primary rat hippocampal neuron cells Search Results


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iCell Gene Therapeutics rat primary hippocampal neuronal cells
miR-129-3p directly regulates MCU expression in glucose fluctuation-exposed <t>hippocampal</t> neuronal neuronal cells. Rat primary hippocampal neuronal cells were exposed to normal glucose (control, CT), low glucose (LG), high glucose (HG) and glucose fluctuation (GV) conditions. ( A and B ) Protein levels of MCU. ( C ) mRNA levels of miR-129-3p. ( D ) Predicted mi R-129-3p target sequence in the MCU-3 ‘ UTR. Target sequences of MCU-3 ‘UTR were mutated. ( E ) Luciferase assay of cells transfected with MCU-WT or MCU-MUT reporter together with miR-129-3p mimic or miR-NC. ( F ) mRNA levels of MCU in cells transfected with miR-129-3p inhibitor or mimics and miR-NC. Data are presented as the means ± SD ; ** p < 0.01; (n = 5).
Rat Primary Hippocampal Neuronal Cells, supplied by iCell Gene Therapeutics, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Rat Hippocampal Neuron Primary Cell Culture Complete Media with Serum. This product is also available without Serum Cat# M12050-02 This product would require pre-coated flasks with Rat Hippocampal Neuron Primary Cell Culture Extra-cellular Matrix Cat#
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Rat Hippocampal Neuron Primary Cell Culture Serum Free Media. This Product is also available with Serum Cat# M12050-02S This product would require pre-coated flasks with Rat Hippocampal Neuron Primary Cell Culture Extra-cellular Matrix Cat# E12050-02
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miR-129-3p directly regulates MCU expression in glucose fluctuation-exposed hippocampal neuronal neuronal cells. Rat primary hippocampal neuronal cells were exposed to normal glucose (control, CT), low glucose (LG), high glucose (HG) and glucose fluctuation (GV) conditions. ( A and B ) Protein levels of MCU. ( C ) mRNA levels of miR-129-3p. ( D ) Predicted mi R-129-3p target sequence in the MCU-3 ‘ UTR. Target sequences of MCU-3 ‘UTR were mutated. ( E ) Luciferase assay of cells transfected with MCU-WT or MCU-MUT reporter together with miR-129-3p mimic or miR-NC. ( F ) mRNA levels of MCU in cells transfected with miR-129-3p inhibitor or mimics and miR-NC. Data are presented as the means ± SD ; ** p < 0.01; (n = 5).

Journal: Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy

Article Title: miR-129-3p Targeting of MCU Protects Against Glucose Fluctuation-Mediated Neuronal Damage via a Mitochondrial-Dependent Intrinsic Apoptotic Pathway

doi: 10.2147/DMSO.S285179

Figure Lengend Snippet: miR-129-3p directly regulates MCU expression in glucose fluctuation-exposed hippocampal neuronal neuronal cells. Rat primary hippocampal neuronal cells were exposed to normal glucose (control, CT), low glucose (LG), high glucose (HG) and glucose fluctuation (GV) conditions. ( A and B ) Protein levels of MCU. ( C ) mRNA levels of miR-129-3p. ( D ) Predicted mi R-129-3p target sequence in the MCU-3 ‘ UTR. Target sequences of MCU-3 ‘UTR were mutated. ( E ) Luciferase assay of cells transfected with MCU-WT or MCU-MUT reporter together with miR-129-3p mimic or miR-NC. ( F ) mRNA levels of MCU in cells transfected with miR-129-3p inhibitor or mimics and miR-NC. Data are presented as the means ± SD ; ** p < 0.01; (n = 5).

Article Snippet: Rat primary hippocampal neuronal cells (iCell, China) were cultured in a primary neuronal cell culture system (iCell, China) at 37 °C in 5% CO 2 .

Techniques: Expressing, Control, Sequencing, Luciferase, Transfection

miR-129-3p overexpression alleviates oxidative stress in glucose fluctuation-exposed hippocampal neuronal cells by targeting MCU. Rat primary hippocampal neuronal cells were transfected with miR-NC, miR-129-3p mimics, miR-129-3p mimics+vector, or miR-129-3p mimics+MCU followed by glucose fluctuation treatment. ( A – C ) The concentration of mitochondrial Ca 2+ and O 2 − was detected using immunofluorescence. Scale bars = 50 μm. ( D ) GSH/GSSG ratio. ( E ) MnSOD activity. Data are presented as the means ± SD ; * p < 0.05, ** p < 0.01; (n = 5). CT, normal glucose; GV, glucose fluctuation; vector, MCU negative control (pcDNA3.1 vector).

