SD of 3 experiments performed in triplicate. (<b>C</b>) <b>C</b>aspase-3 activated cells was determined by flow cytometry using a CaspGlow kit as described in M&M. Histograms are representative of two independent experiments performed in duplicate.</p

ZAC1, SSTR2 and SSTR3 expression in NFPA, somatotropinomas and normal pituitaries.

<div><p>Comparison of <i>ZAC1</i> (A), <i>SSTR2</i> (B) and <i>SSTR3</i> (C) mRNA expression levels among normal pituitaries (NP), somatotropinomas (somatotroph) and non-functioning pituitary adenomas (NFPA). The outliers were excluded.</p> <p>The Kruskall-Wallis test was used to compare the mRNA expression among the three groups and the Mann-Whitney test for comparison between NFPA and normal pituitaries and somatotropinomas.</p></div

Lung mechanics.

<p>Lung static elastance (<i>Est</i>,<i>L</i>). Resistive pressure (ΔP1) and viscoelastic pressure (ΔP2). White bars: DMSO; gray bars: DAS. Values are means (± SD) of 8–9 animals per group. *Significantly different from C-DMSO group (<i>p <</i> 0.05). #DMSO <i>vs</i>. DAS (<i>p <</i> 0.05).</p

Renal Function Parameters.

<p>Renal Function Parameters.</p

Mild glomerular morphologic changes are observed in Pla2g5^−/− mice.

<p>PAS reagent was used for analysis of the mesangial surface of corticomedullary (A, B) and subcapsular glomeruli (C, D), as described in the Materials and Methods. Representative photomicrographs (magnification 40×) of (A) the corticomedullary glomerulus and (C) the subcapsular glomerulus. (B) Quantitative analysis of the corticomedullary and (D) subcapsular glomeruli (n = 6 per group). The results are expressed as means ± SE. *Statistically significant in relation to WT mice (P < 0.05).</p

GV sPLA2 upregulates activity and expression of cortical (Na+ + K+)-ATPase.

<p>Expression and activity of (Na⁺ + K⁺)-ATPase in WT and <i>Pla2g-5</i>^{<i>−/−</i>} mice. ATPase activity from the renal cortex (A) and medulla homogenate (C) was determinate by the colorimetric method. Immunoblotting was performed for the (Na⁺ + K⁺)-ATPase α1 subunit in (B) the renal cortex and (D) the medullar preparation of both WT and <i>Pla2g5</i>^{<i>−/−</i>} mice, as described in the Materials and Methods (<i>n</i> = 8 per group). The results are expressed as means ± SE. *Statistically significant in relation to WT mice (<i>P</i> < 0.05).</p

Study design.

<p>Thirty-four C57BL6 female mice (8–12 weeks, 20–25 g) were divided into two groups: control group (C, n = 16) instilled with sterile saline (50 μL, intratracheally [i.t.]) and silicosis group (SIL, n = 18), instilled with silica particle (20mg in 50 μL saline, i.t.). Fourteen days after disease induction, the animals were randomized to receive a solution of dimethyl sulfoxide (DMSO 1% in saline solution, 100 μL, oral gavage, n = 8/9) or dasatinib (DAS 1 mg/kg body weight in DMSO 1%, 100 μL, oral gavage, n = 8/9).</p