WordNet

the science or study of drugs: their preparation and properties and uses and effects (同)pharmacological medicine, materia_medica
of or relating to pharmacology (同)pharmacologic
the study of drugs that affect the mind
of or relating to psychopharmacology

PrepTutorEJDIC

薬学,薬物学,薬理学

English Journal

Selective ETA receptor blockade protects against cisplatin-induced acute renal failure in male rats.

Helmy MM1, Helmy MW2, Abd Allah DM3, Abo Zaid AM2, Mohy El-Din MM4.Author information 1Department of Pharmacology and Toxicology, Faculty of Pharmacy, Alexandria University, Azarita, PO Box 21521, Alexandria, Egypt. Electronic address: meeshoo7@hotmail.com.2Department of Pharmacology and Toxicology, Faculty of Pharmacy and Drug Manufacturing, Pharos University in Alexandria, Alexandria, Egypt.3Department of Clinical Pathology, Faculty of Medicine, Alexandria University, Azarita, Alexandria, Egypt.4Department of Pharmacology and Toxicology, Faculty of Pharmacy, Alexandria University, Azarita, PO Box 21521, Alexandria, Egypt.AbstractThe present study aims to investigate the possibility that inhibiting the physiological function of endothelin-1 (ET-1) by blocking its receptors would significantly decrease the nephrotoxic effect of cisplatin. Therefore the study was designed to investigate the effect of treatment with BQ-123, the selective endothelin receptor-A (ETA) blocker, and bosentan, the non-selective endothelin receptor blocker, on the cisplatin-induced structural, functional, and biochemical alterations in the rat kidney. Rats were divided into four groups: control (given a single dose of normal saline, i.p.), cisplatin (given a single dose of cisplatin, 6mg/kg, i.p.), cisplatin+BQ-123 (1mg/kg, i.p.), and cisplatin+bosentan (30mg/kg, orally via gavage). Each of the two blockers was administered in two doses; 1h before and one day after the cisplatin dose. Acute cisplatin administration resulted in significant increases in blood urea nitrogen and serum creatinine concentrations at 96h following cisplatin injection. Increased concentrations of malondialdehyde, tumor necrosis factor-α (TNF-α) and caspase-3, decreased nitric oxide (NO) production and superoxide dismutase (SOD) activity in kidney homogenates were observed at 96h following cisplatin injection, in addition to a typical 'acute tubular necrosis' pattern. BQ-123 ameliorated the structural and functional injuries caused by cisplatin mainly via restoring SOD activity, in addition to other antioxidant parameters, NO, TNF-α and caspase-3 concentrations. This study further proves that ETA but not ETB receptors are involved in cisplatin-induced nephrotoxicity. The selective ETA antagonist BQ-123 ameliorated the cisplatin-induced deleterious effects and showed reno-protective effect against cisplatin-induced acute renal damage.
European journal of pharmacology.Eur J Pharmacol.2014 May 5;730:133-9. doi: 10.1016/j.ejphar.2014.03.002. Epub 2014 Mar 14.
The present study aims to investigate the possibility that inhibiting the physiological function of endothelin-1 (ET-1) by blocking its receptors would significantly decrease the nephrotoxic effect of cisplatin. Therefore the study was designed to investigate the effect of treatment with BQ-123, the
PMID 24632086

Protective effect of geranylgeranylacetone via enhanced induction of HSPB1 and HSPB8 in mitochondria of the failing heart following myocardial infarction in rats.

Marunouchi T1, Inomata S1, Sanbe A2, Takagi N1, Tanonaka K3.Author information 1Department of Molecular and Cellular Pharmacology, Tokyo University of Pharmacy and Life Sciences, 1432-1 Horinouchi, Hachioji, Tokyo 192-0392, Japan.2Department of Pharmacotherapeutics, School of Pharmacy, Iwate Medical University, 2-1-1 Nishitokuta, Yahaba, Siwa, Iwate 028-3603, Japan.3Department of Molecular and Cellular Pharmacology, Tokyo University of Pharmacy and Life Sciences, 1432-1 Horinouchi, Hachioji, Tokyo 192-0392, Japan. Electronic address: tanonaka@toyaku.ac.jp.AbstractThe mechanisms underlying mitochondrial impairment in the failing heart are not yet clear. In a previous study, we found that the levels of small heat shock proteins (HSP) such as mitochondrial HSPB1 and HSPB8 in the failing heart following myocardial infarction were decreased. In the present study, to verify the hypothesis that mitochondrial dysfunction in the failing heart is associated with alterations in mitochondrial small heat shock proteins, we examined the effects of geranylgeranylacetone, a heat shock protein inducer, on the cardiac mitochondrial function after myocardial infarction. When hemodynamic parameters of rats with myocardial infarction were measured at the 8th (8W) week after coronary artery ligation (CAL), the 8W-CAL showed signs of chronic heart failure concomitant with a reduced mitochondrial oxygen consumption rate. HSPB1 and HSPB8 contents in the mitochondrial fraction prepared from the failing heart were decreased, suggesting that an attenuation of mitochondrial translocation of HSPB1 and HSPB8 had led to an impairment of mitochondrial energy-producing ability. Geranylgeranylacetone treatment from the 2nd to 8th week after myocardial infarction attenuated the reduction in mitochondrial HSPB1 and HSPB8 contents. Furthermore, the mitochondrial energy-producing ability and cardiac pump function were preserved by orally administered geranylgeranylacetone during the development of heart failure. These results suggest that the induction of small heat shock proteins in the infarcted heart by geranylgeranylacetone treatment contributed to the preservation of mitochondrial function, leading to an improvement of cardiac contractile function.
European journal of pharmacology.Eur J Pharmacol.2014 May 5;730:140-7. doi: 10.1016/j.ejphar.2014.02.037. Epub 2014 Mar 11.
The mechanisms underlying mitochondrial impairment in the failing heart are not yet clear. In a previous study, we found that the levels of small heat shock proteins (HSP) such as mitochondrial HSPB1 and HSPB8 in the failing heart following myocardial infarction were decreased. In the present study,
PMID 24631258

