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Luca Parente - One of the best experts on this subject based on the ideXlab platform.
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inhibition of interleukin 1β induced pyresis in the rabbit by peptide 204 212 of Lipocortin 5
European Journal of Pharmacology, 1995Co-Authors: Mitri Palmi, Mauro Perretti, C Becherucci, Maria Frosini, Gian Pietro Sgaragli, Luca ParenteAbstract:Abstract The intracerebroventricular administration of interleukin-1β (12.5 ng/kg) in rabbits caused a prompt rise of prostaglandin E 2 concentration (+632.6 ± 243.9%) in the cerebrospinal fluid followed by hyperthermia (+1.61 ± 0.14 Δ°C). The intracerebroventricular administration of an anti-inflammatory nonapeptide (amino acids 204–212, SHLRKVFDK) derived from Lipocortin 5, thereafter referred to as Lipocortin 5-(204–212)-peptide, inhibited in a significant manner both the increase in cerebrospinal fluid [prostaglandin E 2 ] and the febrile response induced by the cytokine. This inhibitory effect is probably due to interference by the peptide with phospholipase A 2 activity. A control peptide (FKRVHDLKS) formed by the same amino acids in a randomly shuffled sequence had no effect. These results show that, in addition to the anti-inflammatory effect previously reported, the peptide 204–212 of Lipocortin 5 possesses, like glucocorticoids, anti-pyretic activity. The research on Lipocortin-derived peptides may lead to the development of novel anti-inflammatory and anti-pyretic compounds.
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Inhibition of interleukin-1β-induced pyresis in the rabbit by peptide 204–212 of Lipocortin 5
European Journal of Pharmacology, 1995Co-Authors: Mitri Palmi, Mauro Perretti, C Becherucci, Maria Frosini, Gian Pietro Sgaragli, Luca ParenteAbstract:Abstract The intracerebroventricular administration of interleukin-1β (12.5 ng/kg) in rabbits caused a prompt rise of prostaglandin E 2 concentration (+632.6 ± 243.9%) in the cerebrospinal fluid followed by hyperthermia (+1.61 ± 0.14 Δ°C). The intracerebroventricular administration of an anti-inflammatory nonapeptide (amino acids 204–212, SHLRKVFDK) derived from Lipocortin 5, thereafter referred to as Lipocortin 5-(204–212)-peptide, inhibited in a significant manner both the increase in cerebrospinal fluid [prostaglandin E 2 ] and the febrile response induced by the cytokine. This inhibitory effect is probably due to interference by the peptide with phospholipase A 2 activity. A control peptide (FKRVHDLKS) formed by the same amino acids in a randomly shuffled sequence had no effect. These results show that, in addition to the anti-inflammatory effect previously reported, the peptide 204–212 of Lipocortin 5 possesses, like glucocorticoids, anti-pyretic activity. The research on Lipocortin-derived peptides may lead to the development of novel anti-inflammatory and anti-pyretic compounds.
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The effect of steroid treatment on Lipocortin immunoreactivity of rat brain
Mediators of Inflammation, 1994Co-Authors: K. G. Go, Egle Solito, Luca Parente, J. G. Ter Haar, F. Zuiderveen, W. M. MolenaarAbstract:Lipocortin-1, Lipocortin-2 and Lipocortin-5 were immunohistochemically assessed in rats. Apart from animals receiving no treatment, other animals received pretreatment with methylprednisolone, or the 21-aminosteroid U-74389F. Whereas Hpocortin immunoreactivity was absent in the greater part of the brain in animals not pretreated with steroid (except in sporadic microglial cells and choroid plexus), there was obvious immunostaining of parenchymatous elements in steroid pretreated animals. In the steroid pretreated animals Lipocortin immunoreactivity of the brain tissue may indicate local formation of Lipocortin under the influence of steroids that had entered the tissue. The cellular elements which showed immunostaining included meningeal cells, neurones, ependyma, oligodendroglia and capillary endotheHum.