Journal: Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy

Article Title: miR-129-3p Targeting of MCU Protects Against Glucose Fluctuation-Mediated Neuronal Damage via a Mitochondrial-Dependent Intrinsic Apoptotic Pathway

doi: 10.2147/DMSO.S285179

Figure Lengend Snippet: miR-129-3p overexpression alleviates oxidative stress in glucose fluctuation-exposed hippocampal neuronal cells by targeting MCU. Rat primary hippocampal neuronal cells were transfected with miR-NC, miR-129-3p mimics, miR-129-3p mimics+vector, or miR-129-3p mimics+MCU followed by glucose fluctuation treatment. ( A – C ) The concentration of mitochondrial Ca 2+ and O 2 − was detected using immunofluorescence. Scale bars = 50 μm. ( D ) GSH/GSSG ratio. ( E ) MnSOD activity. Data are presented as the means ± SD ; * p < 0.05, ** p < 0.01; (n = 5). CT, normal glucose; GV, glucose fluctuation; vector, MCU negative control (pcDNA3.1 vector).

Article Snippet: Rat primary hippocampal neuronal cells (iCell, China) were cultured in a primary neuronal cell culture system (iCell, China) at 37 °C in 5% CO 2 .

Techniques: Over Expression, Transfection, Plasmid Preparation, Concentration Assay, Immunofluorescence, Activity Assay, Negative Control

miR-129-3p overexpression inhibits apoptosis in glucose fluctuation-exposed hippocampal neuronal cells apoptosis by targeting MCU. Rat primary hippocampal neuronal cells were transfected with miR-NC, miR-129-3p mimics, miR-129-3p mimics+vector, or miR-129-3p mimics+MCU followed by glucose fluctuation treatment. ( A ) Flow cytometry was performed to detect apoptosis of hippocampal neuronal cells. ( B ) Apoptosis rate (%). Data are presented as the means ± SD ; ** p < 0.01 (n = 5). CT, normal glucose; GV, glucose fluctuation; vector, MCU negative control (pcDNA3.1 vector).

Journal: Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy

Article Title: miR-129-3p Targeting of MCU Protects Against Glucose Fluctuation-Mediated Neuronal Damage via a Mitochondrial-Dependent Intrinsic Apoptotic Pathway

doi: 10.2147/DMSO.S285179

Figure Lengend Snippet: miR-129-3p overexpression inhibits apoptosis in glucose fluctuation-exposed hippocampal neuronal cells apoptosis by targeting MCU. Rat primary hippocampal neuronal cells were transfected with miR-NC, miR-129-3p mimics, miR-129-3p mimics+vector, or miR-129-3p mimics+MCU followed by glucose fluctuation treatment. ( A ) Flow cytometry was performed to detect apoptosis of hippocampal neuronal cells. ( B ) Apoptosis rate (%). Data are presented as the means ± SD ; ** p < 0.01 (n = 5). CT, normal glucose; GV, glucose fluctuation; vector, MCU negative control (pcDNA3.1 vector).

Article Snippet: Rat primary hippocampal neuronal cells (iCell, China) were cultured in a primary neuronal cell culture system (iCell, China) at 37 °C in 5% CO 2 .

Techniques: Over Expression, Transfection, Plasmid Preparation, Flow Cytometry, Negative Control

miR-129-3p overexpression inhibits the mitochondrial-dependent intrinsic apoptosis pathway in glucose fluctuation-treated hippocampal neuronal cells by targeting MCU. Rat primary hippocampal neuronal cells were transfected with miR-NC, miR-129-3p mimics, miR-129-3p mimics+vector, or miR-129-3p mimics+MCU followed by glucose fluctuation treatment. ( A ) Mitochondrial cytochrome c, and ( B ) cytosolic cytochrome c. mRNA levels of ( C ) caspase-9 and ( D ) caspase-3. ( E – H ) Protein levels of MCU, caspase-9, and caspase-3. Data are presented as the means ± SD ; * p < 0.05, ** p < 0.01; (n = 5). CT, normal glucose; GV, glucose fluctuation; vector, MCU negative control (pcDNA3.1 vector).

