The intermediary role of the central cyclooxygenase/lipoxygenase enzymes in intracerebroventricular injected nesfatin-1-evoked cardiovascular effects in rats


GÜVENÇ BAYRAM G., YALÇIN M.

NEUROSCIENCE LETTERS, cilt.756, 2021 (SCI-Expanded, Scopus) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 756
  • Basım Tarihi: 2021
  • Doi Numarası: 10.1016/j.neulet.2021.135961
  • Dergi Adı: NEUROSCIENCE LETTERS
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, Animal Behavior Abstracts, BIOSIS, CAB Abstracts, Chemical Abstracts Core, EMBASE, MEDLINE, Veterinary Science Database
  • Anahtar Kelimeler: Nesfatin-1, Intracerebroventricular, Cyclooxygenase, Lipoxygenase, Mean arterial blood pressure, Heart rate
  • Dokuz Eylül Üniversitesi Adresli: Hayır

Özet

That nesfatin-1 is a neuromodulatory peptide for the cardiovascular system is well documented. Several central receptors have been shown to mediate the cardiovascular effects of nesfatin-1. Immunohistochemistry and Western blot studies showed that nesfatin-1 activated the expression of the central cyclooxygenase (COX) -1, -2 and lipoxygenase (LOX). In addition, microdialysis study showed that nesfatin-1 increased the release of total prostaglandins and leukotrienes from the hypothalamus. The present study investigated whether the central COX and LOX enzymes have a direct mediating role in the MAP and HR responses of nesfatin-1. Intracerebroventricularly administered nesfatin-1 produced dose-dependent pressor and phasic HR responses in normotensive conscious rats Sprague Dawley. Central pretreatment with a COX1/2 inhibitor, ibuprofen, completely blocked the nesfatin-1-induced responses. However, central pretreatment with a nonselective LOX inhibitor, nordihydroguaiaretic acid, partially attenuated the cardiovascular responses induced by nesfatin-1. The results suggest that centrally administered nesfatin-1 activates the central enzymes COX and LOX, which may be involved in the cardiovascular responses as a novel central mechanism for nesfatin-1.