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opencc-by-4.0May 2023View details →

Underlying data for Evaluation of the effect of Modern Sulfonylureas on Oxidative Stress and Hepatorenal Function among Type 2 Diabetic Patients beyond Glycemic Control: an observational study

Underlying data for Evaluation of the effect of Modern Sulfonylureas on Oxidative Stress and Hepatorenal Function among Type 2 Diabetic Patients beyond Glycemic Control: an observational study

opencc-by-4.0Jun 2023View details →

Mammalian animal & human retinal organ culture as pre-clinical model to evaluate oxidative stress and antioxidant intraocular therapeutics

Oxidative stress (OS) is involved in the pathogenesis of retinal neurodegenerative diseases like age-related macular degeneration (AMD) and diabetic retinopathy (DR) and an important target of therapeutic treatments. New therapeutics are tested in vivo despite limits in transferability and ethical concerns. Retina cultures using human tissue can deliver critical information and significantly reduce the number of animal experiments along with increased transferability. We cultured up to 32 retina samples derived from one eye, analyzed models’ quality, induced OS, and tested efficiency of antioxidative therapeutics. Bovine, porcine, rat, and human retinae were cultured in different experimental settings for 3-14 d. OS was induced by high-glucose or hydrogen peroxide (H2O2) and treated by Scutellarin, pigment epithelium-derived factor (PEDF), and/or granulocyte macrophage-colony stimulating factor (GM-CSF). Tissue morphology, cell viability, inflammation, and glutathione level were determined. Retina samples showed only moderate necrosis (23.83±5.05 increased to 27.00±1.66 AU PI-staining over 14 d) after 14 days in culture. OS was successfully induced (reduced ATP content of 288.3±59.9 vs. 435.7±166.8 nM ATP in controls); antioxidants reduced OS-induced apoptosis (from 124.20±51.09 to 60.80±319.66 cells/image after Scutellarin-treatment). Enhanced mammalian animal and human retina cultures allow reliable, highly transferable research on OS-triggered age-related diseases and pre-clinical testing during drug development.

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Camponotus fellah cDNA lists for: Social isolation shortens lifespan through oxidative stress in ants

Social isolation negatively affects health, induces detrimental behaviors, and shortens lifespan in social species. Little is known about the mechanisms underpinning these effects because model species are typically short-lived and non-social. Using colonies of carpenter ant Camponotus fellah, we show that social isolation induces hyperactivity, alters space-use, and reduces lifespan via changes in the expression of genes with key roles in oxidation-reduction and an associated accumulation of reactive oxygen species. These physiological effects are localized to the fat body and oenocytes, which perform liver-like functions in insects. We use pharmacological manipulations to demonstrate that the oxidation-reduction pathway causally underpins the detrimental effects of social isolation on behavior and lifespan. These findings have important implications for our understanding of how social isolation affects behavior and lifespan in general.

opencc-zeroAug 2023View details →

Fig. 12 in Verniciflavanol A, a profisetinidin-type-4-arylflavan-3-ol from toxicodendron vernicifluum protects SH-SY5Y cells against H2O2-Induced oxidative stress

Fig. 12. Effects of vernicivanol A (9) on MAPKs pathway. (A) Immunoblot analysis of the indicated molecules in SH-SY5Y cells. (B) Grey intensity analysis of p-p38 and p-ERK. Data are presented as the mean SD of three independent experiments. *p <0.05 and ***p <0.001 compared with indicated control. &p <0.05 and ± &&&p <0.001 compared with the H O -treated group.

Fig. 8 in Verniciflavanol A, a profisetinidin-type-4-arylflavan-3-ol from toxicodendron vernicifluum protects SH-SY5Y cells against H2O2-Induced oxidative stress

Fig. 8. Effects of verniciflavanol A (9) on apoptosis-related proteins. (A) Immunoblot analysis of the apoptosis-related molecules in SH-SY5Y cells. (B) Grey intensity analysis of Bax/Bcl-2, Cl-PARP, and p53. Data are presented as the mean ± SD of three independent experiments. *p <0.05 and **p <0.01 compared with indicated control. &&p <0.01 and &&&p <0.001 compared with the H O -treated group.