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inhibition of smooth muscle contraction and platelet aggregation by peptide 204 212 of Lipocortin 5 an attempt to define some structure requirements
Mediators of Inflammation, 1993Co-Authors: K G Mugridge, C Becherucci, Luca Parente, Mauro PerrettiAbstract:Peptide 204–212 of Lipocortin (LC) 5 inhibited porcine pancreatic phospholipase A2 (PLA2) induced rat stomach strip contractions and ADP induced rabbit platelet aggregation in a concentration dependent manner (IC30 of 10 μM and 400 μM, respectively). The first two amino acids are not necessary since the eptapeptide 206–212 was equipotent in both assays (IC30 of 12.5 μM and 420 μM). Of the two pentapeptides 204–208 and 208–212 only the latter showed inhibitory activity in both models although the potency was much reduced (IC30 of 170 μM and 630 μM) compared with that of the parent nonapeptide. Comparison of peptide 204–212 effects with those of its analogues on LC1 and LC2 indicate that lysine 208 and aspartic acid 211 are essential in order to maintain a fully active nonapeptide.
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peptide 204 212 of Lipocortin 5 inhibits the generation of a prostacyclin like factor from rat aorta preparations in vitro
Prostaglandins, 1992Co-Authors: G J Douglas, Luca Parente, R J Flower, Mauro PerrettiAbstract:Abstract The release of an endogenous prostacyclin-like factor (PLF) from rat thoracic aorta rings was evaluated through inhibition of platelet ADP-induced aggregation and assessed with a micro-method using 96-multiwell plates. Aggregation was assessed in an ELISA reader by measuring changes of optical density at 620 nm in each well. The generation of endogenous PLF by aortic rings was time-dependent and was inhibited by indomethacin (3 μM). ADP-induced aggregation was inhibited by iloprost in a dose-dependent manner. Incubation of rat aorta rings with peptide 204–212 of human Lipocortin 5 (1–100 μg/ml) resulted in a dose-dependent inhibition of PLF release with a maximal inhibition of 90–95%. The effect of peptide 204–212 was reversible. A control peptide (amino-acids 104–112 of Lipocortin 5) was without any significant effect. Peptide 204–212 (100 μg/ml) did not modify PLF release from rat aorta preparations challenged with arachidonic acid (10 −6 -10 −4 M).
Mauro Perretti - One of the best experts on this subject based on the ideXlab platform.
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Inhibition of interleukin-1β-induced pyresis in the rabbit by peptide 204–212 of Lipocortin 5
European Journal of Pharmacology, 1995Co-Authors: Mitri Palmi, Mauro Perretti, C Becherucci, Maria Frosini, Gian Pietro Sgaragli, Luca ParenteAbstract:Abstract The intracerebroventricular administration of interleukin-1β (12.5 ng/kg) in rabbits caused a prompt rise of prostaglandin E 2 concentration (+632.6 ± 243.9%) in the cerebrospinal fluid followed by hyperthermia (+1.61 ± 0.14 Δ°C). The intracerebroventricular administration of an anti-inflammatory nonapeptide (amino acids 204–212, SHLRKVFDK) derived from Lipocortin 5, thereafter referred to as Lipocortin 5-(204–212)-peptide, inhibited in a significant manner both the increase in cerebrospinal fluid [prostaglandin E 2 ] and the febrile response induced by the cytokine. This inhibitory effect is probably due to interference by the peptide with phospholipase A 2 activity. A control peptide (FKRVHDLKS) formed by the same amino acids in a randomly shuffled sequence had no effect. These results show that, in addition to the anti-inflammatory effect previously reported, the peptide 204–212 of Lipocortin 5 possesses, like glucocorticoids, anti-pyretic activity. The research on Lipocortin-derived peptides may lead to the development of novel anti-inflammatory and anti-pyretic compounds.
