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Published on: April 11, 2012
Methylguanidine reduces the development of non septic shock induced by zymosan in mice
Stefania Marzocco1, Rosanna Di Paola, Tiziana Genovese
1Department of Pharmaceutical Sciences, University of Salerno, Via Ponte Don Melillo 11/c, 84084, Fisciano--Salerno, Italy. smarzocco@unisa.it
Abstract:
In the present study we evaluate the effect of methylguanidine (MG), a product of protein catabolism, in a model of acute inflammation (zymosan induced inflammation) in mice where oxyradical and nitric oxide (NO) play a crucial role. Our data show that MG, given intraperitoneally at the dose of 30 mg/Kg, inhibits the inflammatory response reducing significantly (P < 0.05) peritoneal exudates formation, mononuclear cell infiltration and histological injury in mice. Furthermore, our data suggests that there is a significant (P < 0.05) reduction in kidney, liver and pancreas injury as demonstrated by the reduction in amylase, lipase, creatinine, AST, ALT, bilirubine and alkaline phosfatase levels. MG is also able to reduce the appearance of nitrotyrosine and of the nuclear enzyme poly (adenosine diphosphate [ADP]-ribose) synthase (PARS) immunoreactivity in the inflamed intestinal and lung tissues. The histological examination revealed a significant reduction in zymosan-induced intestinal and lung damage in MG-treated mice. Taken together, the present results demonstrate that MG exerts potent anti-inflammatory effects on zymosan-induced shock.
Insights
Methylguanidine (MG), a protein breakdown product, significantly reduces inflammation and organ damage in a mouse model. This study shows MG
Area of Science:
- Biochemistry and Molecular Biology
- Immunology
- Pharmacology
Background:
- Acute inflammation involves complex pathways including oxyradicals and nitric oxide (NO).
- Methylguanidine (MG) is a known product of protein catabolism.
- Zymosan-induced inflammation in mice is a standard model for studying acute inflammatory responses.
Purpose of the Study:
- To evaluate the anti-inflammatory effects of methylguanidine (MG) in a zymosan-induced acute inflammation model.
- To investigate MG's impact on inflammatory markers and organ damage.
- To explore MG's potential role in modulating pathways involving nitrotyrosine and poly (ADP-ribose) synthase (PARS).
Main Methods:
- Administration of methylguanidine (MG) intraperitoneally at 30 mg/Kg to mice.
- Induction of acute inflammation using zymosan.
- Assessment of peritoneal exudates, cell infiltration, and histological injury.
- Measurement of serum markers for kidney, liver, and pancreas function.
- Immunohistochemical analysis for nitrotyrosine and PARS in inflamed tissues.
Main Results:
- MG significantly inhibited peritoneal exudates formation, mononuclear cell infiltration, and histological injury.
- MG treatment led to a significant reduction in markers of kidney, liver, and pancreas injury.
- MG decreased nitrotyrosine and PARS immunoreactivity in inflamed intestinal and lung tissues.
- Histological examination showed reduced zymosan-induced intestinal and lung damage in MG-treated mice.
Conclusions:
- Methylguanidine (MG) demonstrates potent anti-inflammatory effects in a model of acute inflammation.
- MG mitigates organ damage associated with zymosan-induced shock.
- These findings suggest MG as a potential therapeutic agent for inflammatory conditions.