Fig. 7 in Verniciflavanol A, a profisetinidin-type-4-arylflavan-3-ol from toxicodendron vernicifluum protects SH-SY5Y cells against H2O2-Induced oxidative stress

Fig. 7. Effects of verniciflavanol A (9) on cell apoptosis of H2O2 treated SH-SY5Y cells. (A–B) The apoptosis rate was determined by flow cytometry in SH-SY5Y cells. Data are presented as the mean SD of three independent experiments. ***p <0.001 compared with indicated control. &p <0.05 and &&p <0.01 compared with the ± H2O2-treated group.

Fig. 10 in Verniciflavanol A, a profisetinidin-type-4-arylflavan-3-ol from toxicodendron vernicifluum protects SH-SY5Y cells against H2O2-Induced oxidative stress

Fig. 10. Effects of verniciflavanol A (9) on PI3K/Akt/mTOR pathway. (A) The protein levels of PI3K/Akt/mTOR pathway in SH-SY5Y cells are analyzed by Western Blot. (B) Grey intensity analysis of p-PI3K, p-Akt, p-mTOR. Data are presented as the mean ± SD of three independent experiments. *p <0.05 and ***p <0.001 compared with indicated control. &p <0.05, &&p <0.01, and &&&p <0.001 compared with the H O -treated group.

Fig. 4 in Verniciflavanol A, a profisetinidin-type-4-arylflavan-3-ol from toxicodendron vernicifluum protects SH-SY5Y cells against H2O2-Induced oxidative stress

Fig. 4. Effects of compounds 9–12 against H2O2-induced oxidative damage in SH-SY5Y cells using MTT assay. Data are presented as the mean ± SD of three independent experiments. ***p <0.001 compared with indicated control. &p <0.05, &&p <0.01, and &&&p <0.001 compared with the H O -treated group.

Fig. 6 in Verniciflavanol A, a profisetinidin-type-4-arylflavan-3-ol from toxicodendron vernicifluum protects SH-SY5Y cells against H2O2-Induced oxidative stress

Fig. 6. Effects of verniciflavanol A (9) on mitochondrial membrane potential of H2O2 treated SH-SY5Y cells. (A) Immunofluorescence staining and (B–C) flow cytometry was employed to test mitochondrial membrane potential in SH-SY5Y cells according to kit instructions. Data are presented as the mean ± SD of three independent experiments. ***p <0.001 compared with indicated control. &p <0.05 and &&&p <0.001 compared with the H O -treated group.

Fig. 9 in Verniciflavanol A, a profisetinidin-type-4-arylflavan-3-ol from toxicodendron vernicifluum protects SH-SY5Y cells against H2O2-Induced oxidative stress

Fig. 9. Effects of verniciflavanol A (9) on Nrf2/HO-1 signaling. (A) Proteins in SH-SY5Y cells are analyzed by Western Blot. (B) Grey intensity analysis of HO-1 and Nrf2. **p <0.01 and ***p <0.001 compared with indicated control. &&p <0.01 and &&&p <0.001 compared with the H O -treated group.

Fig. 5 in Verniciflavanol A, a profisetinidin-type-4-arylflavan-3-ol from toxicodendron vernicifluum protects SH-SY5Y cells against H2O2-Induced oxidative stress

Fig. 5. Effects of verniciflavanol A (9) on intracellular ROS production of H2O2 treated SH-SY5Y cells. (A) Immunofluorescence staining and (B–C) flow cytometry was employed to test the ROS production caused by H2O2 in SH-SY5Y cells. Data are presented as the mean ± SD of three independent experiments. ***p <0.001 compared with indicated control. &p <0.05 and &&p <0.01 compared with the H O -treated group.

Fig. 8 in Melatonin mitigates UV-B stress via regulating oxidative stress response, cellular redox and alternative electron sinks in Arabidopsis thaliana

Fig. 8. Accumulation of UV-B absorbing compounds extractable with acidic methanol. Values obtained from absorbance measurements between 280 and 330 nm with 10 nm intervals were used to draw the curves. The area below each curve was used as an indicator of UV-B absorbing capacity.

