min6 β-cell line Search Results


90
Procell Inc min6 islet β-cells lot no. cl-0674
Min6 Islet β Cells Lot No. Cl 0674, supplied by Procell Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/min6 islet β-cells lot no. cl-0674/product/Procell Inc
Average 90 stars, based on 1 article reviews
min6 islet β-cells lot no. cl-0674 - by Bioz Stars, 2026-02
90/100 stars
  Buy from Supplier

90
Keygen Biotech mouse pancreatic β-cell line min6
∆nFGF1 relieves β -cell apoptosis in db / db mice. (a) H&E staining of pancreas tissue from mice sacrificed after intraperitoneal (i.p.) injection of ∆nFGF1 or saline for 8 weeks (left panel). The black dotted lines indicate the borders of <t>pancreatic</t> islets. Pancreatic islet areas were quantified using ImageJ (right panel). (b) Coimmunofluorescence staining of insulin (green) and C-caspase 3 (red) in pancreatic islets. DAPI was used to stain nuclei. The white arrows indicate insulin/C-caspase 3 double-positive β -cells. (c) Representative PCNA-positive cells in pancreas sections (left panel). The black dotted lines indicate the borders of pancreatic islets. PCNA-positive cells were quantified using ImageJ (right panel). All data are presented as mean values ± SEM. n = 5 mice per group. ∗∗∗ p < 0.001; n.s.: no significance.
Mouse Pancreatic β Cell Line Min6, supplied by Keygen Biotech, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/mouse pancreatic β-cell line min6/product/Keygen Biotech
Average 90 stars, based on 1 article reviews
mouse pancreatic β-cell line min6 - by Bioz Stars, 2026-02
90/100 stars
  Buy from Supplier

Image Search Results


∆nFGF1 relieves β -cell apoptosis in db / db mice. (a) H&E staining of pancreas tissue from mice sacrificed after intraperitoneal (i.p.) injection of ∆nFGF1 or saline for 8 weeks (left panel). The black dotted lines indicate the borders of pancreatic islets. Pancreatic islet areas were quantified using ImageJ (right panel). (b) Coimmunofluorescence staining of insulin (green) and C-caspase 3 (red) in pancreatic islets. DAPI was used to stain nuclei. The white arrows indicate insulin/C-caspase 3 double-positive β -cells. (c) Representative PCNA-positive cells in pancreas sections (left panel). The black dotted lines indicate the borders of pancreatic islets. PCNA-positive cells were quantified using ImageJ (right panel). All data are presented as mean values ± SEM. n = 5 mice per group. ∗∗∗ p < 0.001; n.s.: no significance.

Journal: Oxidative Medicine and Cellular Longevity

Article Title: ∆nFGF1 Protects β -Cells against High Glucose-Induced Apoptosis via the AMPK/SIRT1/PGC-1 α Axis

doi: 10.1155/2022/1231970

Figure Lengend Snippet: ∆nFGF1 relieves β -cell apoptosis in db / db mice. (a) H&E staining of pancreas tissue from mice sacrificed after intraperitoneal (i.p.) injection of ∆nFGF1 or saline for 8 weeks (left panel). The black dotted lines indicate the borders of pancreatic islets. Pancreatic islet areas were quantified using ImageJ (right panel). (b) Coimmunofluorescence staining of insulin (green) and C-caspase 3 (red) in pancreatic islets. DAPI was used to stain nuclei. The white arrows indicate insulin/C-caspase 3 double-positive β -cells. (c) Representative PCNA-positive cells in pancreas sections (left panel). The black dotted lines indicate the borders of pancreatic islets. PCNA-positive cells were quantified using ImageJ (right panel). All data are presented as mean values ± SEM. n = 5 mice per group. ∗∗∗ p < 0.001; n.s.: no significance.

Article Snippet: Mouse pancreatic β -cell line MIN6 (Keygen Biotech, Nanjing, China) cells were cultured in RPMI1640 medium (Gibco) accompanied with 10% fetal bovine serum (FBS, Gibco) and 1% penicillin-streptomycin.

