c3ar competitive antagonists Search Results


c3ar competitive antagonists  (MedChemExpress)
95
MedChemExpress c3ar competitive antagonists
Impairment of astrocyte insulin signaling and mitochondrial structure after activation of the <t>C3a‐C3aR</t> pathway. (a–c) Western blotting analysis of C3aR and CD11b expression in wild‐type (WT, 6 months old) and C3 +/+ mice (6 months old) ( n = 4 WT, n = 5 C3 +/+ ; unpaired Student's t ‐test). (d) ELISA analysis of C3a levels in brain tissue from WT ( n = 5) and C3 transgenic mice ( n = 5) (unpaired Student's t ‐test). (e, f) CCK‐8 assay of U251 cell survival after C3a (200 nM) and C3a + <t>SB290157</t> treatments ( n = 6 per group; unpaired Student's t ‐test). (g) qPCR analysis of insulin receptor (IR) mRNA levels in U251 cells after C3a treatment ( n = 4 per group; unpaired Student's t ‐test). (h–j) Western blotting analysis of IR protein expression in U251 cells after C3a (200 nM) ( n = 7 per group ) and C3a + SB290157 treatments ( n = 5 per group; unpaired Student's t ‐test). (k–m) qPCR analysis of mitochondrial function‐related genes in U251 cells ( n = 4 per group; unpaired Student's t ‐test). (n) Quantitative analysis of mitochondrial area (unpaired Student's t ‐test). (o) Schematic representation of mitochondrial morphology as observed by transmission electron microscopy. (p, q) Measurement of reactive oxygen species (ROS) production in U251 cells: (p) C3a versus vehicle control; (q) C3a + C3aR antagonist (SB290157, 100 nM) versus vehicle control (unpaired Student's t ‐test). All data are presented as mean ± standard deviation (SD).
C3ar Competitive Antagonists, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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competitive antagonist against c3ar  (MedChemExpress)
94
MedChemExpress competitive antagonist against c3ar
Impairment of astrocyte insulin signaling and mitochondrial structure after activation of the <t>C3a‐C3aR</t> pathway. (a–c) Western blotting analysis of C3aR and CD11b expression in wild‐type (WT, 6 months old) and C3 +/+ mice (6 months old) ( n = 4 WT, n = 5 C3 +/+ ; unpaired Student's t ‐test). (d) ELISA analysis of C3a levels in brain tissue from WT ( n = 5) and C3 transgenic mice ( n = 5) (unpaired Student's t ‐test). (e, f) CCK‐8 assay of U251 cell survival after C3a (200 nM) and C3a + <t>SB290157</t> treatments ( n = 6 per group; unpaired Student's t ‐test). (g) qPCR analysis of insulin receptor (IR) mRNA levels in U251 cells after C3a treatment ( n = 4 per group; unpaired Student's t ‐test). (h–j) Western blotting analysis of IR protein expression in U251 cells after C3a (200 nM) ( n = 7 per group ) and C3a + SB290157 treatments ( n = 5 per group; unpaired Student's t ‐test). (k–m) qPCR analysis of mitochondrial function‐related genes in U251 cells ( n = 4 per group; unpaired Student's t ‐test). (n) Quantitative analysis of mitochondrial area (unpaired Student's t ‐test). (o) Schematic representation of mitochondrial morphology as observed by transmission electron microscopy. (p, q) Measurement of reactive oxygen species (ROS) production in U251 cells: (p) C3a versus vehicle control; (q) C3a + C3aR antagonist (SB290157, 100 nM) versus vehicle control (unpaired Student's t ‐test). All data are presented as mean ± standard deviation (SD).
Competitive Antagonist Against C3ar, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 94 stars, based on 1 article reviews
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Impairment of astrocyte insulin signaling and mitochondrial structure after activation of the C3a‐C3aR pathway. (a–c) Western blotting analysis of C3aR and CD11b expression in wild‐type (WT, 6 months old) and C3 +/+ mice (6 months old) ( n = 4 WT, n = 5 C3 +/+ ; unpaired Student's t ‐test). (d) ELISA analysis of C3a levels in brain tissue from WT ( n = 5) and C3 transgenic mice ( n = 5) (unpaired Student's t ‐test). (e, f) CCK‐8 assay of U251 cell survival after C3a (200 nM) and C3a + SB290157 treatments ( n = 6 per group; unpaired Student's t ‐test). (g) qPCR analysis of insulin receptor (IR) mRNA levels in U251 cells after C3a treatment ( n = 4 per group; unpaired Student's t ‐test). (h–j) Western blotting analysis of IR protein expression in U251 cells after C3a (200 nM) ( n = 7 per group ) and C3a + SB290157 treatments ( n = 5 per group; unpaired Student's t ‐test). (k–m) qPCR analysis of mitochondrial function‐related genes in U251 cells ( n = 4 per group; unpaired Student's t ‐test). (n) Quantitative analysis of mitochondrial area (unpaired Student's t ‐test). (o) Schematic representation of mitochondrial morphology as observed by transmission electron microscopy. (p, q) Measurement of reactive oxygen species (ROS) production in U251 cells: (p) C3a versus vehicle control; (q) C3a + C3aR antagonist (SB290157, 100 nM) versus vehicle control (unpaired Student's t ‐test). All data are presented as mean ± standard deviation (SD).

Journal: Aging Cell

Article Title: Age‐Related Complement C3 Drives Memory Impairments and Associated Neuropathologies in a Mouse Model

doi: 10.1111/acel.70145

Figure Lengend Snippet: Impairment of astrocyte insulin signaling and mitochondrial structure after activation of the C3a‐C3aR pathway. (a–c) Western blotting analysis of C3aR and CD11b expression in wild‐type (WT, 6 months old) and C3 +/+ mice (6 months old) ( n = 4 WT, n = 5 C3 +/+ ; unpaired Student's t ‐test). (d) ELISA analysis of C3a levels in brain tissue from WT ( n = 5) and C3 transgenic mice ( n = 5) (unpaired Student's t ‐test). (e, f) CCK‐8 assay of U251 cell survival after C3a (200 nM) and C3a + SB290157 treatments ( n = 6 per group; unpaired Student's t ‐test). (g) qPCR analysis of insulin receptor (IR) mRNA levels in U251 cells after C3a treatment ( n = 4 per group; unpaired Student's t ‐test). (h–j) Western blotting analysis of IR protein expression in U251 cells after C3a (200 nM) ( n = 7 per group ) and C3a + SB290157 treatments ( n = 5 per group; unpaired Student's t ‐test). (k–m) qPCR analysis of mitochondrial function‐related genes in U251 cells ( n = 4 per group; unpaired Student's t ‐test). (n) Quantitative analysis of mitochondrial area (unpaired Student's t ‐test). (o) Schematic representation of mitochondrial morphology as observed by transmission electron microscopy. (p, q) Measurement of reactive oxygen species (ROS) production in U251 cells: (p) C3a versus vehicle control; (q) C3a + C3aR antagonist (SB290157, 100 nM) versus vehicle control (unpaired Student's t ‐test). All data are presented as mean ± standard deviation (SD).

Article Snippet: The plates were incubated at 37°C with 5% CO 2 for 24 h. The medium was then replaced with fresh medium containing either 200 nM C3a (HY‐P7862, MCE, USA), a C3aR competitive antagonists (SB290157, HY‐101502A, MCE), or the respective control medium.

Techniques: Activation Assay, Western Blot, Expressing, Enzyme-linked Immunosorbent Assay, Transgenic Assay, CCK-8 Assay, Transmission Assay, Electron Microscopy, Control, Standard Deviation