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Inflammation Research

, Volume 44, Issue 11, pp 466–469 | Cite as

Effects of chlomipramine and fluoxetine on subcutaneous carrageenin-induced inflammation in the rat

  • M. Bianchi
  • G. Rossoni
  • P. Sacerdote
  • A. E. Panerai
  • F. Berti
Article

Abstract

We have previously shown that, after acute administration, antidepressant drugs exert anti-inflammatory actions in rats. In this study we evaluated the effects of 3 different doses of chlomipramine (10, 20, and 40 mg/kg i.p), and fluoxetine (5.0, 10, and 20 mg/kg i.p.) on subcutaneous carrageenin-induced inflammation. Both drugs dose-dependently reduced the inflammatory exudate, as well as the PGE2-like bio- and immuno-activity in the exudate. Chlomipramine dose-dependently reduced substance P concentrations in the exudate, whereas fluoxetine was effective only at the highest dose. Our results confirm that antidepressant drugs are able to reduce the development of inflammation in the rat and suggest that the inhibition of substance P production might play a role in mediating the anti-inflammatory effects of chlomipramine.

Key words

Chlomipramine Fluoxetine Edema Prostaglandins Substance P 

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References

  1. [1]
    Michelson D, Misiewicz-Poltorak B, Raybourne RB, Gold PW, Sternberg EM. Imipramine reduces the local inflammatory response to carrageenin. Agents Actions 1994;42:25–8.PubMedGoogle Scholar
  2. [2]
    Butler SH, Weil-Fugazza J, Godefroy F, Besson J. Reduction of arthritis and pain behavior following chronic administration of amitriptyline or imipramine in rats with adjuvant-induced arthritis. Pain 1985;23:159–75.PubMedGoogle Scholar
  3. [3]
    Bianchi M, Sacerdote P, Panerai AE. Chlomipramine differently affects inflammatory edema and pain in the rat. Pharmacol Biochem Behav 1994;1037–40.Google Scholar
  4. [4]
    Bianchi M, Sacerdote P, Panerai AE. Fluoxetine reduces inflammatory edema in the rat: involvement of the pituitary-adrenal axis. Eur J Pharmacol 1994;263:81–4.PubMedGoogle Scholar
  5. [5]
    Sacerdote P, Bianchi M, Panerai AE. Chlomipramine and nortriptyline but not fluoxetine and fluvoxamine inhibit human polymorphonuclear cell chemotaxis in vitro. Gen Pharmac 1994;25:409–12.Google Scholar
  6. [6]
    Krupp P, West M. Inhibition of prostaglandin synthetase by psychotropic drugs. Experientia 1975;31:330–31.PubMedGoogle Scholar
  7. [7]
    Lembeck F, Holzer P. Substance P as a neurogenic mediator of antidromic vasodilatation and neurogenic plasma extravasation. Naunyn-Schmiedeberg's Arch Pharmac 1979;310:175–83.Google Scholar
  8. [8]
    Barber A. u- and k-opioid receptor agonists produce peripheral inhibition of neurogenic plasma extravasation in rat skin. Eur J Pharmacol 1993;236:113–20.PubMedGoogle Scholar
  9. [9]
    Scott DT, Lam FY, Ferrell WR. Acute joint inflammation-mechanisms and mediators. Gen Pharmac 1994;25:1285–96.Google Scholar
  10. [10]
    Lam FY, Ferrell WR. Inhibition of carrageenan-induced inflammation in the rat knee joint by substance P antagonist. Ann Rheum Dis 1989;48:928–32.PubMedGoogle Scholar
  11. [11]
    Berti F, Galli G, Omini C, Rossoni G, Brunelli G, Daffonchio L et al. Interference of the new antiinflammatory compound flunoxaprofen with eicosanoid formation in various biological systems. Arzneim Forsch Drug Res 1987;37:27–32.Google Scholar
  12. [12]
    Pradelles P, Grassi J, Maclouf J. Enzyme immunoassays of eicosanoids using acetylcholine esterase as label: an alternative to radioimmunoassay. Anal Chem 1985;57:1170–3.PubMedGoogle Scholar
  13. [13]
    Panerai AE, Sacerdote P, Brini A, Bianchi M, Mantegazza P. Central nervous system neuropeptides after peripheral nerve deafferentation. Peptides 1988;9:319–24.PubMedGoogle Scholar
  14. [14]
    Foreman JC. Peptides and neurogenic inflammation. Br Med Bull 1987;43:386–400.PubMedGoogle Scholar
  15. [15]
    Arrigoni Martelli E, Toth E, Segre AD, Corsico N. Mechanism of inhibition of experimental inflammation by antidepressant drugs. Eur J Pharmacol 1967;2:229–33.PubMedGoogle Scholar
  16. [16]
    Maj J, Przegalinsky E, Mogilnica E. Hypothesis concerning the mechanism of action of antidepressant drugs. Rev Physiol Biochem Pharmacol 1984;100:1–74.PubMedGoogle Scholar
  17. [17]
    Richelson E, Pfenning M. Blockade by antidepressants and related compounds of biogenic amine uptake into rat brain synaptosomes: most antidepressants selectively block norepinephrine uptake. Eur J Pharmacol 1984;104:277–86.PubMedGoogle Scholar
  18. [18]
    Szafarczyk AG, Alonso G, Ixart G, Malaval F, Nougyier-Soule J, et al. Serotonergic system and circadian rhythms of ACTH and corticosterone in rats. Am J Physiol 1980;239:482–9.Google Scholar
  19. [19]
    Fuller RW. Serotonergic stimulation of pituitary-adrenocortical function in rats. Neuroendocrinol 1981;32:118–27.Google Scholar

Copyright information

© Birkhäuser Verlag, Basel 1995

Authors and Affiliations

  • M. Bianchi
    • 1
  • G. Rossoni
    • 1
  • P. Sacerdote
    • 1
  • A. E. Panerai
    • 1
  • F. Berti
    • 1
  1. 1.Dept. PharmacologyUniversity of MilanMilanItaly

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