Techniques: Staining, Injection, Saline

∆nFGF1 inhibits apoptosis of MIN6 cells. MIN6 cells were exposed to NG (11.1 mM) and HG+PA (33 mM HG+0.5 mM PA) in the presence or absence of ∆nFGF1 for 24 h. MIN6 cells were exposed for 24 h to HG or PA. (a) The expression of Bcl-2 was analyzed by Western blot (left panel) and quantified using ImageJ (right panel). (b) The expression of Bax and cleaved- (C-) caspase 3 in MIN6 cells under different concentrations of ∆nFGF1 was analyzed by Western blot (upper panel) and quantitated using ImageJ (lower panels). (c) The survival rate of MIN6 cells for above treatments. (d) The proliferation of MIN6 cells after treatment with FGF1 WT and ∆nFGF1. Representative immunofluorescence images of MIN6 cells stained with (e) TUNEL (green) and (f) C-caspase 3 (red). DAPI was used to stain nuclei. (g) The numbers of TUNEL-positive cells (upper panel) and the fluorescence intensity of C-caspase 3 were quantified using ImageJ (lower panel). (h) Bax, Bcl-2, and C-caspase 3 expression was analyzed by Western blot (left panel) and quantitated by ImageJ (right panels). β -Actin was used as a control. All data are presented as mean values ± SEM. NG: normal glucose; HG: high glucose; PA: palmitic acid. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001. n.s.: no significance.

Journal: Oxidative Medicine and Cellular Longevity

Article Title: ∆nFGF1 Protects β -Cells against High Glucose-Induced Apoptosis via the AMPK/SIRT1/PGC-1 α Axis

doi: 10.1155/2022/1231970

Figure Lengend Snippet: ∆nFGF1 inhibits apoptosis of MIN6 cells. MIN6 cells were exposed to NG (11.1 mM) and HG+PA (33 mM HG+0.5 mM PA) in the presence or absence of ∆nFGF1 for 24 h. MIN6 cells were exposed for 24 h to HG or PA. (a) The expression of Bcl-2 was analyzed by Western blot (left panel) and quantified using ImageJ (right panel). (b) The expression of Bax and cleaved- (C-) caspase 3 in MIN6 cells under different concentrations of ∆nFGF1 was analyzed by Western blot (upper panel) and quantitated using ImageJ (lower panels). (c) The survival rate of MIN6 cells for above treatments. (d) The proliferation of MIN6 cells after treatment with FGF1 WT and ∆nFGF1. Representative immunofluorescence images of MIN6 cells stained with (e) TUNEL (green) and (f) C-caspase 3 (red). DAPI was used to stain nuclei. (g) The numbers of TUNEL-positive cells (upper panel) and the fluorescence intensity of C-caspase 3 were quantified using ImageJ (lower panel). (h) Bax, Bcl-2, and C-caspase 3 expression was analyzed by Western blot (left panel) and quantitated by ImageJ (right panels). β -Actin was used as a control. All data are presented as mean values ± SEM. NG: normal glucose; HG: high glucose; PA: palmitic acid. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001. n.s.: no significance.

Article Snippet: Mouse pancreatic β -cell line MIN6 (Keygen Biotech, Nanjing, China) cells were cultured in RPMI1640 medium (Gibco) accompanied with 10% fetal bovine serum (FBS, Gibco) and 1% penicillin-streptomycin.

Techniques: Expressing, Western Blot, Immunofluorescence, Staining, TUNEL Assay, Fluorescence, Control

∆nFGF1 induces activation of AMPK/Sitr1/PGC-1 α signaling. MIN6 cells were exposed to NG (11.1 mM) and HG+PA (33 mM HG+0.5 mM PA) in the absence or presence of ∆nFGF1 for 24 h. (a) The expression of phosphorylated- (p-) AMPK and AMPK analyzed by Western blot (left panel) and quantified by ImageJ (right panel) ( n = 3). (b) The expression levels of SIRT1 and PGC-1 α analyzed by Western blot (left panel) and quantified by ImageJ (right panel) ( n = 3). β -Actin was used as a loading control. (c, d) Immunostaining for SIRT1 (red) and PGC-1 α (green) in paraffin-embedded islets. DAPI was used to stain cell nuclei. n = 5 mice per group. (e) Quantitative analysis of fluorescence intensity of SIRT1 (upper panel) and PGC-1 α (lower panel). All data are presented as mean values ± SEM. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001.

Journal: Oxidative Medicine and Cellular Longevity

Article Title: ∆nFGF1 Protects β -Cells against High Glucose-Induced Apoptosis via the AMPK/SIRT1/PGC-1 α Axis

doi: 10.1155/2022/1231970

Figure Lengend Snippet: ∆nFGF1 induces activation of AMPK/Sitr1/PGC-1 α signaling. MIN6 cells were exposed to NG (11.1 mM) and HG+PA (33 mM HG+0.5 mM PA) in the absence or presence of ∆nFGF1 for 24 h. (a) The expression of phosphorylated- (p-) AMPK and AMPK analyzed by Western blot (left panel) and quantified by ImageJ (right panel) ( n = 3). (b) The expression levels of SIRT1 and PGC-1 α analyzed by Western blot (left panel) and quantified by ImageJ (right panel) ( n = 3). β -Actin was used as a loading control. (c, d) Immunostaining for SIRT1 (red) and PGC-1 α (green) in paraffin-embedded islets. DAPI was used to stain cell nuclei. n = 5 mice per group. (e) Quantitative analysis of fluorescence intensity of SIRT1 (upper panel) and PGC-1 α (lower panel). All data are presented as mean values ± SEM. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001.

