Journal: iScience

Article Title: Increased SIRT3 combined with PARP inhibition rescues motor function of SBMA mice

doi: 10.1016/j.isci.2023.107375

Figure Lengend Snippet: SIRT3 and SOD2 proteins are reduced in AR100Q mice, and activating and increasing SIRT3 reduces ROS and cell death in vitro (A) Western analysis of quadriceps from 11 week-old WT, AR24Q, and AR100Q male mice (n = 3). Top, total SOD2 with tubulin loading control, and densitometry analysis of total SOD2 compared to tubulin. Bottom, a second SDS-PAGE gel probed for acetylated (acetyl-K68) SOD2 with tubulin loading control, and densitometry analysis of acetyl-K68/total SOD2 (from A top) after each were normalized to tubulin loading control. (B) Western analysis of quadriceps from 11 week-old WT, AR24Q, and AR100Q male mice (n = 3). Endogenous SIRT3 and tubulin loading control with densitometry analysis of SIRT3 normalized to tubulin loading control. (C) ROS levels in AR112Q expressing PC12 cells (n = 12) treated with 10 nM DHT plus either DMSO (vehicle control), 1 μM viniferin, 1 μM honokiol, or 100 μM melatonin for 48 h (representative image from 3 experiments). (D) Cell death of AR100Q expressing C2C12 myotubes (n = 3) treated with either DMSO (vehicle control), 1 μM viniferin, 1 μM honokiol, or 100 μM melatonin for 10 days (representative image from 3 experiments). (E) Left, immunoblot of MYC-tagged SIRT3, and tubulin in AR112Q SIRT3-MYC-overexpressing PC12 cells (n = 3). Right, ROS levels in AR112Q SIRT3-MYC-overexpressing PC12 cells (n = 12) after 48 h of DHT treatment (representative image from 3 experiments). (F) Left, immunoblot of MYC-tagged SIRT3, and tubulin loading control from AR100Q SIRT3-MYC-overexpressing C2C12 myoblasts (n = 3). Right, percent cell death of AR100Q SIRT3-MYC-overexpressing C2C12 myoblasts (n = 3) (LDH assay) (representative image from 3 experiments). ∗∗ = Nested two-way t-test, p ≤ 0.01. (A–F) All statistical analysis show mean ± SD, and used a two-way ANOVA and Tukey’s post-hoc (∗ = p ≤ 0.05, ∗∗ = p ≤ 0.01, ∗∗∗ = p ≤ 0.001) unless otherwise noted. WT = wild type, AR24Q = non-polyQ-expanded AR, AR100Q = polyQ-expanded AR, EV = empty vector, SIRT3 = SIRT3-myc-his overexpression, SIRT3-H248Y = SIRT3-myc-his overexpression (deacetylase inactive).

Article Snippet: Cells were treated with honokiol (Tocris), viniferin (Carbosynth), melatonin (Tocris), olaparib (Selleck Chemicals), or a DMSO control for 48 or 96 h before undergoing specific assays.

Techniques: In Vitro, Western Blot, Control, SDS Page, Expressing, Lactate Dehydrogenase Assay, Plasmid Preparation, Over Expression, Histone Deacetylase Assay

Journal: iScience

Article Title: Increased SIRT3 combined with PARP inhibition rescues motor function of SBMA mice

doi: 10.1016/j.isci.2023.107375

Figure Lengend Snippet:

Article Snippet: Cells were treated with honokiol (Tocris), viniferin (Carbosynth), melatonin (Tocris), olaparib (Selleck Chemicals), or a DMSO control for 48 or 96 h before undergoing specific assays.

Techniques: Recombinant, Electron Microscopy, Protease Inhibitor, Lactate Dehydrogenase Assay, Bioassay, Negative Control, DC Protein Assay, Transgenic Assay, Software

Journal: Neural Regeneration Research

Article Title: Neuroprotective mechanisms of ε-viniferin in a rotenone-induced cell model of Parkinson's disease: significance of SIRT3-mediated FOXO3 deacetylation

doi: 10.4103/1673-5374.282264

Figure Lengend Snippet: ε-Viniferin alleviates rotenone-induced mitochondrial depolarization. (A) Depolarization of the mitochondrial membrane potential was shown by red/green fluorescence with JC-1 dye. Compared with the model group, the ratio of red/green fluorescence was markedly higher in the ε-viniferin treatment group, whereas the ratio of red/green fluorescence in the ε-viniferin + SIRT3 shRNA or ε-viniferin + FOXO3 shRNA groups was lower than in the ε-viniferin treatment group. Scale bar: 50 μm. (B) The apoptotic rate induced by mitochondrial depolarization was detected by flow cytometry and JC-1 dye. ε-Viniferin alleviated rotenone-induced mitochondrial depolarization. However, the neuroprotective effect of ε-viniferin on mitochondrial membrane potential was significantly attenuated when cells were pre-transfected with either SIRT3 or FOXO3 shRNA. (C) The apoptotic rate induced by mitochondrial depolarization was detected by flow cytometry. Data are shown as the mean ± SD. * P < 0.05, vs . model group; # P < 0.05, vs . ε-viniferin treatment group (one-way analysis of variance followed by Bonferroni test). VFN: ε-Viniferin.