Journal: Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy

Article Title: miR-129-3p Targeting of MCU Protects Against Glucose Fluctuation-Mediated Neuronal Damage via a Mitochondrial-Dependent Intrinsic Apoptotic Pathway

doi: 10.2147/DMSO.S285179

Figure Lengend Snippet: miR-129-3p overexpression inhibits the mitochondrial-dependent intrinsic apoptosis pathway in glucose fluctuation-treated hippocampal neuronal cells by targeting MCU. Rat primary hippocampal neuronal cells were transfected with miR-NC, miR-129-3p mimics, miR-129-3p mimics+vector, or miR-129-3p mimics+MCU followed by glucose fluctuation treatment. ( A ) Mitochondrial cytochrome c, and ( B ) cytosolic cytochrome c. mRNA levels of ( C ) caspase-9 and ( D ) caspase-3. ( E – H ) Protein levels of MCU, caspase-9, and caspase-3. Data are presented as the means ± SD ; * p < 0.05, ** p < 0.01; (n = 5). CT, normal glucose; GV, glucose fluctuation; vector, MCU negative control (pcDNA3.1 vector).

Article Snippet: Rat primary hippocampal neuronal cells (iCell, China) were cultured in a primary neuronal cell culture system (iCell, China) at 37 °C in 5% CO 2 .

Techniques: Over Expression, Transfection, Plasmid Preparation, Negative Control

Silencing of miR-129-3p inhibits calcium overload and oxidative stress in glucose fluctuation-exposed hippocampal neuronal cells. Rat primary hippocampal neuronal cells were transfected with miR-NC, miR-129-3p mimics, miR-129-3p inhibitor with or without NAC followed by glucose fluctuation treatment. ( A – C ) The concentration of mitochondrial Ca 2+ and O 2 − was detected using immunofluorescence. Scale bars = 50 μm. Data are presented as the means ± SD ; ** p < 0.01; (n = 5). CT, normal glucose; GV, glucose fluctuation; antio, NAC.

Journal: Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy

Article Title: miR-129-3p Targeting of MCU Protects Against Glucose Fluctuation-Mediated Neuronal Damage via a Mitochondrial-Dependent Intrinsic Apoptotic Pathway

doi: 10.2147/DMSO.S285179

Figure Lengend Snippet: Silencing of miR-129-3p inhibits calcium overload and oxidative stress in glucose fluctuation-exposed hippocampal neuronal cells. Rat primary hippocampal neuronal cells were transfected with miR-NC, miR-129-3p mimics, miR-129-3p inhibitor with or without NAC followed by glucose fluctuation treatment. ( A – C ) The concentration of mitochondrial Ca 2+ and O 2 − was detected using immunofluorescence. Scale bars = 50 μm. Data are presented as the means ± SD ; ** p < 0.01; (n = 5). CT, normal glucose; GV, glucose fluctuation; antio, NAC.

Article Snippet: Rat primary hippocampal neuronal cells (iCell, China) were cultured in a primary neuronal cell culture system (iCell, China) at 37 °C in 5% CO 2 .

Techniques: Transfection, Concentration Assay, Immunofluorescence

miR-129-3p inhibits ROS-mediated apoptosis in glucose fluctuation-exposed hippocampal neuronal cells. Rat primary hippocampal neuronal cells were transfected with miR-NC, miR-129-3p mimics, miR-129-3p inhibitor with or without NAC, followed by glucose fluctuation treatment. ( A ) Flow cytometry was performed to detect the apoptosis of hippocampal neuronal cells. ( B ) Apoptosis rate (%). ( C ) Mitochondrial cytochrome c and ( D ) cytosolic cytochrome c. mRNA levels of ( E ) caspase-9 and ( F ) caspase-3. Data are presented as the means ± SD ; * p < 0.05, ** p < 0.01; (n = 5). CT, normal glucose; GV, glucose fluctuation; antio, NAC.

Journal: Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy

Article Title: miR-129-3p Targeting of MCU Protects Against Glucose Fluctuation-Mediated Neuronal Damage via a Mitochondrial-Dependent Intrinsic Apoptotic Pathway

doi: 10.2147/DMSO.S285179

Figure Lengend Snippet: miR-129-3p inhibits ROS-mediated apoptosis in glucose fluctuation-exposed hippocampal neuronal cells. Rat primary hippocampal neuronal cells were transfected with miR-NC, miR-129-3p mimics, miR-129-3p inhibitor with or without NAC, followed by glucose fluctuation treatment. ( A ) Flow cytometry was performed to detect the apoptosis of hippocampal neuronal cells. ( B ) Apoptosis rate (%). ( C ) Mitochondrial cytochrome c and ( D ) cytosolic cytochrome c. mRNA levels of ( E ) caspase-9 and ( F ) caspase-3. Data are presented as the means ± SD ; * p < 0.05, ** p < 0.01; (n = 5). CT, normal glucose; GV, glucose fluctuation; antio, NAC.

Article Snippet: Rat primary hippocampal neuronal cells (iCell, China) were cultured in a primary neuronal cell culture system (iCell, China) at 37 °C in 5% CO 2 .

Techniques: Transfection, Flow Cytometry