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Abstract: Thermolyses of β-hydroxysulfides 2, bearing groups, such as 2-benzothiazolyl and 4-(4-methyl)-4H-1,2,4-triazolyl groups, were studied and found to afford the corresponding substituted styrenes 5 and hydroxy heteroaromatics in good yields, respectively. The product distribution change in the course of the thermolysis of 2a was also studied. The olefin products 5a were considered to be formed by the thermal desulfurization of the corresponding thiiranes 4a initially formed via the five-membered spiro intermediate 6a. [Copyright &y& Elsevier]

Abstract: Convenient and efficient procedures for thiirans have been developed via a one-pot reaction of benzoxazolyl β-ketosulfides with NaBH4 and NaOH in MeOH and THF. The reaction is considered to proceed via the spiro intermediate by the ipso-addition of β-hydroxygroup, which is formed by the NaBH4 reduction of β-keto group, to 2-position of benzoxazole group. [Copyright &y& Elsevier]

Abstract: We have examined the reactivities of α-phosphorylmethyl benzothiazolyl sulfoxides in the thermolyses and in the presence of several amines, such as aniline, benzylamine, piperidine, morpholine, and pyrrolidine. Thermolyses of the derivatives in the presence of 2,3-dimethyl-1,3-butadiene afforded 2-phosphoryl substituted 4,5-dimethyl-3,6-dihydro-2H-thiopyran S-oxide. In the reaction with amines, the complex product mixture, which contains α-phosphorylmethyl benzothiazolyl sulfides (2 and 5), α-phosphorylmethyl disulfides (15 and 16), and 2-amino substituted benzothiazole 14 was found to be formed besides the target phosphinecarbothioamides. Several mechanistic studies were performed to elucidate the formation mechanism, particularly for deoxygenated products from the starting sulfoxides, i.e., 2 and 5 from 3 and 6, respectively. [Copyright &y& Elsevier]

Abstract: We have synthesized α-(phosphoryl)methyl tetrazolyl sulfoxides and examined the reactivities in the thermolyses and in the presence of several amines, such as aniline, benzylamine, piperidine, pyrrolidine, and morpholine. Thermolyses of the derivatives in the presence of 2,3-dimethyl-1,3-butadiene afforded 2-phosphoryl substituted 4,5-dimethyl-3,6-dihydro-2H-thiopyran S-oxide. In addition, novel phosphinecarbothioamides were obtained in the reaction of the derivatives with amines. [Copyright &y& Elsevier]

The expression of inducible nitric oxide synthase (iNOS) and the resultant increased nitric oxide production are associated with endotoxemia and atherosclerotic lesions observed in transplant hearts or balloon-injured artery. Ursodeoxycholic acid has been shown to have cardiovascular protective effects, such as inhibition of the development of transplant arteriosclerosis, but its mechanism remains unclear. Here, we investigated the effects of ursodeoxycholic acid on nitric oxide production and the expression of iNOS in vascular smooth muscle cells isolated from adult rat aorta and rabbit coronary artery. Nitrite released from cells in the culture medium was measured with the Griess reaction. iNOS mRNA and protein were measured by Northern and Western blot analyses. Treatment with ursodeoxycholic acid (30–1000 μM) significantly inhibited lipopolysaccharide plus interferon-γ-induced nitric oxide production in a concentration-dependent manner, but ursodeoxycholic acid showed only small inhibitory effects on nitric oxide production that had already been induced by lipopolysaccharide plus interferon-γ. Ursodeoxycholic acid by itself did not affect basal nitric oxide production. Ursodeoxycholic acid also suppressed lipopolysaccharide plus interferon-γ-induced expression of iNOS mRNA and protein. Ursodeoxycholic acid had the most potent inhibitory effect among various kinds of bile acids examined, i.e. chenodeoxycholic acid, deoxycholic acid, cholic acid and conjugated bile acids such as tauroursodeoxycholic acid. These results suggest that ursodeoxycholic acid inhibits the induction of iNOS and then nitric oxide production in aortic and coronary artery smooth muscle cells, suggesting a possible mechanism for the cardiovascular protective effect of ursodeoxycholic acid under various pathophysiological conditions such as endotoxemia and atherosclerosis. [Copyright &y& Elsevier]