Article Snippet: Mouse pancreatic β -cell line MIN6 (Keygen Biotech, Nanjing, China) cells were cultured in RPMI1640 medium (Gibco) accompanied with 10% fetal bovine serum (FBS, Gibco) and 1% penicillin-streptomycin.

Techniques: Activation Assay, Expressing, Western Blot, Control, Immunostaining, Staining, Fluorescence

∆nFGF1 inhibits glucolipotoxicity-induced apoptosis in MIN6 cells via AMPK/SIRT1/PGC-1 α signaling. MIN6 cells were exposed to NG (11.1 mM) and HG+PA (33 mM HG+0.5 mM PA) with or without the AMPK inhibitor Compound C (CC) in the presence or absence of ∆nFGF1 for 24 h. (a) The protein levels of p-AMPK, SIRT1, and PGC-1 α analyzed by Western blot (left panel) and quantified by ImageJ (right panels) ( n = 3). (b) The protein expression levels of Bcl-2, Bax, and C-caspase 3 analyzed by Western blot (left panel) and quantified by ImageJ (right panels) ( n = 3). (c) MIN6 cells were transfected with AMPK siRNA for 48 h before exposure to NG (11.1 mM) and HG+PA (33 mM HG+0.5 mM PA) in the presence or absence of ∆nFGF1 for 24 h. The protein expression levels of p-AMPK, SIRT1, and PGC-1 α analyzed by Western blot (left panel) and quantified by ImageJ (right panels) ( n = 3). (d) The protein expression levels of Bcl-2, Bax, and C-caspase 3 analyzed by Western blot (left panel) and quantified by ImageJ (right panels) ( n = 3). β -Actin was used as a loading control. (e) Apoptosis of β -cells in each group was evaluated by flow cytometry analysis. The apoptotic rate was calculated as the percentage of Annexin V-positive cells divided by the total number of cells. (f) Schematic diagram illustrating the model of ∆nFGF1-mediated inhibition of pancreatic β -cell apoptosis in T2DM. All data are presented as mean values ± SEM. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001. n.s.: no significance.

Journal: Oxidative Medicine and Cellular Longevity

Article Title: ∆nFGF1 Protects β -Cells against High Glucose-Induced Apoptosis via the AMPK/SIRT1/PGC-1 α Axis

doi: 10.1155/2022/1231970

Figure Lengend Snippet: ∆nFGF1 inhibits glucolipotoxicity-induced apoptosis in MIN6 cells via AMPK/SIRT1/PGC-1 α signaling. MIN6 cells were exposed to NG (11.1 mM) and HG+PA (33 mM HG+0.5 mM PA) with or without the AMPK inhibitor Compound C (CC) in the presence or absence of ∆nFGF1 for 24 h. (a) The protein levels of p-AMPK, SIRT1, and PGC-1 α analyzed by Western blot (left panel) and quantified by ImageJ (right panels) ( n = 3). (b) The protein expression levels of Bcl-2, Bax, and C-caspase 3 analyzed by Western blot (left panel) and quantified by ImageJ (right panels) ( n = 3). (c) MIN6 cells were transfected with AMPK siRNA for 48 h before exposure to NG (11.1 mM) and HG+PA (33 mM HG+0.5 mM PA) in the presence or absence of ∆nFGF1 for 24 h. The protein expression levels of p-AMPK, SIRT1, and PGC-1 α analyzed by Western blot (left panel) and quantified by ImageJ (right panels) ( n = 3). (d) The protein expression levels of Bcl-2, Bax, and C-caspase 3 analyzed by Western blot (left panel) and quantified by ImageJ (right panels) ( n = 3). β -Actin was used as a loading control. (e) Apoptosis of β -cells in each group was evaluated by flow cytometry analysis. The apoptotic rate was calculated as the percentage of Annexin V-positive cells divided by the total number of cells. (f) Schematic diagram illustrating the model of ∆nFGF1-mediated inhibition of pancreatic β -cell apoptosis in T2DM. All data are presented as mean values ± SEM. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001. n.s.: no significance.

Article Snippet: Mouse pancreatic β -cell line MIN6 (Keygen Biotech, Nanjing, China) cells were cultured in RPMI1640 medium (Gibco) accompanied with 10% fetal bovine serum (FBS, Gibco) and 1% penicillin-streptomycin.

Techniques: Western Blot, Expressing, Transfection, Control, Flow Cytometry, Inhibition