8 research outputs found
DMY inhibits T cells proliferation <i>ex</i><i>vivo</i> and T cells infiltration into mouse liver tissues.
<p>(A) Splenic CD4<sup>+</sup> T cells were purified from male ICR mouse and stimulated with vehicle alone or anti-CD3/anti-CD28 mAbs plus 0, 25, 50, or 100 Ī¼M of DMY for 48 h. [<sup>3</sup>H]Thymidine incorporation in T cells was determined. (B) The concentration of IL-2 in cultural media of T cells was determined by ELISA. (C) Immunohistochemistry analysis of mouse liver tissues against CD4 mAb. Data are mean Ā± SEM, <i>n</i> = 3. Means without a common letter differ, <i>P</i> < 0.05.</p
The effect of DMY treatment on NF-ĪŗB and MAPK signaling pathway in LPSāstimulated macrophages.
<p>Cells were pre-treated with 50 Ī¼M DMY for 1 h, then with LPS treatment for 2, 4, and 8 h. Western blot analysis of (A) Phospho- and total IKK, IĪŗBĪ±, JNK1/2 and ERK1/2 levels. (B) Immunofluorescence staining of nuclear translocation of NF-ĪŗB(p65) protein. Cells were stained with DAPI (nuclear marker, blue) and rabbit anti-p65 antibody (red).</p
Working hypothesis of the metabolic mechanisms of LPS/D-GalNā induced hepatic toxicity and protection by DMY.
<p>Symbol circle and square represent the relative metabolite changes in the LPS/D-GalNāchallenged group and the DMY treatment group, respectively. The decrease, increase and no difference in levels with statistical significance are presented in green, red and tan, respectively.</p
The effect of DMY treatment on Jak/STAT signaling pathway in LPSāstimulated macrophages.
<p>Cells were pre-treated with 50 Ī¼M DMY for 1 h, then with LPS treatment for 2, 4, and 8 h. Western blot analysis of (A) Phospho- and total Jak2 and STAT1 levels, (B) Total STAT3, phospho-STAT3, and SOCS3 levels and the levels of STAT3 and phospho-STAT3 in nuclear and cytosolic fractions. PARP and Ī±-tubulin were used as internal control of nuclear and cytosolic proteins, respectively.</p
Immunohistochemistry of liver tissues from LPS/D-GalNāchallenged mice with or without DMY pretreatment.
<p>Immunofluorescence staining and quantification of DMY inhibiting STAT3 and F4/80 (macrophage) infiltration (A) and Ly6G (neutrophil) infiltration (B) in LPS/D-GalNātreated mouse liver. Data are mean Ā± SEM, <i>n</i> = 4. Means without a common letter differ, <i>P</i> < 0.05.</p
Protective effects of DMY on LPS/D-GalNāinduced acute liver dysfunction in mice.
<p>Mice were pretreated with DMY (1 and 10 mg/kg) for three consecutive days, then LPS/D-GalN for 8 h. (A) Serum levels of AST and ALT with or without treatment. Data are mean Ā± SEM, <i>n</i> = 6. Means without a common letter differ, <i>P</i> < 0.05. (B) Hematoxylin and eosin staining of mouse livers. (C) TUNEL assay of apoptosis in mouse liver with LPS/D-GalN challenge or DMY treatment. Representative image of each treatment group is shown. Brownish cells are TUNEL-positive apoptotic cells. (D) Survival rate of LPS/D-GalN-challenged mice with or without DMY-pretreatment. <sup>*,# </sup><i>P</i> < 0.05, significant differences within treatment groups and the LPS/D-GalN group (log rank test).</p
Comparative metabolomic analysis of mouse serum.
<p>Score plots (A, C) and corresponding loading plots (B, D) for PCA of UPLC/QTOF MS data from mice treated with vehicle control, LPS/D-GalN, and LPS/D-GalNāchallenged mice pretreated with DMY1 and DMY10 (<i>n</i> = 3 in each group). <i>Dashed </i><i>circles</i> group pairs of samples from LPS/D-GalNāchallenged group vs. other treatment groups. The ions most responsible for the variance of the score plots are indicated by their distance from the origin. The metabolites are labeled according their retention times in the chromatogram and <i>m</i>/<i>z</i> values. </p
Anti-inflammatory Lanostanoids and Lactone Derivatives from <i>Antrodia camphorata</i>
Four new lanostanoids, ethyl lucidenate
A (<b>1</b>), ethyl
lucidenate F (<b>2</b>), 15-<i>O</i>-acetylganolucidate
A (<b>3</b>), and 3,11,15,23-tetraoxo-27Ī¾-lanosta-8,16-dien-26-oic
acid (<b>4</b>), and two new lactone derivatives, 5-hydroxy-5-(methoxymethyl)-4-methylfuran-2Ā(5<i>H</i>)-one (<b>5</b>) and 3-(4-methoxy-2-oxo-2<i>H</i>-pyran-6-yl)Āpropanoic acid (<b>6</b>), together with
four known compounds, 11Ī±-hydroxy-3,7-dioxolanost-8,24Ā(<i>E</i>)-dien-26- oic acid (<b>7</b>), 3,7,11-trioxo-5Ī±-lanosta-8,24Ā(<i>E</i>)-dien-26-oic acid (<b>8</b>), methyl 3,7,11,12,15,23-hexaoxo-5Ī±-lanost-8-en-26-oate
(<b>9</b>), and ethyl 3,7,11,12,15,23-hexaoxo-5Ī±-lanost-8-en-26-oate
(<b>10</b>), were characterized from <i>Antrodia camphorata</i>. The structures of these new compounds were determined by analysis
of their spectroscopic data, including 1D and 2D NMR experiments.
Ten components were evaluated for anti-inflammatory activity by examining
their effect on LPS-iNOS-dependent NO production in murine macrophage
(RAW 264.7) cells. Among them, compounds <b>1</b>, <b>3</b>, <b>7</b>, <b>8</b>, <b>9</b>, and <b>10</b> significantly suppressed the NO concentration in LPS-treated RAW
264.7 cells with IC<sub>50</sub> values ā¤ 10 Ī¼M