The relevance of kalikrein-kinin system via activation of B receptor in LPS-induced fever in rats.

Purpose: This study evaluated the involvement of endogenous kallikrein-kinin system and the bradykinin (BK) B and B receptors on LPS- induced fever and the POA cells involved in this response.

Material And Methods: Male Wistar rats received either i.v.

Virtual screening and biological evaluation of novel antipyretic compounds.

Due to the absence of safety of the antipyretics to patients with cardiovascular dysfunction, new targets to treat inflammation have been pursued. mPGES-1 is a promising target because its inhibition would not cause the side-effects related to COX inhibition. To identify novel inhibitors of mPGES-1, we developed a ligand-based pharmacophore model that differentiates true inhibitors from decoys and enlightens the structure-activity relationships for known mPGES-1 inhibitors.

Dipyrone metabolite 4-MAA induces hypothermia and inhibits PGE2 -dependent and -independent fever while 4-AA only blocks PGE2 -dependent fever.

Background And Purpose: The antipyretic and hypothermic prodrug dipyrone prevents PGE2 -dependent and -independent fever induced by LPS from Escherichia coli and Tityus serrulatus venom (Tsv) respectively. We aimed to identify the dipyrone metabolites responsible for the antipyretic and hypothermic effects.

Experimental Approach: Male Wistar rats were treated i.

Chemokine ligand (CCL)-3 promotes an integrated febrile response when injected within pre-optic area (POA) of rats and induces calcium signaling in cells of POA microcultures but not TNF-α or IL-6 synthesis.

Although studies have shown that chemokines are pyrogenic when injected into the brain, there are no data indicating which cell types and receptors in the CNS are employed by chemokines such as CCL3 (synonym: MIP-1α) to induce fever in rats. We aimed to study, whether CCL3 induces fever when injected directly into the thermoregulatory center within the pre-optic area (POA). Moreover, we investigated whether CCL3 activates cells from POA microcultures resulting in intracellular Ca++ mobilization and synthesis/release of TNF-α and IL-6.

Involvement of PGE2 and RANTES in Staphylococcus aureus-induced fever in rats.

This study investigated the involvement of prostaglandins and regulated on activation, normal T cell expressed and secreted (RANTES), in fever induced by live Staphylococcus aureus (no. 25923, American Type Culture Collection) injection in rats. S.

Febrile response induced by cecal ligation and puncture (CLP) in rats: involvement of prostaglandin E2 and cytokines.

The purpose of the present study was to better understand the events involved in the febrile response induced by cecal ligation and puncture (CLP), a complex infectious process. To this end, we conducted in vivo experiments in rats examining (1) fever development, (2) bacterial number in the infection focus and in blood, (3) peripheral and hypothalamic synthesis of cytokines, (4) hypothalamic and cerebrospinal fluid (CSF) synthesis of prostaglandin E(2) (PGE(2)), (5) the effect of anti-IL-6 antibody on fever, and (6) the effect of celecoxib on fever and hypothalamic synthesis of PGE(2) after CLP induction. We found that CLP promotes fever and animal death depending on the number of punctures.

Cyclooxygenase-independent mechanism of ibuprofen-induced antipyresis: the role of central vasopressin V₁ receptors.

This study compared the antipyretic effects of ibuprofen and indomethacin regarding the efficacy in blocking fevers induced by lipopolysaccharide (LPS from E. coli) or pyrogenic mediators that act on prostaglandin (PG)-dependent and PG-independent pathways. The content of PGE₂ in the cerebrospinal fluid (CSF) and the dependence on central arginine vasopressin (AVP) release by both antipyretics were also compared during the reduction of LPS-induced fever.

Hypotensive effect of the nitrosyl ruthenium complex nitric oxide donor in renal hypertensive rats.

We have described a new compound (trans-[RuCl([15]aneN(4))NO](2+)), which in vitro releases NO by the action of a reducing agent such as catecholamines. We investigated the effect of this NO donor in lowering the mean arterial pressure (MAP) in severe and moderate renal hypertensive 2K-1C rats. MAP was measured before and after intravenous in bolus injection of the compound in conscious 2K-1C and normotensive (2K) rats.

Cytokine-induced neutrophil chemoattractant (CINC)-1 induces fever by a prostaglandin-dependent mechanism in rats.

Cytokine-induced neutrophil chemoattractant-1 (CINC-1), a member of the ELR+CXC subfamily [ELR motif (glutamic acid-leucine-arginine) adjacent to the cysteine-X-cysteine (CXC) motif located at the N-terminus of the protein], is an acute-phase protein and its synthesis is induced by endogenous and exogenous pyrogens. However, there are no studies on the pyrogenic property of CINC-1. Therefore, the present study evaluates whether centrally administered CINC-1 promotes an integrated febrile response along with an increase in the prostaglandin (PG)E2 content of the cerebrospinal fluid (CSF) of rats.