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The antinociceptive activity of Muntingia calabura aqueous extract and the involvement of l ‐arginine/nitric oxide/cyclic guanosine monophosphate pathway in its observed activity in mice
Author(s) -
Zakaria Zainul Amiruddin,
Sulaiman Mohd Roslan,
Jais Abdul Manan Mat,
Somchit Muhammad Nazrul,
Jayaraman Kogilla Vani,
Balakhrisnan Ganesh,
Abdullah Fatimah Corazon
Publication year - 2006
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1111/j.1472-8206.2006.00412.x
Subject(s) - chemistry , nitric oxide , cyclic guanosine monophosphate , arginine , guanosine , pharmacology , distilled water , methylene blue , biochemistry , chromatography , medicine , amino acid , organic chemistry , photocatalysis , catalysis
The present study was carried out to investigate on the possible involvement of l ‐arginine/nitric oxide/cyclic guanosine monophosphate ( l ‐arginine/NO/cGMP) pathway in the aqueous extract of Muntingia calabura (AEMC) leaves antinociception in mice assessed by abdominal constriction test. The AEMC, obtained by soaking the dried leaves in distilled water (DH 2 O) (1 : 2; w/v) for 24 h, was prepared in concentrations of 10%, 50% and 100% that were approximately equivalent to doses of 27, 135 and 270 mg/kg, and administered subcutaneously (s.c.) 5 min after pre‐treatment (s.c.) of mice with DH 2 O, l ‐arginine (20 mg/kg), N G ‐monomethyl‐ l ‐arginine acetate ( l ‐NMMA; 20 mg/kg), N G ‐nitro‐ l ‐arginine methyl esters ( l ‐NAME; 20 mg/kg), methylene blue (MB) (20 mg/kg), respectively. The AEMC was found to exhibit a concentration‐dependent antinociception after pre‐challenge with DH 2 O. Interestingly, pre‐treatment with l ‐arginine was found to block significantly ( P < 0.05) the AEMC antinociception but only at the highest concentration (100%) of AEMC used. On the other hand, pre‐treatment with l ‐NAME was found to significantly ( P < 0.05) enhance the low concentration but inhibit the high concentration AEMC antinociception. MB was found to significantly ( P < 0.05) enhance AEMC antinociception at all concentrations used. Except for the higher concentration of AEMC used, co‐treatment with l ‐NAME was found to insignificantly and significantly ( P < 0.05) reverse the l ‐arginine effect when given alone or with low concentration AEMC, respectively. In addition, co‐treatment with MB significantly ( P < 0.05) reversed the l ‐arginine effect when given alone or with 10% concentration AEMC but failed to affect the activity of the rest of concentrations used. As a conclusion, this study has demonstrated the involvement of l ‐arginine/NO/cGMP pathway in AEMC antinociception.