Barium chloride impaired Kir2.1 inward rectification in its stably transfected HEK 293 cell lines.

Shen N1, Zheng J2, Liu H3, Xu K4, Chen Q4, Chen Y5, Shen Y5, Jiang L2, Chen Y6.Author information 1Cardiovascular Division, Zhejiang Province People׳s Hospital, 158 Shangtang Road, Hangzhou 310014, PR China.2Cardiovascular Division, Jiaxing No. 2 Hospital, 1882 Central Circle Road South, Jiaxing 314001, PR China.3Chinese Herb Medicine Division, The Nurturing Station for the State Key Laboratory of Subtropical Silviculture, Zhejiang Agriculture and Forestry University, 88 North Circle Road, Lin'an 311300, PR China.4Safety Pharmacology Division, Olivepharmasolutions Ltd., 333 Changhong Road, Wukang 313200, PR China.5Pathophysiolog department, Medical School, Zhejiang University, Hangzhou 310058, PR China.6Chinese Herb Medicine Division, The Nurturing Station for the State Key Laboratory of Subtropical Silviculture, Zhejiang Agriculture and Forestry University, 88 North Circle Road, Lin'an 311300, PR China. Electronic address: ychen@zafu.edu.cn.AbstractKir2.1 channel is a typical inward rectified channel with little outward currents when the membrane depolarized. Barium blocks the inward Kir2.1 currents in a voltage-dependent manner. However, in this study we found that barium would impair the rectification and open Kir2.1 outward currents at a depolarized voltage, causing increment of outward current amplitudes by 43±7% (n=5, P<0.01) after 200s barium application. In the meanwhile, a higher barium concentration did block the outward currents by 17.5±4.3% (n=4, P<0.01) and temporarily twisted current upward tendency. The increment was likely barium specific since both calcium and Kir2.1 specific blocker, Chloroethylclonidine (CEC), did not enhance the current amplitudes. The rectification of Kir2.1 was not recovered by washing barium off, which suggested a non-competitive mechanism. Since the currents occurred at phase 1, 2 of cardiac action potential, it would likely shorten the action potential plateau and it would decrease QT duration in electrocardiography (ECG).
European journal of pharmacology.Eur J Pharmacol.2014 May 5;730:164-70. doi: 10.1016/j.ejphar.2014.02.025. Epub 2014 Mar 12.
Kir2.1 channel is a typical inward rectified channel with little outward currents when the membrane depolarized. Barium blocks the inward Kir2.1 currents in a voltage-dependent manner. However, in this study we found that barium would impair the rectification and open Kir2.1 outward currents at a de
PMID 24631257

Japanese Journal

P-042 うま味胃内投与がラット内側視索前野ヒスタミン遊離に及ぼす影響(ポスターセッション,2012年度日本味と匂学会第46回大会)

石塚智子,硲哲崇,大和谷厚,大浦清
日本味と匂学会誌 19(3), 361-364, 2012-12-00
NAID 110009578276

P-053 食物嫌悪学習の想起に対する扁桃体中心核ヒスタミンH_1受容体の関与(ポスターセッション,2011年度日本味と匂学会第45回大会)

石塚智子,硲哲崇,大和谷厚 [他],大浦清
日本味と匂学会誌 18(3), 303-306, 2011-12-00
NAID 110009441224

Polyoxyethylene hydrogenated castor oil modulates benzalkonium chloride toxicity: comparison of acute corneal barrier dysfunction induced by travoprost Z and travoprost.

Uematsu Masafumi,Kumagami Takeshi,Shimoda Kenichiro,Kusano Mao,Teshima Mugen,To Hideto,Kitahara Takashi,Kitaoka Takashi,Sasaki Hitoshi
Journal of Ocular Pharmacology and Therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics 27(5), 437-444, 2011-10-01
To determine the element that modulates benzalkonium chloride (BAC) toxicity by using a new electrophysiological method to evaluate acute corneal barrier dysfunction induced by travoprost Z with sofZi …
NAID 120003751861

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