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inhibition of interleukin 1β induced pyresis in the rabbit by peptide 204 212 of Lipocortin 5
European Journal of Pharmacology, 1995Co-Authors: Mitri Palmi, Mauro Perretti, C Becherucci, Maria Frosini, Gian Pietro Sgaragli, Luca ParenteAbstract:Abstract The intracerebroventricular administration of interleukin-1β (12.5 ng/kg) in rabbits caused a prompt rise of prostaglandin E 2 concentration (+632.6 ± 243.9%) in the cerebrospinal fluid followed by hyperthermia (+1.61 ± 0.14 Δ°C). The intracerebroventricular administration of an anti-inflammatory nonapeptide (amino acids 204–212, SHLRKVFDK) derived from Lipocortin 5, thereafter referred to as Lipocortin 5-(204–212)-peptide, inhibited in a significant manner both the increase in cerebrospinal fluid [prostaglandin E 2 ] and the febrile response induced by the cytokine. This inhibitory effect is probably due to interference by the peptide with phospholipase A 2 activity. A control peptide (FKRVHDLKS) formed by the same amino acids in a randomly shuffled sequence had no effect. These results show that, in addition to the anti-inflammatory effect previously reported, the peptide 204–212 of Lipocortin 5 possesses, like glucocorticoids, anti-pyretic activity. The research on Lipocortin-derived peptides may lead to the development of novel anti-inflammatory and anti-pyretic compounds.
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inhibition of smooth muscle contraction and platelet aggregation by peptide 204 212 of Lipocortin 5 an attempt to define some structure requirements
Mediators of Inflammation, 1993Co-Authors: K G Mugridge, C Becherucci, Luca Parente, Mauro PerrettiAbstract:Peptide 204–212 of Lipocortin (LC) 5 inhibited porcine pancreatic phospholipase A2 (PLA2) induced rat stomach strip contractions and ADP induced rabbit platelet aggregation in a concentration dependent manner (IC30 of 10 μM and 400 μM, respectively). The first two amino acids are not necessary since the eptapeptide 206–212 was equipotent in both assays (IC30 of 12.5 μM and 420 μM). Of the two pentapeptides 204–208 and 208–212 only the latter showed inhibitory activity in both models although the potency was much reduced (IC30 of 170 μM and 630 μM) compared with that of the parent nonapeptide. Comparison of peptide 204–212 effects with those of its analogues on LC1 and LC2 indicate that lysine 208 and aspartic acid 211 are essential in order to maintain a fully active nonapeptide.
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peptide 204 212 of Lipocortin 5 inhibits the generation of a prostacyclin like factor from rat aorta preparations in vitro
Prostaglandins, 1992Co-Authors: G J Douglas, Luca Parente, R J Flower, Mauro PerrettiAbstract:Abstract The release of an endogenous prostacyclin-like factor (PLF) from rat thoracic aorta rings was evaluated through inhibition of platelet ADP-induced aggregation and assessed with a micro-method using 96-multiwell plates. Aggregation was assessed in an ELISA reader by measuring changes of optical density at 620 nm in each well. The generation of endogenous PLF by aortic rings was time-dependent and was inhibited by indomethacin (3 μM). ADP-induced aggregation was inhibited by iloprost in a dose-dependent manner. Incubation of rat aorta rings with peptide 204–212 of human Lipocortin 5 (1–100 μg/ml) resulted in a dose-dependent inhibition of PLF release with a maximal inhibition of 90–95%. The effect of peptide 204–212 was reversible. A control peptide (amino-acids 104–112 of Lipocortin 5) was without any significant effect. Peptide 204–212 (100 μg/ml) did not modify PLF release from rat aorta preparations challenged with arachidonic acid (10 −6 -10 −4 M).
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a novel anti inflammatory peptide from human Lipocortin 5
British Journal of Pharmacology, 1991Co-Authors: Mauro Perretti, C Becherucci, K G Mugridge, Egle Solito, S Silvestri, Luca ParenteAbstract:1 A novel anti-inflammatory peptide (residues 204–212) of human recombinant Lipocortin 5 (hrLC5) found on the high similarity region with uteroglobin is described. 2 Peptide 204–212 dose-dependently inhibited the contractions of rat isolated stomach strips elicited by porcine pancreatic phospholipase A2 (PLA2). Contractions caused by arachidonic acid (AA), prostaglandin E2 (PGE2) and 5-hydroxytryptamine were not affected. No direct enzyme inhibition was observed in a radiochemical assay. 3 PGE2 release by both human fibroblasts and rat macrophages was reduced by peptide 204–212 in a dose-dependent manner. 4 The development of carrageenin-induced oedema in rats was significantly inhibited by the local administration of peptide 204–212. 5 The pattern and potency of the biological effects of peptide 204–212 are similar to those of antiflammin 2, a Lipocortin 1-derived peptide. 6 It is suggested that peptide 204–212 may represent the active site responsible for the anti-inflammatory properties of Lipocortin 5.
