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rat beta insulinoma cells rinm5f  (ATCC)


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    ATCC rat beta insulinoma cells rinm5f
    Characterization of microbubbles (MBs) and their interaction with ultrasound. (A) Bright-field microscopy image of synthesized MBs (scale bar: 10 μm). (B) Size distribution of MBs (mean diameter: 2.01 ± 0.31 μm), analyzed from (A) using MATLAB. (C) Frequency spectrum of backscattered signals from MB suspension during sonication (0.5 MHz, 50-cycle tone burst, 0.38 MPa peak negative pressure). Fundamental frequency (green dot) and harmonics (blue diamonds) are labeled. (D) RMS power of 2nd–8th harmonics in degassed water (black) versus MB suspension (red) across increasing acoustic pressures (0.11–0.38 MPa). (E) Cytocompatibility of MBs assessed by MTS assay. <t>RINm5F</t> cell viability (normalized to MB-free controls) after 12–60 h exposure to MBs ( n = 3 biological replicates; mean ± SEM; ns: not significant by one-way ANOVA)
    Rat Beta Insulinoma Cells Rinm5f, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 76 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rat+beta+cells+rin+m5f/Rin-M5F%3B+Insulinoma%3B+Rat/pmc12836977-113-0-7
    Average 94 stars, based on 76 article reviews
    rat beta insulinoma cells rinm5f - by Bioz Stars, 2026-09
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    1) Product Images from "Microbubble-enhanced ultrasound stimulation of β-cells improves insulin release and glycemic control in mice"

    Article Title: Microbubble-enhanced ultrasound stimulation of β-cells improves insulin release and glycemic control in mice

    Journal: Journal of Nanobiotechnology

    doi: 10.1186/s12951-025-03926-6

    Characterization of microbubbles (MBs) and their interaction with ultrasound. (A) Bright-field microscopy image of synthesized MBs (scale bar: 10 μm). (B) Size distribution of MBs (mean diameter: 2.01 ± 0.31 μm), analyzed from (A) using MATLAB. (C) Frequency spectrum of backscattered signals from MB suspension during sonication (0.5 MHz, 50-cycle tone burst, 0.38 MPa peak negative pressure). Fundamental frequency (green dot) and harmonics (blue diamonds) are labeled. (D) RMS power of 2nd–8th harmonics in degassed water (black) versus MB suspension (red) across increasing acoustic pressures (0.11–0.38 MPa). (E) Cytocompatibility of MBs assessed by MTS assay. RINm5F cell viability (normalized to MB-free controls) after 12–60 h exposure to MBs ( n = 3 biological replicates; mean ± SEM; ns: not significant by one-way ANOVA)
    Figure Legend Snippet: Characterization of microbubbles (MBs) and their interaction with ultrasound. (A) Bright-field microscopy image of synthesized MBs (scale bar: 10 μm). (B) Size distribution of MBs (mean diameter: 2.01 ± 0.31 μm), analyzed from (A) using MATLAB. (C) Frequency spectrum of backscattered signals from MB suspension during sonication (0.5 MHz, 50-cycle tone burst, 0.38 MPa peak negative pressure). Fundamental frequency (green dot) and harmonics (blue diamonds) are labeled. (D) RMS power of 2nd–8th harmonics in degassed water (black) versus MB suspension (red) across increasing acoustic pressures (0.11–0.38 MPa). (E) Cytocompatibility of MBs assessed by MTS assay. RINm5F cell viability (normalized to MB-free controls) after 12–60 h exposure to MBs ( n = 3 biological replicates; mean ± SEM; ns: not significant by one-way ANOVA)

    Techniques Used: Microscopy, Synthesized, Suspension, Sonication, Labeling, MTS Assay