Article Snippet: Next, ε-viniferin (Wako Pure Chemical Industries, Osaka, Japan) was used as a therapeutic agent, and its ability to attenuate rotenone-induced neurotoxicity in the PD SH-SY5Y cell model was investigated.

Techniques: Fluorescence, shRNA, Flow Cytometry, Transfection

Journal: Neural Regeneration Research

Article Title: Neuroprotective mechanisms of ε-viniferin in a rotenone-induced cell model of Parkinson's disease: significance of SIRT3-mediated FOXO3 deacetylation

doi: 10.4103/1673-5374.282264

Figure Lengend Snippet: ε-Viniferin decreases rotenone-induced oxidative stress and increases ATP production. (A, B) Intracellular ROS generation in cells was evaluated by flow cytometry using DCFH-DA. (C) ATP content was evaluated using an ATP assay. ε-Viniferin alleviated rotenone-induced ROS generation and ATP depletion. However, the protective effect of ε-viniferin was significantly decreased when cells were pre-transfected with either SIRT3 or FOXO3 shRNA. Data are shown as the mean ± SD. * P < 0.05, vs . model group; # P < 0.05, vs . ε-viniferin treatment group (one-way analysis of variance followed by Bonferroni test). VFN: ε-Viniferin.

Article Snippet: Next, ε-viniferin (Wako Pure Chemical Industries, Osaka, Japan) was used as a therapeutic agent, and its ability to attenuate rotenone-induced neurotoxicity in the PD SH-SY5Y cell model was investigated.

Techniques: Flow Cytometry, ATP Assay, Transfection, shRNA

Journal: Neural Regeneration Research

Article Title: Neuroprotective mechanisms of ε-viniferin in a rotenone-induced cell model of Parkinson's disease: significance of SIRT3-mediated FOXO3 deacetylation

doi: 10.4103/1673-5374.282264

Figure Lengend Snippet: ε-Viniferin mitigates rotenone-induced apoptosis. Flow cytometry of apoptosis in cells exposed to rotenone. The dot-plot display yield from Annexin V-FITC/PI is shown. Representative histograms and graphs of flow cytometry show the apoptotic rate. ε-Viniferin alleviated rotenone-induced apoptosis. However, the protective effect of ε-viniferin was significantly decreased when cells were pre-transfected with either SIRT3 or FOXO3 shRNA. Data are shown as the mean ± SD. * P < 0.05, vs . model group; # P < 0.05, vs . ε-viniferin treatment group (one-way analysis of variance followed by Bonferroni test). VFN: ε-Viniferin.

Article Snippet: Next, ε-viniferin (Wako Pure Chemical Industries, Osaka, Japan) was used as a therapeutic agent, and its ability to attenuate rotenone-induced neurotoxicity in the PD SH-SY5Y cell model was investigated.

Techniques: Flow Cytometry, Transfection, shRNA

Journal: Neural Regeneration Research

Article Title: Neuroprotective mechanisms of ε-viniferin in a rotenone-induced cell model of Parkinson's disease: significance of SIRT3-mediated FOXO3 deacetylation

doi: 10.4103/1673-5374.282264

Figure Lengend Snippet: FOXO3 deacetylation induced by ε-viniferin promotes SIRT3 expression and FOXO3 nuclear localization. (A) Expression of SIRT3 after ε-viniferin treatment. The expression and distribution of SIRT3 was detected using immunofluorescence staining for SIRT3 (red staining by Alexa Fluor 568) and DAPI (blue), and merged. Scale bar: 50 μm. (B) Fractionated cellular extracts (cytosolic, nuclear, and mitochondrial fractions) were prepared in the ε-viniferin treatment, control, and model groups. FOXO3 in the ε-viniferin treatment group was prone to nuclear localization compared with the model and control groups. These results suggest that ε-viniferin promotes FOXO3 nuclear localization by activating SIRT3. (C) ε-Viniferin significantly promoted SIRT3 expression compared with the model and control groups. Data are shown as the mean ± SD. † P < 0.05, vs . model and control groups (one-way analysis of variance followed by Bonferroni test). VFN: ε-Viniferin.

Article Snippet: Next, ε-viniferin (Wako Pure Chemical Industries, Osaka, Japan) was used as a therapeutic agent, and its ability to attenuate rotenone-induced neurotoxicity in the PD SH-SY5Y cell model was investigated.