C Becherucci - One of the best experts on this subject based on the ideXlab platform.
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Inhibition of interleukin-1β-induced pyresis in the rabbit by peptide 204–212 of Lipocortin 5
European Journal of Pharmacology, 1995Co-Authors: Mitri Palmi, Mauro Perretti, C Becherucci, Maria Frosini, Gian Pietro Sgaragli, Luca ParenteAbstract:Abstract The intracerebroventricular administration of interleukin-1β (12.5 ng/kg) in rabbits caused a prompt rise of prostaglandin E 2 concentration (+632.6 ± 243.9%) in the cerebrospinal fluid followed by hyperthermia (+1.61 ± 0.14 Δ°C). The intracerebroventricular administration of an anti-inflammatory nonapeptide (amino acids 204–212, SHLRKVFDK) derived from Lipocortin 5, thereafter referred to as Lipocortin 5-(204–212)-peptide, inhibited in a significant manner both the increase in cerebrospinal fluid [prostaglandin E 2 ] and the febrile response induced by the cytokine. This inhibitory effect is probably due to interference by the peptide with phospholipase A 2 activity. A control peptide (FKRVHDLKS) formed by the same amino acids in a randomly shuffled sequence had no effect. These results show that, in addition to the anti-inflammatory effect previously reported, the peptide 204–212 of Lipocortin 5 possesses, like glucocorticoids, anti-pyretic activity. The research on Lipocortin-derived peptides may lead to the development of novel anti-inflammatory and anti-pyretic compounds.
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inhibition of interleukin 1β induced pyresis in the rabbit by peptide 204 212 of Lipocortin 5
European Journal of Pharmacology, 1995Co-Authors: Mitri Palmi, Mauro Perretti, C Becherucci, Maria Frosini, Gian Pietro Sgaragli, Luca ParenteAbstract:Abstract The intracerebroventricular administration of interleukin-1β (12.5 ng/kg) in rabbits caused a prompt rise of prostaglandin E 2 concentration (+632.6 ± 243.9%) in the cerebrospinal fluid followed by hyperthermia (+1.61 ± 0.14 Δ°C). The intracerebroventricular administration of an anti-inflammatory nonapeptide (amino acids 204–212, SHLRKVFDK) derived from Lipocortin 5, thereafter referred to as Lipocortin 5-(204–212)-peptide, inhibited in a significant manner both the increase in cerebrospinal fluid [prostaglandin E 2 ] and the febrile response induced by the cytokine. This inhibitory effect is probably due to interference by the peptide with phospholipase A 2 activity. A control peptide (FKRVHDLKS) formed by the same amino acids in a randomly shuffled sequence had no effect. These results show that, in addition to the anti-inflammatory effect previously reported, the peptide 204–212 of Lipocortin 5 possesses, like glucocorticoids, anti-pyretic activity. The research on Lipocortin-derived peptides may lead to the development of novel anti-inflammatory and anti-pyretic compounds.
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inhibition of smooth muscle contraction and platelet aggregation by peptide 204 212 of Lipocortin 5 an attempt to define some structure requirements
Mediators of Inflammation, 1993Co-Authors: K G Mugridge, C Becherucci, Luca Parente, Mauro PerrettiAbstract:Peptide 204–212 of Lipocortin (LC) 5 inhibited porcine pancreatic phospholipase A2 (PLA2) induced rat stomach strip contractions and ADP induced rabbit platelet aggregation in a concentration dependent manner (IC30 of 10 μM and 400 μM, respectively). The first two amino acids are not necessary since the eptapeptide 206–212 was equipotent in both assays (IC30 of 12.5 μM and 420 μM). Of the two pentapeptides 204–208 and 208–212 only the latter showed inhibitory activity in both models although the potency was much reduced (IC30 of 170 μM and 630 μM) compared with that of the parent nonapeptide. Comparison of peptide 204–212 effects with those of its analogues on LC1 and LC2 indicate that lysine 208 and aspartic acid 211 are essential in order to maintain a fully active nonapeptide.