    Microbubble-enhanced ultrasound stimulation triggers Ca²⁺ influx and insulin release in RINm5F β-cells. (A) Experimental setup for ultrasound stimulation (0.5 MHz, 0.5 ms pulse width, 1 ms interval, 300 ms duration, 3 s repetition) and live-cell Ca²⁺ imaging. MBs were suspended in culture medium above adherent RINm5F cells. (B) Bright-field microscopy showing uniform MB distribution among cells (scale bar: 50 μm). (C) Representative Fura-2 fluorescence images showing intracellular Ca²⁺ levels before and after ultrasound stimulation (0.14 MPa) with MBs (0–1.65.65 × 10⁹/mL). (D) Ca²⁺ response kinetics under 0.14 MPa ultrasound with increasing MB concentrations ( n = 28–30 cells/group; mean ± SEM; *** p < 0.001, **** p < 0.0001, one-way ANOVA with Dunn’s post-hoc tests). (E) Ultrasound intensity-dependent Ca²⁺ responses with/without MBs (1.65 × 10⁹/mL; n = 10–55 cells/group). (F) Insulin release measured by ELISA 15 min post-stimulation ( n = 4 biological replicates). Data: mean ± SEM; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 (two-way ANOVA)
    Figure Legend Snippet: Microbubble-enhanced ultrasound stimulation triggers Ca²⁺ influx and insulin release in RINm5F β-cells. (A) Experimental setup for ultrasound stimulation (0.5 MHz, 0.5 ms pulse width, 1 ms interval, 300 ms duration, 3 s repetition) and live-cell Ca²⁺ imaging. MBs were suspended in culture medium above adherent RINm5F cells. (B) Bright-field microscopy showing uniform MB distribution among cells (scale bar: 50 μm). (C) Representative Fura-2 fluorescence images showing intracellular Ca²⁺ levels before and after ultrasound stimulation (0.14 MPa) with MBs (0–1.65.65 × 10⁹/mL). (D) Ca²⁺ response kinetics under 0.14 MPa ultrasound with increasing MB concentrations ( n = 28–30 cells/group; mean ± SEM; *** p < 0.001, **** p < 0.0001, one-way ANOVA with Dunn’s post-hoc tests). (E) Ultrasound intensity-dependent Ca²⁺ responses with/without MBs (1.65 × 10⁹/mL; n = 10–55 cells/group). (F) Insulin release measured by ELISA 15 min post-stimulation ( n = 4 biological replicates). Data: mean ± SEM; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 (two-way ANOVA)

    Techniques Used: Imaging, Microscopy, Fluorescence, Enzyme-linked Immunosorbent Assay

    Microbubble-enhanced ultrasound stimulation promotes insulin release and improves glycemic control in mice. (A) Experimental timeline and setup: RINm5F cells were implanted subcutaneously 24 h before the intraperitoneal glucose injection (2 g/kg). The MB + US group received microbubble injection followed by ultrasound stimulation (0.5 MHz, 0.38 MPa, 50% duty cycle, 300 ms pulse duration, 3 s interval) for 15 min post-glucose challenge. Blood was collected for glucose and insulin measurements at 0 (before US) and 15 min (immediately after US). (B) Plasma insulin levels normalized to baseline (t = 0). MB + US group showed significant enhancement vs. Ctrl and US-only groups ( n = 5 mice/group; mean ± SEM; * p < 0.05, *** p < 0.001, one-way ANOVA with Holm-Šídák’s multiple comparisons test). (C) Blood glucose performance normalized to baseline (t = 0). MB + US group exhibited accelerated glucose clearance ( n = 5 mice/group; mean ± SEM; * p < 0.05, *** p < 0.001 vs. Ctrl at matched timepoint, one-way ANOVA with Holm-Šídák’s multiple comparisons test). (D) Representative nonlinear contrast ultrasound images confirming stable MB distribution at implantation sites
    Figure Legend Snippet: Microbubble-enhanced ultrasound stimulation promotes insulin release and improves glycemic control in mice. (A) Experimental timeline and setup: RINm5F cells were implanted subcutaneously 24 h before the intraperitoneal glucose injection (2 g/kg). The MB + US group received microbubble injection followed by ultrasound stimulation (0.5 MHz, 0.38 MPa, 50% duty cycle, 300 ms pulse duration, 3 s interval) for 15 min post-glucose challenge. Blood was collected for glucose and insulin measurements at 0 (before US) and 15 min (immediately after US). (B) Plasma insulin levels normalized to baseline (t = 0). MB + US group showed significant enhancement vs. Ctrl and US-only groups ( n = 5 mice/group; mean ± SEM; * p < 0.05, *** p < 0.001, one-way ANOVA with Holm-Šídák’s multiple comparisons test). (C) Blood glucose performance normalized to baseline (t = 0). MB + US group exhibited accelerated glucose clearance ( n = 5 mice/group; mean ± SEM; * p < 0.05, *** p < 0.001 vs. Ctrl at matched timepoint, one-way ANOVA with Holm-Šídák’s multiple comparisons test). (D) Representative nonlinear contrast ultrasound images confirming stable MB distribution at implantation sites

