c3ar antagonist  (MedChemExpress)

Journal: Journal of Neurochemistry

Article Title: Complement C3a and C5a Receptors Are Presented in Mouse Sciatic and Human Sural Nerves and Selectively Modulate the Neuronal Function of Large‐Caliber Fibers in Mice

doi: 10.1111/jnc.70129

Figure Lengend Snippet: C3aR is localized to the paranodal region. Longitudinal and cross‐sections of human sural nerves were analyzed by immunofluorescence using an anti‐C3aR antibody (red, A, D). The paranodal region was stained with an anti‐Caspr antibody (green, B), and the axons were stained with an anti‐peripherin antibody (green, E). Double‐stained images are merged (C, F). Teased mouse sciatic fibers were stained for C3aR (red, G, J, M), Caspr (green, H, K), and peripherin (green, N). The white arrow points to the Schmidt–Lanterman incisures (G). Double‐stained images are merged (I, L, O). Caspr‐contactin‐associated protein; n = 10 mice; Scale bar, 20 μM.

Article Snippet: The C3aR agonist TLQP‐21 (500 nM, Cat. No. HY‐P1345A, MedChemExpress, NJ, USA), the C3aR antagonist JR14‐a (100 nM, Cat. No. HY‐138161, MedChemExpress) and the combination were applied at the same concentrations as described above.

Techniques: Immunofluorescence, Staining

Journal: Journal of Neurochemistry

Article Title: Complement C3a and C5a Receptors Are Presented in Mouse Sciatic and Human Sural Nerves and Selectively Modulate the Neuronal Function of Large‐Caliber Fibers in Mice

doi: 10.1111/jnc.70129

Figure Lengend Snippet: mRNA and protein expression in the mouse sciatic nerve. Quantitative PCR (qPCR) analysis and western blotting were performed on sciatic nerves from 13‐week‐old mice ( n = 6 nerves). Intrinsic expression of the complement receptors and factors is seen (A). The outcomes are presented relative to hypoxanthine guanine phosphoribosyltransferase expression using the 2 −ΔCT method calculation method. Proteins C3aR and C5aR1 are present in mouse sciatic nerves ( n = 6 nerves) (B, C). HPRT‐hypoxanthine guanine phosphoribosyltransferase; ** p < 0.01.

Article Snippet: The C3aR agonist TLQP‐21 (500 nM, Cat. No. HY‐P1345A, MedChemExpress, NJ, USA), the C3aR antagonist JR14‐a (100 nM, Cat. No. HY‐138161, MedChemExpress) and the combination were applied at the same concentrations as described above.

Techniques: Expressing, Real-time Polymerase Chain Reaction, Western Blot

Journal: Journal of Neurochemistry

Article Title: Complement C3a and C5a Receptors Are Presented in Mouse Sciatic and Human Sural Nerves and Selectively Modulate the Neuronal Function of Large‐Caliber Fibers in Mice

doi: 10.1111/jnc.70129

Figure Lengend Snippet: TLQP‐21 C3aR agonist‐induced neuronal sensitivity. Representative recruitment curves from a control nerve (A) and a nerve treated with the C3aR agonist (B) are shown. TLQP‐21‐treated nerves responded to a lower stimulation current compared to control nerves, prevented by the application of the antagonist (C). EC50 is presented as the EC50 plus 95% CI (profile likelihood) (D). Control n = 10; TLQP‐21 n = 13; JR14a n = 7; TLQP‐21 JR14a n = 10. **** p < 0.0001.

Article Snippet: The C3aR agonist TLQP‐21 (500 nM, Cat. No. HY‐P1345A, MedChemExpress, NJ, USA), the C3aR antagonist JR14‐a (100 nM, Cat. No. HY‐138161, MedChemExpress) and the combination were applied at the same concentrations as described above.

Techniques: Control

Journal: Journal of Neurochemistry

Article Title: Complement C3a and C5a Receptors Are Presented in Mouse Sciatic and Human Sural Nerves and Selectively Modulate the Neuronal Function of Large‐Caliber Fibers in Mice

doi: 10.1111/jnc.70129

Figure Lengend Snippet: The C3aR agonist modulates excitatory neuronal activity. Panel (A) shows a representative example of the refractory response in a control nerve (black, top) compared with a nerve treated with the C3aR agonist (green, bottom). The application of the C3aR agonist led to a reduction in the refractory period, which was prevented by the application of an antagonist (B). In Panel (C), representative examples of the response to high‐frequency stimulation (600–1000 Hz) are presented, comparing a control nerve (black, top) with a nerve following C3aR agonist application (green, bottom). In panel (D), representative examples of the slope at 1000 Hz are presented for a control nerve (black, left) compared with a C3aR agonist‐treated nerve (green, right). The slope in the C3aR agonist‐treated nerves was less steep than that in the control nerves, with the antagonist preventing this excitatory response (E). In panel (F), representative examples of the compound action potential response to 1000 Hz are shown (control: black, top; C3aR agonist: green, bottom). The difference between consecutive compound action potentials was greater in the control nerves than in the C3aR agonist‐treated nerves (G). Control n = 9, TLQP‐21 n = 13, and TLQP‐21 + JR14a n = 10, **** p < 0.0001.