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a novel anti inflammatory peptide from human Lipocortin 5
British Journal of Pharmacology, 1991Co-Authors: Mauro Perretti, C Becherucci, K G Mugridge, Egle Solito, S Silvestri, Luca ParenteAbstract:1 A novel anti-inflammatory peptide (residues 204–212) of human recombinant Lipocortin 5 (hrLC5) found on the high similarity region with uteroglobin is described. 2 Peptide 204–212 dose-dependently inhibited the contractions of rat isolated stomach strips elicited by porcine pancreatic phospholipase A2 (PLA2). Contractions caused by arachidonic acid (AA), prostaglandin E2 (PGE2) and 5-hydroxytryptamine were not affected. No direct enzyme inhibition was observed in a radiochemical assay. 3 PGE2 release by both human fibroblasts and rat macrophages was reduced by peptide 204–212 in a dose-dependent manner. 4 The development of carrageenin-induced oedema in rats was significantly inhibited by the local administration of peptide 204–212. 5 The pattern and potency of the biological effects of peptide 204–212 are similar to those of antiflammin 2, a Lipocortin 1-derived peptide. 6 It is suggested that peptide 204–212 may represent the active site responsible for the anti-inflammatory properties of Lipocortin 5.
Mitri Palmi - One of the best experts on this subject based on the ideXlab platform.
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Role of the nitric oxide/cyclic GMP/Ca^2+ signaling pathway in the pyrogenic effect of interleukin-1β
Molecular Neurobiology, 2002Co-Authors: Mitri Palmi, Antonella MeiniAbstract:Interleukin-1β (IL-1β) has a wide spectrum of inflammatory, metabolic, haemopoietic, and immunological properties. Because it produces fever when injected into animals and humans, it is considered an endogenous pyrogen. There is evidence to suggest that Ca^2+ plays a critical role in the central mechanisms of thermoregulation, and in the intracellular signaling pathways controlling fever induced by IL-1β and other pyrogens. Data from different labs indicate that Ca^2+ and Na^+ determine the temperature set point in the posterior hypothalamus (PH) of various mammals and that changes in Ca^2+ and PGE_2 concentrations in the cerebrospinal fluid (CSF) of these animals are associated with IL-1β-induced fever. Antipyretic drugs such as acetylsalicylic acid, dexamethasone, and Lipocortin 5-(204–212) peptide counteract IL-1β-induced fever and abolish changes in Ca^2+ and PGE_2 concentrations in CSF. In vitro studies have established that activation of the nitric oxide (NO)/cyclic GMP (cGMP) pathway is part of the signaling cascade transducing Ca^2+ mobilization in response to IL-1β and that the ryanodine (RY)- and inositol-(1,4,5)-trisphosphate (IP_3)-sensitive pools are the main source of the mobilized Ca^2+. It is concluded that the NO/cGMP/Ca^2+ pathway is part of the signaling cascade subserving some of the multiple functions of IL-1β.
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inhibition of interleukin 1β induced pyresis in the rabbit by peptide 204 212 of Lipocortin 5
European Journal of Pharmacology, 1995Co-Authors: Mitri Palmi, Mauro Perretti, C Becherucci, Maria Frosini, Gian Pietro Sgaragli, Luca ParenteAbstract:Abstract The intracerebroventricular administration of interleukin-1β (12.5 ng/kg) in rabbits caused a prompt rise of prostaglandin E 2 concentration (+632.6 ± 243.9%) in the cerebrospinal fluid followed by hyperthermia (+1.61 ± 0.14 Δ°C). The intracerebroventricular administration of an anti-inflammatory nonapeptide (amino acids 204–212, SHLRKVFDK) derived from Lipocortin 5, thereafter referred to as Lipocortin 5-(204–212)-peptide, inhibited in a significant manner both the increase in cerebrospinal fluid [prostaglandin E 2 ] and the febrile response induced by the cytokine. This inhibitory effect is probably due to interference by the peptide with phospholipase A 2 activity. A control peptide (FKRVHDLKS) formed by the same amino acids in a randomly shuffled sequence had no effect. These results show that, in addition to the anti-inflammatory effect previously reported, the peptide 204–212 of Lipocortin 5 possesses, like glucocorticoids, anti-pyretic activity. The research on Lipocortin-derived peptides may lead to the development of novel anti-inflammatory and anti-pyretic compounds.