    Techniques Used: Control, Injection, Clinical Proteomics

    Mechanistic role of mechanosensitive ion channels in microbubble-enhanced ultrasound stimulation of insulin release. (A) Proposed mechanism: MB-mediated ultrasound activates mechanosensitive channels to induce Ca²⁺ influx and insulin exocytosis. (B) qPCR analysis of mechanosensitive channel expression in RINm5F cells ( n = 3 biological replicates). (C) Quantification of Ca²⁺ influx in RINm5F cells. Cells were treated with ultrasound alone (US), the combination of microbubbles and ultrasound (MB + US), or MB + US following pretreatment with GsMTx4 (MB + US + GsMTx4). Data are presented as mean ± SEM; **** p < 0.0001, one-way ANOVA with post-hoc test). (D) Quantified Ca²⁺ responses in the indicated groups ( n = 32–45 cells/group). Data are shown as mean ± SEM, * p <0.05, ** p < 0.01, **** p < 0.0001. one-way ANOVA followed by Tukey’s multiple comparisons test. (E) Insulin release in the indicated groups ( n = 3 biological replicates). Data are shown as mean ± SEM, **** p < 0.0001. one-way ANOVA followed by Tukey’s multiple comparisons test
    Figure Legend Snippet: Mechanistic role of mechanosensitive ion channels in microbubble-enhanced ultrasound stimulation of insulin release. (A) Proposed mechanism: MB-mediated ultrasound activates mechanosensitive channels to induce Ca²⁺ influx and insulin exocytosis. (B) qPCR analysis of mechanosensitive channel expression in RINm5F cells ( n = 3 biological replicates). (C) Quantification of Ca²⁺ influx in RINm5F cells. Cells were treated with ultrasound alone (US), the combination of microbubbles and ultrasound (MB + US), or MB + US following pretreatment with GsMTx4 (MB + US + GsMTx4). Data are presented as mean ± SEM; **** p < 0.0001, one-way ANOVA with post-hoc test). (D) Quantified Ca²⁺ responses in the indicated groups ( n = 32–45 cells/group). Data are shown as mean ± SEM, * p <0.05, ** p < 0.01, **** p < 0.0001. one-way ANOVA followed by Tukey’s multiple comparisons test. (E) Insulin release in the indicated groups ( n = 3 biological replicates). Data are shown as mean ± SEM, **** p < 0.0001. one-way ANOVA followed by Tukey’s multiple comparisons test

    Techniques Used: Expressing

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    Cell Culture:

    Article Title: Promotion of beta cell proliferation through DYRK kinase inhibition using the marine natural product breitfussin C
    Article Snippet: .. Rat beta cells RIN-M5F (purchased from ATCC, Manassas, VA, USA, product code ATCC-CRL-11605, passage number below 40 for all experiments presented in this manuscript) were cultured in RPMI-1640 (cat# R5886, Sigma-Aldrich, Saint Louis, MO, USA) supplemented with 10% FBS (Biowest, Nauillé, France), 2 mM L-glutamine (Biowest), 1 mM sodium pyruvate (Merck, Darmstadt, Germany) and 1x Penicillin-Streptomycin (Sigma-Aldrich) according to manufacturer’s instructions. ..



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    Characterization of microbubbles (MBs) and their interaction with ultrasound. (A) Bright-field microscopy image of synthesized MBs (scale bar: 10 μm). (B) Size distribution of MBs (mean diameter: 2.01 ± 0.31 μm), analyzed from (A) using MATLAB. (C) Frequency spectrum of backscattered signals from MB suspension during sonication (0.5 MHz, 50-cycle tone burst, 0.38 MPa peak negative pressure). Fundamental frequency (green dot) and harmonics (blue diamonds) are labeled. (D) RMS power of 2nd–8th harmonics in degassed water (black) versus MB suspension (red) across increasing acoustic pressures (0.11–0.38 MPa). (E) Cytocompatibility of MBs assessed by MTS assay. <t>RINm5F</t> cell viability (normalized to MB-free controls) after 12–60 h exposure to MBs ( n = 3 biological replicates; mean ± SEM; ns: not significant by one-way ANOVA)
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    Image Search Results