Fig. 5 in Melatonin mitigates UV-B stress via regulating oxidative stress response, cellular redox and alternative electron sinks in Arabidopsis thaliana

Fig. 5. Expressions of GPX1-8 genes of UV-B treated (90 min) A. thaliana plants with or without 10 μM melatonin supplement. Experiments were repeated two times, and each data point was the mean of three replicates (n = 6). Significant differences (P <0.05) were marked with different letters (a–d) in the charts.

Fig. 4 in Melatonin mitigates UV-B stress via regulating oxidative stress response, cellular redox and alternative electron sinks in Arabidopsis thaliana

Fig. 4. Activities of APX, GR, POX (90 and 180 min) and expressions of APX1 and GR1 genes (at 90 min) of UV-B treated A. thaliana plants with or without 10 μM melatonin supplement. Experiments were repeated two times, and each data point was the mean of three replicates (n = 6). Significant differences (P <0.05) were marked with different letters (a–d) in the charts.

Fig. 1 in Melatonin mitigates UV-B stress via regulating oxidative stress response, cellular redox and alternative electron sinks in Arabidopsis thaliana

Fig. 1. TBARS and Fv/Fm (maximum efficiency of PSII) values of UV-B treated (90 and 180 min) A. thaliana plants with or without melatonin supplement. C90 and C180: control groups, UV90 and UV180: plants treated with UV-B for 90 or 180 min. M90 and M180: melatonin (10 μM), UVM90 and UVM180: UV-B + melatonin treated plants. Note that Y-axis of Fv/Fm starts from 0.5 for better reflection of differences between treatment groups.

Fig. 3 in Melatonin mitigates UV-B stress via regulating oxidative stress response, cellular redox and alternative electron sinks in Arabidopsis thaliana

Fig. 3. Native activity gel of CAT, CAT activity (90 and 180 min) and expression of CAT1 gene (at 90 min) of UV-B treated A. thaliana plants with or without 10 μM melatonin supplement. Experiments were repeated two times, and each data point was the mean of three replicates (n = 6). Significant differences (P <0.05) were marked with different letters (a–d) in the charts.

Fig. 7 in Melatonin mitigates UV-B stress via regulating oxidative stress response, cellular redox and alternative electron sinks in Arabidopsis thaliana

Fig. 7. Expressions of alternative oxidase (AOX1a-d) and plastid terminal oxidase (PTOX) genes of UV-B treated (90 min) A. thaliana plants with or without 10 μM melatonin supplement. Experiments were repeated two times, and each data point was the mean of three replicates (n = 6). Significant differences (P <0.05) were marked with different letters (a–d) in the charts.

opennotspecifiedAug 2020View details →

Fig. 8. Compounds 1–3 in Phenolics from Archidendron clypearia (Jack) I.C.Nielsen protect SH-SY5Y cells against H O -induced oxidative stress

Fig. 8. Compounds 1–3 reduced mitochondrial dysfunction in H2O2-induced SH-SY5Y cells. Cells were pretreated with 1, 2, 3 (50 μM), then treated with H2O2 (200 μM) for 4h. The loss of ΔΨm was determined by JC-1 staining and measured by flow cytometric analysis. ##P <0.01 compared with the control group, **P <0.01, *P <0.05 compared with the H2O2 group.

opennotspecifiedAug 2020View details →

Fig. 6 in Phenolics from Archidendron clypearia (Jack) I.C.Nielsen protect SH-SY5Y cells against H O -induced oxidative stress

Fig. 6. Effects of compounds 1–3 to attenuate apoptosis of H2O2-treated SH-SY5Y cells. Cells were pretreated with 1, 2, 3 (50 μM), then treated with H2O2 (200 μM) for 4 h. Flow cytometry was used to determine the apoptotic ratio after Annexin V-FITC/PI staining. Data were shown as mean ± SD from three separate experiments. ##P <0.01 compared with the control group, *P <0.05, **P <0.01 compared with the H O group.