Biomedical subjects

Nobuaki Matsui

Publications and source records attributed to Nobuaki Matsui.

7 recordsLinked to original sources

PubMed2005

The protective effect of H2-receptor activation against the duration of myocardial hypoxia/reoxygenation-induced ventricular fibrillation in sensitized guinea-pig hearts.

Patients with high serum immunoglobulin E levels were reported to be protected against sudden death during acute myocardial infarction. The protection mechanism might be attributed to the facilitation of histamine release from sensitized mast cells; however, this remains to be clarified. In this study, we examined the influence of sensitization on ventricular fibrillation (VF) induced by myocardial hypoxia/reoxygenation (H/R). Guinea pigs were actively sensitized by subcutaneous injection of ovalbumin in Bordetella pertussis vaccine. Hearts isolated from non-sensitized and sensitized guinea pigs were subjected to 30-min hypoxia / 30-min reoxygenation using a Langendorff apparatus. The amount of histamine released in the sensitized guinea-pig hearts was elevated, and the duration of VF was found to be reduced. The treatment with a histamine H2-receptor antagonist inhibited the reduction of VF duration. Treatment of the non-sensitized hearts with the histamine H2-receptor agonist resulted in the decrease of VF duration to the same level as that in the sensitized hearts. In conclusion, these results suggest that the risk of sudden death during myocardial H/R may be attenuated in the sensitized hearts and that histamine H2-receptor activation due to the released histamine may be involved in the protective effect.

Adrenergic beta-Antagonists↗

PubMed2005

Protective effect of the 5-lipoxygenase inhibitor ardisiaquinone A on hepatic ischemia-reperfusion injury in rats.

The protective effects of the 5-lipoxygenase inhibitor ardisiaquinone A, a compound isolated from Ardisia sieboldii, on hepatic ischemia-reperfusion (I/R) injury was studied in rats. Hepatic I/R injury was induced by occlusion of the portal vein and the hepatic artery for 60 min, followed by reperfusion for 24 h. The content of leukotriene B (4) (LTB (4)) in the liver increased during ischemia. Serum alanine aminotransferase (ALT) levels, a marker of hepatic parenchymal cell injury, and hepatic myeloperoxidase (MPO) activity, a marker of neutrophil accumulation, significantly increased 6 - 9 h after reperfusion. Treatment with ardisiaquinone A (0.1 - 2 mg/kg, i. p.) 30 min prior to ischemia dose-dependently prevented the increase in LTB (4) content during ischemia (ID (50) = 0.645 mg/kg) with a slightly higher potency than that of AA-861 (ID (50) = 0.728 mg/kg), a known reference 5-lipoxygenase inhibitor. Ardisiaquinone A also attenuated the increase in MPO activity and serum ALT levels at 6 h after reperfusion (ID (50) = 1.71 mg/kg and 4.28 mg/kg, respectively). These protective effects were more efficient than those of AA-861 (ID (50) = 1.86 mg/kg and no effect, respectively), LY255283 (ID (50) = 18.1 mg/kg and 11.5 mg/kg, respectively), and ONO-4057 (ID (50) = 8.38 mg/kg and 9.44 mg/kg, respectively), which are LTB (4) receptor antagonists. These results suggest that ardisiaquinone A may protect the liver against damage due to I/R in rats.

Animals↗

PubMed2005

Neurotrophic effect of magnolol in the hippocampal CA1 region of senescence-accelerated mice (SAMP1).

Magnolol has neurotrophic effects in primary cultured rat cortical neurons, which are expressed as the promotion of neurite outgrowth and neuronal survival. In this study, we investigated the protective effect of magnolol against age-related neuronal loss in the hippocampus using senescence-accelerated mouse (SAMP1). Magnolol (5, 10 mg/kg) was orally administered once a day for 14 d to 2- or 4-month-old mice, and evaluation was carried out when the mice were 4 or 6 months old. The density of neurofibrils decreased with aging in the stratum radiatum of the CA1 region in the hippocampus of SAMP1, not SAMR1. Treatment with magnolol significantly prevented the decrease of neurofibrils in the CA1, when it was administered in 2-month-olds. However, administration at 4 months of age did not result in a preventive effect. These findings suggest that the administration of magnolol before the initiation of neuronal loss may result in a protective effect in the hippocampus.

Aging↗

PubMed2005

Enzymatic measurement of tryptase-like protease release from isolated perfused guinea pig heart during ischemia-reperfusion.