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Inhibition of interleukin-1β-induced pyresis in the rabbit by peptide 204–212 of Lipocortin 5
European Journal of Pharmacology, 1995Co-Authors: Mitri Palmi, Mauro Perretti, C Becherucci, Maria Frosini, Gian Pietro Sgaragli, Luca ParenteAbstract:Abstract The intracerebroventricular administration of interleukin-1β (12.5 ng/kg) in rabbits caused a prompt rise of prostaglandin E 2 concentration (+632.6 ± 243.9%) in the cerebrospinal fluid followed by hyperthermia (+1.61 ± 0.14 Δ°C). The intracerebroventricular administration of an anti-inflammatory nonapeptide (amino acids 204–212, SHLRKVFDK) derived from Lipocortin 5, thereafter referred to as Lipocortin 5-(204–212)-peptide, inhibited in a significant manner both the increase in cerebrospinal fluid [prostaglandin E 2 ] and the febrile response induced by the cytokine. This inhibitory effect is probably due to interference by the peptide with phospholipase A 2 activity. A control peptide (FKRVHDLKS) formed by the same amino acids in a randomly shuffled sequence had no effect. These results show that, in addition to the anti-inflammatory effect previously reported, the peptide 204–212 of Lipocortin 5 possesses, like glucocorticoids, anti-pyretic activity. The research on Lipocortin-derived peptides may lead to the development of novel anti-inflammatory and anti-pyretic compounds.
K G Mugridge - One of the best experts on this subject based on the ideXlab platform.
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inhibition of smooth muscle contraction and platelet aggregation by peptide 204 212 of Lipocortin 5 an attempt to define some structure requirements
Mediators of Inflammation, 1993Co-Authors: K G Mugridge, C Becherucci, Luca Parente, Mauro PerrettiAbstract:Peptide 204–212 of Lipocortin (LC) 5 inhibited porcine pancreatic phospholipase A2 (PLA2) induced rat stomach strip contractions and ADP induced rabbit platelet aggregation in a concentration dependent manner (IC30 of 10 μM and 400 μM, respectively). The first two amino acids are not necessary since the eptapeptide 206–212 was equipotent in both assays (IC30 of 12.5 μM and 420 μM). Of the two pentapeptides 204–208 and 208–212 only the latter showed inhibitory activity in both models although the potency was much reduced (IC30 of 170 μM and 630 μM) compared with that of the parent nonapeptide. Comparison of peptide 204–212 effects with those of its analogues on LC1 and LC2 indicate that lysine 208 and aspartic acid 211 are essential in order to maintain a fully active nonapeptide.
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a novel anti inflammatory peptide from human Lipocortin 5
British Journal of Pharmacology, 1991Co-Authors: Mauro Perretti, C Becherucci, K G Mugridge, Egle Solito, S Silvestri, Luca ParenteAbstract:1 A novel anti-inflammatory peptide (residues 204–212) of human recombinant Lipocortin 5 (hrLC5) found on the high similarity region with uteroglobin is described. 2 Peptide 204–212 dose-dependently inhibited the contractions of rat isolated stomach strips elicited by porcine pancreatic phospholipase A2 (PLA2). Contractions caused by arachidonic acid (AA), prostaglandin E2 (PGE2) and 5-hydroxytryptamine were not affected. No direct enzyme inhibition was observed in a radiochemical assay. 3 PGE2 release by both human fibroblasts and rat macrophages was reduced by peptide 204–212 in a dose-dependent manner. 4 The development of carrageenin-induced oedema in rats was significantly inhibited by the local administration of peptide 204–212. 5 The pattern and potency of the biological effects of peptide 204–212 are similar to those of antiflammin 2, a Lipocortin 1-derived peptide. 6 It is suggested that peptide 204–212 may represent the active site responsible for the anti-inflammatory properties of Lipocortin 5.