Immunostaining of GFAP for reactive astrocytes in hippocampus at 4, 5 and 6 months post-lesion.

<p>(A1–A2) In the normal brain, GFAP staining (brown) showed slim astrocyte morphology and HE staining showed normal neuron (blue) number. Higher magnification of insert was presented in A2. (B1–B2) Simvastatin-treated group exhibited astrocytic hypertrophy and moderate reduction in neurons. (C1–C2) Animals with KA-lesion followed by saline administration showed pronounced up-regulation of GFAP expression. GFAP-positive astrocytes exhibited hypertrophy and atrophied processes. The number of neuron was also severely reduced. (D–E) Quantification of GFAP-positive cells in DH area of hippocampus. Scale bar = 400 µm in C1 (applies to A1, B1, C1); scale bar = 100 µm in C2 (applies to A2, B2, C2). (* P<0.05, vs. the control group; # P<0.05, vs. the saline-treated group).</p

Comparison of KA-lesion induced MFS using Timm's staining in DH.

<p>The extent of aberrant MFS in saline-treated group with severe hippocampal injury (A1and A2), simvastatin-treated group with moderate hippocampal injury (B1 and B2) and in comparison with rats with intracerebroventricular saline injection (C1 and C2), visualized by Timm's histochemical staining. Quantitative data for width and density of sprouting into DSGL were presented in (D and E). GCL, granule cell layer, UB, upper blade; LB, lower blade. Scale bars = 500 µm in A1 and 200 µm in A2. (*P<0.05, vs. the simvastatin-treated group).</p

Hippocampal cytoarchitecture visualized with Nissl staining.

<p>A1, A2, A3 and A4 showed hippocampal regions from rats with intracerebroventricular saline injection. B1, B2, B3 and B4 showed regions of hippocampus from KA-injured rat followed by simvastatin treatment. C1, C2, C3 and C4 showed hippocampal regions from KA-injured rat followed by saline-treatment. D showed quantitative data of the number of neurons in DH and CA3. scale bar = 400 µm in A1 (applies to B1, C1, A3, B3, C3); scale bar = 100 µm in A2 (applies to B2, C2, A4, B4, C4 ). (* P<0.05, vs. control group, # P<0.05, vs simvastatin-treated group).</p

Simvastatin altered the expression level of IL-1β and TNF-α.

<p>Bar graphs showed the level of IL-1β (A), TNF-α (B), and IL-6 (C) in the hippocampus 3 days post KA-lesion. KA-injured rats were treated with simvastatin or saline for 3 days. Data were presented as means±standard deviation. *P<0.05 versus control group; #P<0.05 versus the saline group. IL-1β and TNF-α expression was decreased at day 3 after simvastatin treatment compared with that in saline-treated group. However, simvastatin did not suppress the expression of IL-6 compared with the saline-treated group.</p

Simvastatin-treatment decreased the frequency of abnormal spikes of epileptic brain.

<p>Representative EEG recordings from saline-treated group and simvastatin-treated group at 4 months (A), 5 months (B) and 6 months (C). Quantitative data was presented in (D). *P<0.05, vs. the saline-treated group.</p

Additional file 2: of Grifolic acid induces GH3 adenoma cell death by inhibiting ATP production through a GPR120-independent mechanism

The effects of PI3K inhibitor, ERK1/2 inhibitor and p53 inactivator on GH3 cells. PI3K inhibitor Wortmannin (0.1μmol/L), ERK1/2 inhibitor U-0126 (1 μmol/L), and p53 inactivator cyclic pifithrin-α, p-nitro (1 μmol/L) did not induce cell death in GH3 cells respectively, as measured by MTT assay. (P = 0.58, n = 12) (JPG 2759 kb

Additional file 1: of Grifolic acid induces GH3 adenoma cell death by inhibiting ATP production through a GPR120-independent mechanism

The structure of grifolic acid. (JPG 153 kb

Constitutive expression of miR-122 in cervical epithelial carcinoma cells.

<p>The constitutive expression of miR-122 were separately detected in several cell lines by RT-qPCR. U6 was employed as control.</p

Primers sequences list.

<p>Primers sequences list.</p

Inhibition effects of miR-122 on SOCS1 mRNA.

<p>(A–B) Inhibition of SOCS1 by transfecting miR-122 in SiHa cells, detected by RT-qPCR and western blotting at 24 h, 48 h and 72 h separately. (C–D) Up-regulation of SOCS1 by transfecting AMO-122 in SiHa cells at 24 h, 48 h and 72 h separately. (*<i>p</i><0.05, **<i>p</i><0.01).</p