6 results match your criteria: "Kindai University (Formerly Kinki University)[Affiliation]"
J Pharmacol Sci
June 2019
Laboratory of Pharmacology and Pathophysiology, Faculty of Pharmacy, Kindai University (formerly Kinki University), Higashi-Osaka 577-8502, Japan. Electronic address:
We tested whether NNC 55-0396 (NNC), a T-type calcium channel (T-channel) blocker, reduces the brain injury caused by middle cerebral artery occlusion and reperfusion (MCAO/R) in mice. NNC, administered i.c.
View Article and Find Full Text PDFPharmacology
May 2017
Laboratory of Pharmacology and Pathophysiology, Faculty of Pharmacy, Kindai University (Formerly Kinki University), Higashi-osaka, Japan.
We examined the effect of repeated cold (RC) stress on cyclophosphamide (CPA)-induced cystitis/bladder pain in mice, in relation to macrophage activity. CPA, given i.p.
View Article and Find Full Text PDFJ Pharmacol Sci
January 2017
Laboratory of Pharmacology and Pathophysiology, Faculty of Pharmacy, Kindai University (Formerly Kinki University), Higashi-Osaka 577-8502, Japan. Electronic address:
Given that Ca3.2 T-type Ca channels were functionally regulated by asparagine (N)-linked glycosylation, we examined effects of high glucose on the function of Ca3.2, known to regulate secretory function, in neuroendocrine-like differentiated prostate cancer LNCaP cells.
View Article and Find Full Text PDFPharmacology
March 2017
Laboratory of Pharmacology and Pathophysiology, Faculty of Pharmacy, Kindai University (Formerly Kinki University), Higashi-osaka, Japan.
Background: Hydrogen sulfide (H2S), a gasotransmitter, is generated from L-cysteine by mainly 3 enzymes, cystathionine-γ-lyase (CSE), cystathionine-β-synthase, and 3-mercaptopyruvate sulfurtransferase in cooperation with cysteine aminotransferase. The H2S-forming enzymes, particularly CSE, are overexpressed under the pathological conditions such as inflammation, neuronal or neuroendocrine differentiation and cancer development. Given that Cav3.
View Article and Find Full Text PDFToxicology
July 2016
Laboratory of Pharmacology and Pathophysiology, Faculty of Pharmacy, Kindai University (formerly Kinki University), Higashi-Osaka 577-8502, Japan. Electronic address:
Given that high mobility group box 1 (HMGB1), a nuclear protein, once released to the extracellular space, promotes nociception, we asked if inactivation of HMGB1 prevents or reverses chemotherapy-induced painful neuropathy in rats and also examined possible involvement of Toll-like receptor 4 (TLR4) and the receptor for advanced glycation endproduct (RAGE), known as targets for HMGB1. Painful neuropathy was produced by repeated i.p.
View Article and Find Full Text PDFJ Pharmacol Sci
February 2016
Laboratory of Pharmacology and Pathophysiology, Faculty of Pharmacy, Kindai University (formerly Kinki University), Higashi-Osaka 577-8502, Japan. Electronic address:
Nuclear HMGB1 that contains 3 cysteine residues is acetylated and secreted to the extracellular space, promoting inflammation via multiple molecules such as RAGE and TLR4. We thus evaluated and characterized the redox state-dependent effects of peripheral HMGB1 on nociception. Intraplantar (i.
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