    Characterization of microbubbles (MBs) and their interaction with ultrasound. (A) Bright-field microscopy image of synthesized MBs (scale bar: 10 μm). (B) Size distribution of MBs (mean diameter: 2.01 ± 0.31 μm), analyzed from (A) using MATLAB. (C) Frequency spectrum of backscattered signals from MB suspension during sonication (0.5 MHz, 50-cycle tone burst, 0.38 MPa peak negative pressure). Fundamental frequency (green dot) and harmonics (blue diamonds) are labeled. (D) RMS power of 2nd–8th harmonics in degassed water (black) versus MB suspension (red) across increasing acoustic pressures (0.11–0.38 MPa). (E) Cytocompatibility of MBs assessed by MTS assay. RINm5F cell viability (normalized to MB-free controls) after 12–60 h exposure to MBs ( n = 3 biological replicates; mean ± SEM; ns: not significant by one-way ANOVA)

    Journal: Journal of Nanobiotechnology

    Article Title: Microbubble-enhanced ultrasound stimulation of β-cells improves insulin release and glycemic control in mice

    doi: 10.1186/s12951-025-03926-6

    Figure Lengend Snippet: Characterization of microbubbles (MBs) and their interaction with ultrasound. (A) Bright-field microscopy image of synthesized MBs (scale bar: 10 μm). (B) Size distribution of MBs (mean diameter: 2.01 ± 0.31 μm), analyzed from (A) using MATLAB. (C) Frequency spectrum of backscattered signals from MB suspension during sonication (0.5 MHz, 50-cycle tone burst, 0.38 MPa peak negative pressure). Fundamental frequency (green dot) and harmonics (blue diamonds) are labeled. (D) RMS power of 2nd–8th harmonics in degassed water (black) versus MB suspension (red) across increasing acoustic pressures (0.11–0.38 MPa). (E) Cytocompatibility of MBs assessed by MTS assay. RINm5F cell viability (normalized to MB-free controls) after 12–60 h exposure to MBs ( n = 3 biological replicates; mean ± SEM; ns: not significant by one-way ANOVA)

    Article Snippet: Rat beta-insulinoma cells (RINm5F) were obtained from ATCC and cultured in RPMI 1640 medium supplemented with 10% fetal bovine serum (FBS) and 1% penicillin-streptomycin (all from Gibco).

    Techniques: Microscopy, Synthesized, Suspension, Sonication, Labeling, MTS Assay

    Microbubble-enhanced ultrasound stimulation triggers Ca²⁺ influx and insulin release in RINm5F β-cells. (A) Experimental setup for ultrasound stimulation (0.5 MHz, 0.5 ms pulse width, 1 ms interval, 300 ms duration, 3 s repetition) and live-cell Ca²⁺ imaging. MBs were suspended in culture medium above adherent RINm5F cells. (B) Bright-field microscopy showing uniform MB distribution among cells (scale bar: 50 μm). (C) Representative Fura-2 fluorescence images showing intracellular Ca²⁺ levels before and after ultrasound stimulation (0.14 MPa) with MBs (0–1.65.65 × 10⁹/mL). (D) Ca²⁺ response kinetics under 0.14 MPa ultrasound with increasing MB concentrations ( n = 28–30 cells/group; mean ± SEM; *** p < 0.001, **** p < 0.0001, one-way ANOVA with Dunn’s post-hoc tests). (E) Ultrasound intensity-dependent Ca²⁺ responses with/without MBs (1.65 × 10⁹/mL; n = 10–55 cells/group). (F) Insulin release measured by ELISA 15 min post-stimulation ( n = 4 biological replicates). Data: mean ± SEM; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 (two-way ANOVA)

