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mn plasma 1 recombinant human c3a  (R&D Systems)


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    R&D Systems mn plasma 1 recombinant human c3a
    Figure 4. The treatments of C3aR antagonist alleviated plasma level of <t>C3a</t> and glomerular expression of C3aR on Heymann nephritis rats. Sprague-Dawley rats were injected with anti-Fx1A antibody serum via the tail vein. The plasma C3a was significantly elevated in disease controls (A, C). After C3aR antagonist treatments, it was decreased remarkably, both in the early-treatment groups and in the late-treatment groups: SB290157 (B), JR14a (D). In the kidneys, the staining of C3aR was strong in the rats with Heymann nephritis (E), and was attenuated in both treatment groups (F, G). *P,0.05, **P,0.01, ***P,0.001.
    Mn Plasma 1 Recombinant Human C3a, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 20 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mn plasma 1 recombinant human c3a/product/R&D Systems
    Average 94 stars, based on 20 article reviews
    mn plasma 1 recombinant human c3a - by Bioz Stars, 2026-02
    94/100 stars

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    1) Product Images from "Complement C3a and C3a Receptor Activation Mediates Podocyte Injuries in the Mechanism of Primary Membranous Nephropathy"

    Article Title: Complement C3a and C3a Receptor Activation Mediates Podocyte Injuries in the Mechanism of Primary Membranous Nephropathy

    Journal: Journal of the American Society of Nephrology

    doi: 10.1681/asn.2021101384

    Figure 4. The treatments of C3aR antagonist alleviated plasma level of C3a and glomerular expression of C3aR on Heymann nephritis rats. Sprague-Dawley rats were injected with anti-Fx1A antibody serum via the tail vein. The plasma C3a was significantly elevated in disease controls (A, C). After C3aR antagonist treatments, it was decreased remarkably, both in the early-treatment groups and in the late-treatment groups: SB290157 (B), JR14a (D). In the kidneys, the staining of C3aR was strong in the rats with Heymann nephritis (E), and was attenuated in both treatment groups (F, G). *P,0.05, **P,0.01, ***P,0.001.
    Figure Legend Snippet: Figure 4. The treatments of C3aR antagonist alleviated plasma level of C3a and glomerular expression of C3aR on Heymann nephritis rats. Sprague-Dawley rats were injected with anti-Fx1A antibody serum via the tail vein. The plasma C3a was significantly elevated in disease controls (A, C). After C3aR antagonist treatments, it was decreased remarkably, both in the early-treatment groups and in the late-treatment groups: SB290157 (B), JR14a (D). In the kidneys, the staining of C3aR was strong in the rats with Heymann nephritis (E), and was attenuated in both treatment groups (F, G). *P,0.05, **P,0.01, ***P,0.001.

    Techniques Used: Clinical Proteomics, Expressing, Injection, Staining

    Figure 5. The treatments of C3aR antagonist inhibited specific IgG and complement activation on Heymann nephritis rats. Sprague-Dawley rats were injected with anti-Fx1A antibody serum via the tail vein. In the early-treatment groups, C3aR antagonists (SB290157 or JR14a) was administrated daily from day 0. In the late-treatment groups, both C3aR antagonists were administrated from week 3 after proteinuria was detected. Compared with the disease controls treated with normal saline, the plasma level of spe- cific anti-sheep IgG was decreased in treatment groups of both C3aR antagonists, SB290157 (A) and JR14a (B), whereas the level of total IgG was comparable among the groups. In the glomeruli, the deposit of sheep IgG (C) was comparable among the disease controls and treatment groups. However, the deposit of rat IgG (D) was alleviated in both treatment groups. Along with that, the staining of C1q (E), factor B (F), and C5b-9 (G) was significantly decreased in the treatment groups. *P,0.05, **P,0.01, ***P,0.001.
    Figure Legend Snippet: Figure 5. The treatments of C3aR antagonist inhibited specific IgG and complement activation on Heymann nephritis rats. Sprague-Dawley rats were injected with anti-Fx1A antibody serum via the tail vein. In the early-treatment groups, C3aR antagonists (SB290157 or JR14a) was administrated daily from day 0. In the late-treatment groups, both C3aR antagonists were administrated from week 3 after proteinuria was detected. Compared with the disease controls treated with normal saline, the plasma level of spe- cific anti-sheep IgG was decreased in treatment groups of both C3aR antagonists, SB290157 (A) and JR14a (B), whereas the level of total IgG was comparable among the groups. In the glomeruli, the deposit of sheep IgG (C) was comparable among the disease controls and treatment groups. However, the deposit of rat IgG (D) was alleviated in both treatment groups. Along with that, the staining of C1q (E), factor B (F), and C5b-9 (G) was significantly decreased in the treatment groups. *P,0.05, **P,0.01, ***P,0.001.

