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Updated: May 19, 2026

Valorization of the Red Seaweed Gracilaria gracilis Through a Biorefinery Approach
Published on: November 21, 2023
Edematogenic activity of a sulfated galactan from the red marine algae Gelidium crinale
Ana Maria Sampaio Assreuy1, Renata Morais Ferreira Amorim, Luiz André Cavalcante Brizeno
1Laboratório de Fisio-Farmacologia da Inflamação-LAFFIN, Instituto Superior de Ciências Biomédicas, Universidade Estadual do Ceará, Fortaleza-CE, Brazil. anassreuy@gmail.com
Context:
The red algae Gelidium crinale (Turner) Gaillon (Gelidiaceae), encountered along the Southeast and Northeast Brazilian sea coast, contains a sulfated galactan presenting a similar saccharide backbone compared to λ carrageenan. Inflammatory effects of other galactans were reported, but not for that obtained from G. crinale (SG-Gc).
Objective:
To investigate the in vivo edematogenic effect of SG-Gc in comparison to λ carrageenan.
Methods:
SG-Gc was isolated by ion exchange chromatography. Paw edema was induced by subcutaneous (s.c.) intraplantar injection of SG-Gc or λ carrageenan and evaluated by hydroplethysmometry. Data were expressed as the increase in paw volume subtracted from the basal volume or area under curve-AUC. To investigate the participation of early and late-phase inflammatory mediators, rats were treated with pyrilamine, compound 48/80, indomethacin, NG-nitro-L-arginine methyl ester (L-NAME), or pentoxifylline before SG-Gc.
Results:
SG-Gc edematogenic effect was initiated at 0.5 h, peaked at 2 h (1.26 ± 0.05 mL) and lasted until 6 h (0.21 ± 0.03 mL), whereas the carrageenan-induced edema started at 1 h. The first phase (1-3 h) of SG-Gc-induced edema was 176 ± 15 (AUC) versus carrageenan (114.5 ± 14), whereas the second phase (3-5 h) was 95 ± 12 (AUC) versus carrageenan (117.5 ± 11). Treatment with compound 48/80, pyrilamine, indomethacin, L-NAME, and pentoxifylline inhibited the effect of SG-Gc by 32, 40, 69, 72, and 49%, respectively.
Discussion And Conclusion:
SG-Gc and λ carrageenan induce different profile of inflammatory response in the paw edema model, that involves histamine, cytokines, prostaglandins, and nitric oxide (NO), but with different degree of participation.
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