    Journal: Journal of Nanobiotechnology

    Article Title: Microbubble-enhanced ultrasound stimulation of β-cells improves insulin release and glycemic control in mice

    doi: 10.1186/s12951-025-03926-6

    Figure Lengend Snippet: Microbubble-enhanced ultrasound stimulation triggers Ca²⁺ influx and insulin release in RINm5F β-cells. (A) Experimental setup for ultrasound stimulation (0.5 MHz, 0.5 ms pulse width, 1 ms interval, 300 ms duration, 3 s repetition) and live-cell Ca²⁺ imaging. MBs were suspended in culture medium above adherent RINm5F cells. (B) Bright-field microscopy showing uniform MB distribution among cells (scale bar: 50 μm). (C) Representative Fura-2 fluorescence images showing intracellular Ca²⁺ levels before and after ultrasound stimulation (0.14 MPa) with MBs (0–1.65.65 × 10⁹/mL). (D) Ca²⁺ response kinetics under 0.14 MPa ultrasound with increasing MB concentrations ( n = 28–30 cells/group; mean ± SEM; *** p < 0.001, **** p < 0.0001, one-way ANOVA with Dunn’s post-hoc tests). (E) Ultrasound intensity-dependent Ca²⁺ responses with/without MBs (1.65 × 10⁹/mL; n = 10–55 cells/group). (F) Insulin release measured by ELISA 15 min post-stimulation ( n = 4 biological replicates). Data: mean ± SEM; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 (two-way ANOVA)

    Article Snippet: Rat beta-insulinoma cells (RINm5F) were obtained from ATCC and cultured in RPMI 1640 medium supplemented with 10% fetal bovine serum (FBS) and 1% penicillin-streptomycin (all from Gibco).

    Techniques: Imaging, Microscopy, Fluorescence, Enzyme-linked Immunosorbent Assay

    Microbubble-enhanced ultrasound stimulation promotes insulin release and improves glycemic control in mice. (A) Experimental timeline and setup: RINm5F cells were implanted subcutaneously 24 h before the intraperitoneal glucose injection (2 g/kg). The MB + US group received microbubble injection followed by ultrasound stimulation (0.5 MHz, 0.38 MPa, 50% duty cycle, 300 ms pulse duration, 3 s interval) for 15 min post-glucose challenge. Blood was collected for glucose and insulin measurements at 0 (before US) and 15 min (immediately after US). (B) Plasma insulin levels normalized to baseline (t = 0). MB + US group showed significant enhancement vs. Ctrl and US-only groups ( n = 5 mice/group; mean ± SEM; * p < 0.05, *** p < 0.001, one-way ANOVA with Holm-Šídák’s multiple comparisons test). (C) Blood glucose performance normalized to baseline (t = 0). MB + US group exhibited accelerated glucose clearance ( n = 5 mice/group; mean ± SEM; * p < 0.05, *** p < 0.001 vs. Ctrl at matched timepoint, one-way ANOVA with Holm-Šídák’s multiple comparisons test). (D) Representative nonlinear contrast ultrasound images confirming stable MB distribution at implantation sites

    Journal: Journal of Nanobiotechnology

    Article Title: Microbubble-enhanced ultrasound stimulation of β-cells improves insulin release and glycemic control in mice

    doi: 10.1186/s12951-025-03926-6

    Figure Lengend Snippet: Microbubble-enhanced ultrasound stimulation promotes insulin release and improves glycemic control in mice. (A) Experimental timeline and setup: RINm5F cells were implanted subcutaneously 24 h before the intraperitoneal glucose injection (2 g/kg). The MB + US group received microbubble injection followed by ultrasound stimulation (0.5 MHz, 0.38 MPa, 50% duty cycle, 300 ms pulse duration, 3 s interval) for 15 min post-glucose challenge. Blood was collected for glucose and insulin measurements at 0 (before US) and 15 min (immediately after US). (B) Plasma insulin levels normalized to baseline (t = 0). MB + US group showed significant enhancement vs. Ctrl and US-only groups ( n = 5 mice/group; mean ± SEM; * p < 0.05, *** p < 0.001, one-way ANOVA with Holm-Šídák’s multiple comparisons test). (C) Blood glucose performance normalized to baseline (t = 0). MB + US group exhibited accelerated glucose clearance ( n = 5 mice/group; mean ± SEM; * p < 0.05, *** p < 0.001 vs. Ctrl at matched timepoint, one-way ANOVA with Holm-Šídák’s multiple comparisons test). (D) Representative nonlinear contrast ultrasound images confirming stable MB distribution at implantation sites

    Article Snippet: Rat beta-insulinoma cells (RINm5F) were obtained from ATCC and cultured in RPMI 1640 medium supplemented with 10% fetal bovine serum (FBS) and 1% penicillin-streptomycin (all from Gibco).

