Cholestenone functions as an antibiotic against by inhibiting biosynthesis of the cell wall component CGL.

, a pathogen responsible for gastric cancer, contains a unique glycolipid, cholesteryl-α-D-glucopyranoside (CGL), in its cell wall. Moreover, -glycans having α1,4-linked -acetylglucosamine residues (αGlcNAc) are secreted from gland mucous cells of gastric mucosa. Previously, we demonstrated that CGL is critical for survival and that αGlcNAc serves as antibiotic against by inhibiting CGL biosynthesis.

β3-adrenoceptor-mediated increased circulating transaminase levels in mice treated with its agonist BRL 37344.

Treatment with the selective β(3)-adrenoceptor agonist BRL 37344 increased circulating levels of alanine transaminase (ALT) and aspartate transaminase (AST) in mice without causing hepatocellular injury. To clarify whether this was a β(3)-adrenoceptor-mediated effect, the inhibitory effect of the selective β(3)-adrenoceptor antagonist SR 59230A on the increase in circulating transaminase levels induced by BRL 37344 was examined. A single intraperitoneal dose of BRL 37344 alone initially increased insulin and non-esterified fatty acid (NEFA) dose-proportionally at 0.

Renoprotective effect of the L/N-type calcium channel antagonist cilnidipine on puromycin aminonucleoside-induced nephrosis in rats.

The renoprotective effect of cilnidipine ((+/-)-2-methoxyethyl 3-phenyl-2(E)-propenyl 1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridinedicarboxylate, CAS 132203-70-4), a L/N-type calcium channel antagonist, on puromycin aminonucleoside (PAN)-induced nephrosis was investigated in rats. In the Experiment I, rats were given an intravenous injection of PAN (70 mg/kg). Cilnidipine (3 mg/kg/day) and enalapril (CAS 75847-73-3, 5 mg/kg/day) were administered orally from 6 days after treatment with PAN (day 6) to day 26, and urinary analysis was performed on days 9, 15, 20 and 27.