Involvement of the NO/cGMP/PKG/K_ATP pathway and endogenous opioids in the antinociceptive effect of a sulphated-polysaccharide fraction extracted from the red algae, Gracilaria caudata

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• 作者：Francisco das Chagas Vieira Jú ; nior^a ; Adriano Bezerra Sales^a ; Francisco Clark Nogueira Barros^c ; Luciano de Sousa Chaves^c ; Ana Lú ; cia Ponte Freitas^c ; Mariana Lima Vale^b ; Ronaldo de Albuquerque Ribeiro^b ; Marcellus Henrique Loiola Ponte Souza^b ; Jand-Venes Rolim Medeiros^a ; André ; Luiz dos Reis Barbosa^a ; ^{andreluiz@ufpi.edu.br}
• 关键词：Sulfated-polysaccharide ; Hypernociception ; Oxide nitric ; Opioids
• 刊名：Biomedicine & Preventive Nutrition
• 出版年：2012
• 出版时间：October-December, 2012
• 年：2012
• 卷：2
• 期：4
• 页码：303-309
• 全文大小：879 K

文摘

We investigated the antinociceptive activity of a sulphated-polysaccharide (PLS) fraction extracted from the sea algae Gracilaria caudata against carrageenan-induced hypernociception in mice and the mechanism underlying the antinociceptive activity. Mechanical inflammatory hypernociception was measured with an electronic version of the Von Frey^? test. Mice were treated with PLS (2.5, 5.0, and 10 mg/kg, 0.5 mL, p.o.) 1 h before carrageenan treatment. l-Noarg (100 ng/paw; 50 ¦ÌL) was administered 1 h before carrageenan administration. l-Arg (l-Arginine; 200 mg/kg; 0.5 mL, p.o.) was administered 10 min before l-Noarg injection. ODQ (8 ¦Ìg/paw), KT 5823 (1.5 ¦Ìg/paw), glibenclamide (160 ¦Ìg/paw), and naloxone (1.0 ¦Ìg/paw) were administered 30 min before carrageenan administration. PLS reduced carrageenan-induced hypernociception (300 ¦Ìg/paw, 50 ¦ÌL, intraplantar injection). PLS-induced analgesia was reversed by l-Noarg, and the effect of l-Noarg was prevented by l-Arg. The soluble guanylyl cyclase inhibitor ODQ, the protein kinase G inhibitor KT 5823, the K_ATP blocker glibenclamide, and the opioid receptor antagonist naloxone, significantly reversed (P < 0.05) the antinociceptive effect of PLS. The present study showed an intrinsic peripheral antinociceptive action of PLS administration in mice. This antinociceptive effect seemed to be mediated by activation of the NO/cGMP/PKG pathway followed by the opening of K_ATP channels, and depended on endogenous opioids.