    Techniques: Control, Injection, Clinical Proteomics

    Mechanistic role of mechanosensitive ion channels in microbubble-enhanced ultrasound stimulation of insulin release. (A) Proposed mechanism: MB-mediated ultrasound activates mechanosensitive channels to induce Ca²⁺ influx and insulin exocytosis. (B) qPCR analysis of mechanosensitive channel expression in RINm5F cells ( n = 3 biological replicates). (C) Quantification of Ca²⁺ influx in RINm5F cells. Cells were treated with ultrasound alone (US), the combination of microbubbles and ultrasound (MB + US), or MB + US following pretreatment with GsMTx4 (MB + US + GsMTx4). Data are presented as mean ± SEM; **** p < 0.0001, one-way ANOVA with post-hoc test). (D) Quantified Ca²⁺ responses in the indicated groups ( n = 32–45 cells/group). Data are shown as mean ± SEM, * p <0.05, ** p < 0.01, **** p < 0.0001. one-way ANOVA followed by Tukey’s multiple comparisons test. (E) Insulin release in the indicated groups ( n = 3 biological replicates). Data are shown as mean ± SEM, **** p < 0.0001. one-way ANOVA followed by Tukey’s multiple comparisons test

    Journal: Journal of Nanobiotechnology

    Article Title: Microbubble-enhanced ultrasound stimulation of β-cells improves insulin release and glycemic control in mice

    doi: 10.1186/s12951-025-03926-6

    Figure Lengend Snippet: Mechanistic role of mechanosensitive ion channels in microbubble-enhanced ultrasound stimulation of insulin release. (A) Proposed mechanism: MB-mediated ultrasound activates mechanosensitive channels to induce Ca²⁺ influx and insulin exocytosis. (B) qPCR analysis of mechanosensitive channel expression in RINm5F cells ( n = 3 biological replicates). (C) Quantification of Ca²⁺ influx in RINm5F cells. Cells were treated with ultrasound alone (US), the combination of microbubbles and ultrasound (MB + US), or MB + US following pretreatment with GsMTx4 (MB + US + GsMTx4). Data are presented as mean ± SEM; **** p < 0.0001, one-way ANOVA with post-hoc test). (D) Quantified Ca²⁺ responses in the indicated groups ( n = 32–45 cells/group). Data are shown as mean ± SEM, * p <0.05, ** p < 0.01, **** p < 0.0001. one-way ANOVA followed by Tukey’s multiple comparisons test. (E) Insulin release in the indicated groups ( n = 3 biological replicates). Data are shown as mean ± SEM, **** p < 0.0001. one-way ANOVA followed by Tukey’s multiple comparisons test

    Article Snippet: Rat beta-insulinoma cells (RINm5F) were obtained from ATCC and cultured in RPMI 1640 medium supplemented with 10% fetal bovine serum (FBS) and 1% penicillin-streptomycin (all from Gibco).

    Techniques: Expressing

    Effects of LSE in combination with H 2 O 2 on beta-cell viability and oxidative injury. ( a – b ) Rat pancreatic beta-cells (RIN-m5F) were treated with various doses of LSE (0–100 μg/mL) alone ( a ) or the indicated doses of LSE (0.5 and 1.0 μg/mL) in combination with 200 μM of H 2 O 2 ( b ) for 24 h. The cell viability was evaluated by the MTT method. ( c – e ) Under the same co-treatment conditions, the insulin secretion ( c ), lipid peroxidation ( d ), and intracellular reactive oxygen species (ROS) level ( e ) were assessed by measuring the glucose-stimulated insulin secretion (GSIS), thiobarbituric acid relative substance (TBARS), and dichlorofluorescein diacetate (DCFH-DA) assay, receptively. The results are represented as mean ± SD ( n ≥ 3) from three independent experiments. # p < 0.05, ## p < 0.01, compared with untreated control; * p < 0.05, ** p < 0.01, compared with the H 2 O 2 group.