Article Snippet: The C3aR agonist TLQP‐21 (500 nM, Cat. No. HY‐P1345A, MedChemExpress, NJ, USA), the C3aR antagonist JR14‐a (100 nM, Cat. No. HY‐138161, MedChemExpress) and the combination were applied at the same concentrations as described above.

Techniques: Activity Assay, Control

Journal: Journal of Neurochemistry

Article Title: Complement C3a and C5a Receptors Are Presented in Mouse Sciatic and Human Sural Nerves and Selectively Modulate the Neuronal Function of Large‐Caliber Fibers in Mice

doi: 10.1111/jnc.70129

Figure Lengend Snippet: C3aR neuronal hyperexcitability through potassium channel mediation. The slope of the response to high frequencies was similar for low KCl and low KCl + TLQP‐21 (A) Control = white; TLQP‐21 = green. A decreased response to high‐frequency firing rates was observed in the TEA and TEA‐TLQP‐21 nerves (B). Control n = 9; TLQP‐21 n = 12; Low KCl n = 4; Low KCl + TLQP‐21 n = 5; TEA n = 4; TEA + TLQP‐21 n = 6; TEA‐ tetraethyl ammonium chloride; ** p < 0.01.

Article Snippet: The C3aR agonist TLQP‐21 (500 nM, Cat. No. HY‐P1345A, MedChemExpress, NJ, USA), the C3aR antagonist JR14‐a (100 nM, Cat. No. HY‐138161, MedChemExpress) and the combination were applied at the same concentrations as described above.

Techniques: Control

Journal: Computational and structural biotechnology journal

Article Title: The complement C3a/C3aR pathway is associated with treatment resistance to gemcitabine-based neoadjuvant therapy in pancreatic cancer.

doi: 10.1016/j.csbj.2024.09.032

Figure Lengend Snippet: Fig. 7. Knockdown of C3aR does not affect the progression of pancreatic cancer cells in vitro. A.A-F Panc-1 cells were infected with C3aR shRNA to knock down the C3aR expression (sh#1, sh#2), or infected with a scrambled shRNA as the control group (sh-Scr). (A) Western blotting was used to detect C3aR expression in control cells and C3aR-deficient cells to evaluate the transfection efficiency. (B) CCK8 assay was used to evaluate the cell proliferation, and the relative optical density of each group at day 0, 1, 2, 3 and 4 was measured. The line chart showed that C3aR knockdown did not change the proliferation capacity of Panc-1 cells. (C) Representative images of EdU assays showed that the knockdown of C3aR did not affect the proliferation capacity of Panc-1 cells. (D) The bar plot showed the percentage of EdU+

Article Snippet: Recombinant human complement C3a protein (MedChemExpress, MCE; HY-P7862), recombinant mouse complement C3a protein (MCE; HY-P7863) and C3aR antagonist, SB290157 (TargetMol) were used according to the manufacturer’s instructions.

Techniques: Knockdown, In Vitro, Infection, shRNA, Expressing, Control, Western Blot, Transfection, CCK-8 Assay

Journal: Computational and structural biotechnology journal

Article Title: The complement C3a/C3aR pathway is associated with treatment resistance to gemcitabine-based neoadjuvant therapy in pancreatic cancer.

doi: 10.1016/j.csbj.2024.09.032

Figure Lengend Snippet: Fig. 8. C3aR antagonist (SB290157) attenuated the effects of C3a activation in pancreatic cancer. (A) Representative images of EdU assays showed that the treatment of SB290157 attenuated C3a-induced proliferation in Panc-1 cells. (B) The bar plot showed the percentage of EdU+ cells per field. (C) Representative images of Transwell assays showed that the treatment of SB290157 attenuated C3a-induced migration in Panc-1 cells. (D) The bar plot showed the percentage of migrated cells per field. (E) CCK-8 assay showed that the treatment of SB290157 attenuated C3a-induced gemcitabine resistance in Panc-1 cells. F-K A mouse subcutaneous tumor model of Panc-1 cells was constructed. The mice were randomly grouped and treated with vehicle, 20 mg/kg gemcitabine, 20 mg/kg SB290157, 20 mg/kg gem- citabine combined with 20 mg/kg SB29015 by intraperitoneal injection once a day. (F) Line charts of volume changes of subcutaneous tumor. (G) On the 14th day of treatment, subcutaneous tumors were separated to show tumor size. Frozen sections were prepared from tumor tissues. IF staining with antibodies to Ki-67 (in red color, (H)) and CC3 (in red color, (J)) was performed to detect proliferation and apoptosis of Panc-1 cells. And the percentage of Ki-67+ cells (I) or CC3+ cells (K) per field was shown by bar plots. * P < 0.05, * * P < 0.01, * ** P < 0.001. GEM, gemcitabine.

Article Snippet: Recombinant human complement C3a protein (MedChemExpress, MCE; HY-P7862), recombinant mouse complement C3a protein (MCE; HY-P7863) and C3aR antagonist, SB290157 (TargetMol) were used according to the manufacturer’s instructions.

Techniques: Activation Assay, Migration, CCK-8 Assay, Construct, Injection, Staining