    Techniques Used: Activation Assay, Injection, Saline, Clinical Proteomics, Staining



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    mn plasma 1 recombinant human c3a  (R&D Systems)
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    R&D Systems mn plasma 1 recombinant human c3a
    Figure 4. The treatments of C3aR antagonist alleviated plasma level of <t>C3a</t> and glomerular expression of C3aR on Heymann nephritis rats. Sprague-Dawley rats were injected with anti-Fx1A antibody serum via the tail vein. The plasma C3a was significantly elevated in disease controls (A, C). After C3aR antagonist treatments, it was decreased remarkably, both in the early-treatment groups and in the late-treatment groups: SB290157 (B), JR14a (D). In the kidneys, the staining of C3aR was strong in the rats with Heymann nephritis (E), and was attenuated in both treatment groups (F, G). *P,0.05, **P,0.01, ***P,0.001.
    Mn Plasma 1 Recombinant Human C3a, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mn plasma 1 recombinant human c3a/product/R&D Systems
    Average 94 stars, based on 1 article reviews
    mn plasma 1 recombinant human c3a - by Bioz Stars, 2026-02
    94/100 stars
    		  Buy from Supplier

    Image Search Results


    Figure 4. The treatments of C3aR antagonist alleviated plasma level of C3a and glomerular expression of C3aR on Heymann nephritis rats. Sprague-Dawley rats were injected with anti-Fx1A antibody serum via the tail vein. The plasma C3a was significantly elevated in disease controls (A, C). After C3aR antagonist treatments, it was decreased remarkably, both in the early-treatment groups and in the late-treatment groups: SB290157 (B), JR14a (D). In the kidneys, the staining of C3aR was strong in the rats with Heymann nephritis (E), and was attenuated in both treatment groups (F, G). *P,0.05, **P,0.01, ***P,0.001.

    Journal: Journal of the American Society of Nephrology

    Article Title: Complement C3a and C3a Receptor Activation Mediates Podocyte Injuries in the Mechanism of Primary Membranous Nephropathy

    doi: 10.1681/asn.2021101384

    Figure Lengend Snippet: Figure 4. The treatments of C3aR antagonist alleviated plasma level of C3a and glomerular expression of C3aR on Heymann nephritis rats. Sprague-Dawley rats were injected with anti-Fx1A antibody serum via the tail vein. The plasma C3a was significantly elevated in disease controls (A, C). After C3aR antagonist treatments, it was decreased remarkably, both in the early-treatment groups and in the late-treatment groups: SB290157 (B), JR14a (D). In the kidneys, the staining of C3aR was strong in the rats with Heymann nephritis (E), and was attenuated in both treatment groups (F, G). *P,0.05, **P,0.01, ***P,0.001.