    Journal: Antioxidants

    Article Title: Flavonoids Identification and Pancreatic Beta-Cell Protective Effect of Lotus Seedpod

    doi: 10.3390/antiox9080658

    Figure Lengend Snippet: Effects of LSE in combination with H 2 O 2 on beta-cell viability and oxidative injury. ( a – b ) Rat pancreatic beta-cells (RIN-m5F) were treated with various doses of LSE (0–100 μg/mL) alone ( a ) or the indicated doses of LSE (0.5 and 1.0 μg/mL) in combination with 200 μM of H 2 O 2 ( b ) for 24 h. The cell viability was evaluated by the MTT method. ( c – e ) Under the same co-treatment conditions, the insulin secretion ( c ), lipid peroxidation ( d ), and intracellular reactive oxygen species (ROS) level ( e ) were assessed by measuring the glucose-stimulated insulin secretion (GSIS), thiobarbituric acid relative substance (TBARS), and dichlorofluorescein diacetate (DCFH-DA) assay, receptively. The results are represented as mean ± SD ( n ≥ 3) from three independent experiments. # p < 0.05, ## p < 0.01, compared with untreated control; * p < 0.05, ** p < 0.01, compared with the H 2 O 2 group.

    Article Snippet: The rat pancreatic beta-cell line (RIN-m5F), obtained from the Bioresource Collection and Research Center (Food Industry Research and Development Institute, Hsinchu City, Taiwan, ROC), was cultured in RPMI-1640 medium supplemented with 10% fetal bovine serum (FBS, Thermo Fisher Scientific, Inc., Waltham, MA, USA) and 1% penicillin-streptomycin (Gibco/BRL, Gaithersburg, MD, USA).

    Techniques: DCFH-DA Assay, Control

    In vivo effect of LSE on diabetes mellitus (DM) symptoms and pancreatic beta-cell dysfunction. BALB/c mice fed on a high-fat diet (HFD) combined with streptozotocin (STZ) injection (HFD/STZ) were randomly divided into four experimental groups. Among groups, two of these groups were fed with LSE at 1% and 2%, whereas the metformin group was administered intragastrically a metformin hydrochloride water solution (300 mg/kg). These mice were sacrificed after 12 weeks. The glucose tolerance ( a ) and insulin resistance ( b ) were, respectively, determined by oral glucose tolerance test (OGTT) and homeostasis model of insulin resistance (HOMA-IR). ( c ) The pancreatic tissues were collected for H&E stain ( upper panel ), and pancreatic islet apoptosis (red-brown color) was analyzed by TUNEL assay ( lower panel ). Images were taken at 200× magnification; scale bar, 50 μm. ( d ) The pancreatic islet areas ( left axis ), relative to the total pancreas, and apoptotic index ( right axis ) were, respectively, measured in the total islet tissues of four groups. Values are expressed as mean ± SD, n = 10; ( e ) The intracellular lipid peroxidation ( left axis ) and H 2 O 2 production ( right axis ) of pancreatic tissues were measured by TBARS and H 2 O 2 assays, respectively. ( f , g ) Western blotting of active-caspase 3, Bcl-2, Bax, p-Bad, Bad ( f ), LC3-I/II, Atg5/12 conjugate, class III PI3K, and Beclin-1 ( g ) protein expressions was performed with the tissue extracts from them. α-tubulin was served as an internal control. The quantitative results are expressed as the mean ± SD ( n = 10) from one independent experiment. # p < 0.05, ## p < 0.01, compared with the negative control (NC); * p < 0.05, ** p < 0.01, compared with the HFD/STZ group. ( h ) Schematic representation of in vivo beta-cell protective effects of LSE against oxidative injury. HFD/STZ induces intracellular ROS production, leading to pancreatic beta-cell apoptosis and autophagy. While apoptosis contributes to cell injury (by bold arrows), autophagy is induced as a pro-survival mechanism (by regular arrows). LSE performs against ROS via the downregulation of apoptosis and upregulation of autophagy, subsequently mediating the ameliorated effects on pancreatic beta-cell oxidative injury and DM development.