Techniques: Expressing, Immunofluorescence, Staining

Journal: Neural Regeneration Research

Article Title: Neuroprotective mechanisms of ε-viniferin in a rotenone-induced cell model of Parkinson's disease: significance of SIRT3-mediated FOXO3 deacetylation

doi: 10.4103/1673-5374.282264

Figure Lengend Snippet: ε-Viniferin drives the expression of mitochondrial homeostasis-related proteins. Western blot assays demonstrated that ε-viniferin treatment increases the expression levels of mitochondrial biosynthesis-related proteins (PGC-1α and TFAM); mitochondrial fusion and fission proteins (DRP1, MFN2, and FIS1), and mitophagy-related proteins (BNIP3, NIX, and Parkin), and decreases the expression levels of P62. Data are shown as the mean ± SD. # P < 0.05, vs . ε-viniferin treatment group (one-way analysis of variance followed by Bonferroni test). 1: Model group; 2: ε-viniferin treatment group; 3: ε-viniferin + SIRT3 shRNA group; 4: ε-viniferin + FOXO3 shRNA group; 5: ε-viniferin + control shRNA group. VFN: ε-Viniferin.

Article Snippet: Next, ε-viniferin (Wako Pure Chemical Industries, Osaka, Japan) was used as a therapeutic agent, and its ability to attenuate rotenone-induced neurotoxicity in the PD SH-SY5Y cell model was investigated.

Techniques: Expressing, Western Blot, shRNA

Journal: Neural Regeneration Research

Article Title: Neuroprotective mechanisms of ε-viniferin in a rotenone-induced cell model of Parkinson's disease: significance of SIRT3-mediated FOXO3 deacetylation

doi: 10.4103/1673-5374.282264

Figure Lengend Snippet: Mitophagy was observed by transmission electron microscopy. Autophagic vacuoles and typical mitophagy structures (black arrow) were observed in the ε-viniferin treatment group (A) compared with the control group (B). In the model group (C), mitochondria were obviously swollen following rotenone treatment, suggesting mitochondrial dysfunction. Scale bars: 500 nm.

Article Snippet: Next, ε-viniferin (Wako Pure Chemical Industries, Osaka, Japan) was used as a therapeutic agent, and its ability to attenuate rotenone-induced neurotoxicity in the PD SH-SY5Y cell model was investigated.

Techniques: Transmission Assay, Electron Microscopy

Journal: Foods

Article Title: A Comparative Study of the Influence of Various Fungal-Based Pretreatments of Grape Pomace on Phenolic Compounds Recovery

doi: 10.3390/foods11111665

Figure Lengend Snippet: Content of individual phenolic compounds in GP extract obtained before SSF (at ‘0’ day, C o ) and after SSF (max. content of phenolic compounds in GP extract regardless of duration SSF and used microorganism, C i, max. ).

Article Snippet: Quercetin, 3,4-dihydroxybenzoic acid, and vanillic acid were obtained from Acros Organics (Geel, Belgium). ε-Viniferin was obtained from AppliChem (Darmstadt, Germany).

Techniques:

Journal: Foods

Article Title: A Comparative Study of the Influence of Various Fungal-Based Pretreatments of Grape Pomace on Phenolic Compounds Recovery

doi: 10.3390/foods11111665

Figure Lengend Snippet: UHPLC chromatograms of phenolic compounds in GP extracts after 1, 10 and 15 days of SSF with CS: (1) gallic acid, (2) 3.4-dihydroxybenzoic acid, (3) p -hydroxybenzoic acid, (4) procyanidin B1, (5) vanillic acid, (6) syringic acid, (7) procyanidin B2, (8) p -coumaric acid, (9) gallocatechin gallate, (10) ferulic acid, (11) epicatechin gallate, (12) o -coumaric acid, (13) ellagic acid, (14) resveratrol, (15) quercetin, (16) ε-viniferin, (17) kaempferol.

Article Snippet: Quercetin, 3,4-dihydroxybenzoic acid, and vanillic acid were obtained from Acros Organics (Geel, Belgium). ε-Viniferin was obtained from AppliChem (Darmstadt, Germany).

Techniques:

Journal: Foods

Article Title: A Comparative Study of the Influence of Various Fungal-Based Pretreatments of Grape Pomace on Phenolic Compounds Recovery

doi: 10.3390/foods11111665

Figure Lengend Snippet: Dimensionless content ( C = C i / C o ) of resveratrol ( a , b ) and ε-viniferin ( c , d ) in GP extracts before biological treatment (‘0’ day) and after 1–15 days of biological treatment with TV6, TV8, TV AG613, GL, GR, RO ( a , c ), and PC, CS, PE, HG, TG ( b , d ).

Article Snippet: Quercetin, 3,4-dihydroxybenzoic acid, and vanillic acid were obtained from Acros Organics (Geel, Belgium). ε-Viniferin was obtained from AppliChem (Darmstadt, Germany).

Techniques: