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Modulation of IL-1 beta gene expression by lipid peroxidation inhibition after kainic acid-induced rat brain injury.
Exp Neurol. 2004 Jul; 188(1):178-86.EN

Abstract

Brain injury was induced by intraperitoneal administration of kainic acid (KA, 10 mg/kg). Animals were randomized to receive either IRFI 042 (20 mg/kg i.p.), a lipid peroxidation inhibitor, or its vehicle (NaCl 0.9% DMSO 10% 1 ml/kg i.p.) 30 min before KA administration. A first set of animals was sacrificed 6 h after KA injection to measure malondialdehyde (MDA) content, glutathione-reduced (GSH) levels and the mRNA for interleukin-1beta (IL-1beta) in the cortex and in the hippocampus. A second set of animals was sacrificed 48 h after KA administration for histological analysis. All animals were observed for monitoring the behavioral sequelae and for evaluating latency of convulsions. Sham brain injury rats were used as controls. Intraperitoneal administration of IRFI 042 significantly decreased brain MDA (cortex: KA + vehicle = 0.285 +/- 0.04 nmol/mg protein; KA + IRFI 042 = 0.156 +/- 0.02 nmol/mg protein, P < 0.005; hippocampus: KA + vehicle = 0.350 +/- 0.03 nmol/mg protein; KA + IRFI 042 = 0.17 +/- 0.04 nmol/mg protein, P < 0.005), prevented the brain loss of GSH in both cortex (KA + vehicle = 7.81 +/- 1 micromol/g protein; KA + IRFI 042 = 12.1 +/- 1 micromol/g protein; P < 0.005) and hippocampus (KA + vehicle = 5 +/- 0.8 micromol/g protein; KA + IRFI 042 = 9.4 +/- 1.8 micromol/g protein; P < 0.005), reduced both brain IL-1beta mRNA expression and oedema, and increased latency of convulsions. Histological analysis showed a reduction of cell damage in IRFI 042-treated samples. The present data indicate that lipid peroxidation inhibition reduces IL-1beta gene expression and protects against kainic acid-induced brain damage.

Authors+Show Affiliations

Section of Pharmacology, Department of Clinical and Experimental Medicine and Pharmacology, University of Messina, Messina, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

15191814

Citation

Marini, Herbert, et al. "Modulation of IL-1 Beta Gene Expression By Lipid Peroxidation Inhibition After Kainic Acid-induced Rat Brain Injury." Experimental Neurology, vol. 188, no. 1, 2004, pp. 178-86.
Marini H, Altavilla D, Bellomo M, et al. Modulation of IL-1 beta gene expression by lipid peroxidation inhibition after kainic acid-induced rat brain injury. Exp Neurol. 2004;188(1):178-86.
Marini, H., Altavilla, D., Bellomo, M., Adamo, E. B., Marini, R., Laureanti, F., Bonaccorso, M. C., Seminara, P., Passaniti, M., Minutoli, L., Bitto, A., Calapai, G., & Squadrito, F. (2004). Modulation of IL-1 beta gene expression by lipid peroxidation inhibition after kainic acid-induced rat brain injury. Experimental Neurology, 188(1), 178-86.
Marini H, et al. Modulation of IL-1 Beta Gene Expression By Lipid Peroxidation Inhibition After Kainic Acid-induced Rat Brain Injury. Exp Neurol. 2004;188(1):178-86. PubMed PMID: 15191814.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Modulation of IL-1 beta gene expression by lipid peroxidation inhibition after kainic acid-induced rat brain injury. AU - Marini,Herbert, AU - Altavilla,Domenica, AU - Bellomo,Maria, AU - Adamo,Elena Bianca, AU - Marini,Rolando, AU - Laureanti,Floriana, AU - Bonaccorso,Maria Carmela, AU - Seminara,Paolo, AU - Passaniti,Maria, AU - Minutoli,Letteria, AU - Bitto,Alessandra, AU - Calapai,Gioacchino, AU - Squadrito,Francesco, PY - 2003/11/12/received PY - 2004/03/29/revised PY - 2004/03/30/accepted PY - 2004/6/12/pubmed PY - 2004/8/11/medline PY - 2004/6/12/entrez SP - 178 EP - 86 JF - Experimental neurology JO - Exp Neurol VL - 188 IS - 1 N2 - Brain injury was induced by intraperitoneal administration of kainic acid (KA, 10 mg/kg). Animals were randomized to receive either IRFI 042 (20 mg/kg i.p.), a lipid peroxidation inhibitor, or its vehicle (NaCl 0.9% DMSO 10% 1 ml/kg i.p.) 30 min before KA administration. A first set of animals was sacrificed 6 h after KA injection to measure malondialdehyde (MDA) content, glutathione-reduced (GSH) levels and the mRNA for interleukin-1beta (IL-1beta) in the cortex and in the hippocampus. A second set of animals was sacrificed 48 h after KA administration for histological analysis. All animals were observed for monitoring the behavioral sequelae and for evaluating latency of convulsions. Sham brain injury rats were used as controls. Intraperitoneal administration of IRFI 042 significantly decreased brain MDA (cortex: KA + vehicle = 0.285 +/- 0.04 nmol/mg protein; KA + IRFI 042 = 0.156 +/- 0.02 nmol/mg protein, P < 0.005; hippocampus: KA + vehicle = 0.350 +/- 0.03 nmol/mg protein; KA + IRFI 042 = 0.17 +/- 0.04 nmol/mg protein, P < 0.005), prevented the brain loss of GSH in both cortex (KA + vehicle = 7.81 +/- 1 micromol/g protein; KA + IRFI 042 = 12.1 +/- 1 micromol/g protein; P < 0.005) and hippocampus (KA + vehicle = 5 +/- 0.8 micromol/g protein; KA + IRFI 042 = 9.4 +/- 1.8 micromol/g protein; P < 0.005), reduced both brain IL-1beta mRNA expression and oedema, and increased latency of convulsions. Histological analysis showed a reduction of cell damage in IRFI 042-treated samples. The present data indicate that lipid peroxidation inhibition reduces IL-1beta gene expression and protects against kainic acid-induced brain damage. SN - 0014-4886 UR - https://www.unboundmedicine.com/medline/citation/15191814/Modulation_of_IL_1_beta_gene_expression_by_lipid_peroxidation_inhibition_after_kainic_acid_induced_rat_brain_injury_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014488604001311 DB - PRIME DP - Unbound Medicine ER -