    Journal: Antioxidants

    Article Title: Flavonoids Identification and Pancreatic Beta-Cell Protective Effect of Lotus Seedpod

    doi: 10.3390/antiox9080658

    Figure Lengend Snippet: In vivo effect of LSE on diabetes mellitus (DM) symptoms and pancreatic beta-cell dysfunction. BALB/c mice fed on a high-fat diet (HFD) combined with streptozotocin (STZ) injection (HFD/STZ) were randomly divided into four experimental groups. Among groups, two of these groups were fed with LSE at 1% and 2%, whereas the metformin group was administered intragastrically a metformin hydrochloride water solution (300 mg/kg). These mice were sacrificed after 12 weeks. The glucose tolerance ( a ) and insulin resistance ( b ) were, respectively, determined by oral glucose tolerance test (OGTT) and homeostasis model of insulin resistance (HOMA-IR). ( c ) The pancreatic tissues were collected for H&E stain ( upper panel ), and pancreatic islet apoptosis (red-brown color) was analyzed by TUNEL assay ( lower panel ). Images were taken at 200× magnification; scale bar, 50 μm. ( d ) The pancreatic islet areas ( left axis ), relative to the total pancreas, and apoptotic index ( right axis ) were, respectively, measured in the total islet tissues of four groups. Values are expressed as mean ± SD, n = 10; ( e ) The intracellular lipid peroxidation ( left axis ) and H 2 O 2 production ( right axis ) of pancreatic tissues were measured by TBARS and H 2 O 2 assays, respectively. ( f , g ) Western blotting of active-caspase 3, Bcl-2, Bax, p-Bad, Bad ( f ), LC3-I/II, Atg5/12 conjugate, class III PI3K, and Beclin-1 ( g ) protein expressions was performed with the tissue extracts from them. α-tubulin was served as an internal control. The quantitative results are expressed as the mean ± SD ( n = 10) from one independent experiment. # p < 0.05, ## p < 0.01, compared with the negative control (NC); * p < 0.05, ** p < 0.01, compared with the HFD/STZ group. ( h ) Schematic representation of in vivo beta-cell protective effects of LSE against oxidative injury. HFD/STZ induces intracellular ROS production, leading to pancreatic beta-cell apoptosis and autophagy. While apoptosis contributes to cell injury (by bold arrows), autophagy is induced as a pro-survival mechanism (by regular arrows). LSE performs against ROS via the downregulation of apoptosis and upregulation of autophagy, subsequently mediating the ameliorated effects on pancreatic beta-cell oxidative injury and DM development.

    Article Snippet: The rat pancreatic beta-cell line (RIN-m5F), obtained from the Bioresource Collection and Research Center (Food Industry Research and Development Institute, Hsinchu City, Taiwan, ROC), was cultured in RPMI-1640 medium supplemented with 10% fetal bovine serum (FBS, Thermo Fisher Scientific, Inc., Waltham, MA, USA) and 1% penicillin-streptomycin (Gibco/BRL, Gaithersburg, MD, USA).

    Techniques: In Vivo, Injection, Staining, TUNEL Assay, Western Blot, Control, Negative Control

    Pretreatment with CUR or nCUR prevents STZ induced cell death in RIN‐m5f cells. (A) Cell death was identified by PI staining (20× magnification, scale bar represents 200 μm). (B) The presence of active caspase‐8 was examined by immunofluorescence using antibodies specific for cleaved caspase‐8 (40× magnification, scale bar represents 100 μm).

    Journal: British Journal of Pharmacology

    Article Title: Nano‐curcumin safely prevents streptozotocin‐induced inflammation and apoptosis in pancreatic beta cells for effective management of Type 1 diabetes mellitus

    doi: 10.1111/bph.13816

    Figure Lengend Snippet: Pretreatment with CUR or nCUR prevents STZ induced cell death in RIN‐m5f cells. (A) Cell death was identified by PI staining (20× magnification, scale bar represents 200 μm). (B) The presence of active caspase‐8 was examined by immunofluorescence using antibodies specific for cleaved caspase‐8 (40× magnification, scale bar represents 100 μm).

    Article Snippet: Rat insulin elisa kits were purchased from Mercodia [10–1250‐01] (Uppsala, Sweden), ProcartaPlex Rat Th complete panel was purchased from Affymetrix, eBiosciences (14plex EPX140–30120‐901, USA) and, Histomount was purchased from Ted Pella Inc. Rat pancreatic beta‐insulinoma cells (RIN‐m5f) were purchased from ATCC and maintained in RPMI‐1640 medium.

    Techniques: Staining, Immunofluorescence