To elucidate the details of tryptase release from the heart during ischemia-reperfusion (I/R), we attempted the enzymatic measurement of tryptase release from the isolated guinea pig heart perfused by the Langendorff mode I/R model. Tryptase-like activity in the effluent was monitored by the hydrolysis of L-Pyr-Gly-Arg-MCA. Tryptase-like protease and histamine were rapidly released from heart during ischemia within 10 min. After reperfusion, tryptase-like protease levels decreased, achieving stabilization. The tryptase-like protease activity in the effluent was inactivated by serine protease inhibitors. The pattern of inhibition was similar to those of guinea pig and human lung tryptase. In conclusion, tryptase was released into the coronary effluent during ischemia, but not during reperfusion in guinea pig heart.

Animals↗

PubMed2005

Inhibiton of NF-kappaB activation during ischemia reduces hepatic ischemia/reperfusion injury in rats.

The aim of this study was to determine whether nuclear factor-kappaB (NF-kappaB) inhibitors are efficient against hepatic ischemia/reperfusion (I/R) injury. We previously demonstrated that xanthine oxidase-derived reactive oxygen species activate NF-kappaB during ischemia. However, the role of NF-kappaB activation during ischemia in post-reperfusion injury remains unclear. Therefore, while we examined the effects of NF-kappaB inhibitors, sulfasalazine and pyrrolidinedithiocarbamate on hepatic I/R injury using a rat lobar hepatic I/R model, we estimated the relationship between NF-kappaB activation during ischemia and following hepatic damage caused by reperfusion. The portal vein and the hepatic artery were clamped for 1 hr followed by reperfusion for up to 24 hr. NF-kappaB activation was determined by Western blot analysis. NF-kappaB activation was observed in the ischemic lobe of the liver, and the activation was prevented by pre-administration with NF-kappaB inhibitors. Although the serum ALT level, hepatic MPO activity and BSP clearance, as an index of hepatic injury, were increased after reperfusion, the increase was attenuated by pre-administration with NF-kappaB inhibitors. These findings suggest that NF-kappaB activation during ischemia is relevant to hepatic I/R injury. Moreover, we first showed that pre-administration with NF-kappaB inhibitors is effective against hepatic I/R injury.

Alanine Transaminase↗

PubMed2004

Het-PDB Navi.: a database for protein-small molecule interactions.

The genomes of more than 100 species have been sequenced, and the biological functions of encoded proteins are now actively being researched. Protein function is based on interactions between proteins and other molecules. One approach to assuming protein function based on genomic sequence is to predict interactions between an encoded protein and other molecules. As a data source for such predictions, knowledge regarding known protein-small molecule interactions needs to be compiled. We have, therefore, surveyed interactions between proteins and other molecules in Protein Data Bank (PDB), the protein three-dimensional (3D) structure database. Among 20,685 entries in PDB (April, 2003), 4,189 types of small molecules were found to interact with proteins. Biologically relevant small molecules most often found in PDB were metal ions, such as calcium, zinc, and magnesium. Sugars and nucleotides were the next most common. These molecules are known to act as cofactors for enzymes and/or stabilizers of proteins. In each case of interactions between a protein and small molecule, we found preferred amino acid residues at the interaction sites. These preferences can be the basis for predicting protein function from genomic sequence and protein 3D structures. The data pertaining to these small molecules were collected in a database named Het-PDB Navi., which is freely available at http://daisy.nagahama-i-bio.ac.jp/golab/hetpdbnavi.html and linked to the official PDB home page.

Adenosine Triphosphate↗

PubMed2002

Inhibitory effect of olopatadine on antigen-induced eosinophil infiltration and the LFA-1 and Mac-1 expression in eosinophils.

The inhibitory effect of olopatadine, a new antiallergic drug, on antigen-induced eosinophil infiltration and its mechanisms were examined using the local sensitized rat allergic rhinitis model and isolated IL-5-stimulated rat peritoneal eosinophils. Olopatadine dose-dependently inhibited antigen-induced eosinophil infiltration in the nasal mucosa. Olopatadine dose-dependently repressed the IL-5-induced expressions of CD11a/CD18 (LFA-1) and CD11b/CD18 (Mac-1) on rat peritoneal eosinophils. However, olopatadine had no effect on IL-5-induced CD49d/CD29 (VLA-4) expression. These results suggest that olopatadine may inhibit antigen-induced eosinophil infiltration through repression of LFA-1 and Mac-1 expression.

Administration, Oral↗