    Article Snippet: Conditionally immortalized human podocytes, kindly provided by Prof. Jochen Reiser (Rush University Medical Center, Chicago, IL), were cultivated and allowed to differentiate as described previously.16 The differentiated podocytes on sixwell plates were cultured in RPMI 1640 medium for 6 hours to achieve synchronization, then stimulated in RPMI 1640 medium containing 10% plasma from patients with primary MN, 10% MN plasma 1 C3aR antagonist SB290157 (HY101502A; MedChemExpress, Monmouth Junction, NJ), 10% MN plasma 1 C3aR antagonist JR14a (HY-138161; MedChemExpress), 10% MN plasma 1 recombinant human C3a (2 mg/ml, 3677-C3; R&D Systems, Minneapolis, MN), 10% plasma from healthy controls, C3a, or 5% FBS (10100147; Gibco, CA).

    Techniques: Clinical Proteomics, Expressing, Injection, Staining

    Figure 5. The treatments of C3aR antagonist inhibited specific IgG and complement activation on Heymann nephritis rats. Sprague-Dawley rats were injected with anti-Fx1A antibody serum via the tail vein. In the early-treatment groups, C3aR antagonists (SB290157 or JR14a) was administrated daily from day 0. In the late-treatment groups, both C3aR antagonists were administrated from week 3 after proteinuria was detected. Compared with the disease controls treated with normal saline, the plasma level of spe- cific anti-sheep IgG was decreased in treatment groups of both C3aR antagonists, SB290157 (A) and JR14a (B), whereas the level of total IgG was comparable among the groups. In the glomeruli, the deposit of sheep IgG (C) was comparable among the disease controls and treatment groups. However, the deposit of rat IgG (D) was alleviated in both treatment groups. Along with that, the staining of C1q (E), factor B (F), and C5b-9 (G) was significantly decreased in the treatment groups. *P,0.05, **P,0.01, ***P,0.001.

    Journal: Journal of the American Society of Nephrology

    Article Title: Complement C3a and C3a Receptor Activation Mediates Podocyte Injuries in the Mechanism of Primary Membranous Nephropathy

    doi: 10.1681/asn.2021101384

    Figure Lengend Snippet: Figure 5. The treatments of C3aR antagonist inhibited specific IgG and complement activation on Heymann nephritis rats. Sprague-Dawley rats were injected with anti-Fx1A antibody serum via the tail vein. In the early-treatment groups, C3aR antagonists (SB290157 or JR14a) was administrated daily from day 0. In the late-treatment groups, both C3aR antagonists were administrated from week 3 after proteinuria was detected. Compared with the disease controls treated with normal saline, the plasma level of spe- cific anti-sheep IgG was decreased in treatment groups of both C3aR antagonists, SB290157 (A) and JR14a (B), whereas the level of total IgG was comparable among the groups. In the glomeruli, the deposit of sheep IgG (C) was comparable among the disease controls and treatment groups. However, the deposit of rat IgG (D) was alleviated in both treatment groups. Along with that, the staining of C1q (E), factor B (F), and C5b-9 (G) was significantly decreased in the treatment groups. *P,0.05, **P,0.01, ***P,0.001.

    Article Snippet: Conditionally immortalized human podocytes, kindly provided by Prof. Jochen Reiser (Rush University Medical Center, Chicago, IL), were cultivated and allowed to differentiate as described previously.16 The differentiated podocytes on sixwell plates were cultured in RPMI 1640 medium for 6 hours to achieve synchronization, then stimulated in RPMI 1640 medium containing 10% plasma from patients with primary MN, 10% MN plasma 1 C3aR antagonist SB290157 (HY101502A; MedChemExpress, Monmouth Junction, NJ), 10% MN plasma 1 C3aR antagonist JR14a (HY-138161; MedChemExpress), 10% MN plasma 1 recombinant human C3a (2 mg/ml, 3677-C3; R&D Systems, Minneapolis, MN), 10% plasma from healthy controls, C3a, or 5% FBS (10100147; Gibco, CA).

    Techniques: Activation Assay, Injection, Saline, Clinical Proteomics, Staining