The dinuclear palladium(II) complexes [(PP)Pd(C1–C3-β-dik(2−)-O,O′)Pd(PP)](ClO4)2 containing a β-diketonate dianion as a bridging ligand were prepared by the reactions of the mononuclear complexes [Pd(β-dik(2−)-C1–C3)(PP)] with [Pd(PP)(H2O)2](ClO4)2. In the reactions of [Pd(etac(2−)-C1–C3)(dpe)] with [Pt(PPh3)2(H2O)2](ClO4)2 and [Ni(acac)2] in the 1:1 mole ratio, similar dinuclear complexes [(dpe)Pd(C1–C3-etac(2−)-O,O′)Pt(PPh3)2](ClO4)2 and [(dpe)Pd(C1–C3-etac(2−)-O,O′)Ni(acac)2] were produced, respectively, while the reactions of [Pd(β-dik(2−)-C1–C3)(PP)] with Ni(ClO4)2·6H2O and Mg(ClO4)2 in the 2:1 mole ratio afforded the trinuclear complexes [M{O,O′-β-dik(2−)-C1–C3Pd(PP)}2](ClO4)2 (M=Ni(II) and Mg(II)). The trihapto coordination to palladium(II) and O,O′-chelation to another metal atom of the β-diketonate dianion in these complexes were deduced mainly by IR and NMR spectroscopy.
Accumulating evidence suggests that histamine synthesis induced in several types of tumor tissues modulates tumor immunity. We found that a transient histamine synthesis was induced in CD11b+Gr-1+ splenocytes derived from BALB/c mice transplanted with a syngeneic colon carcinoma, CT-26, when they were co-cultured with CT-26 cells. Significant levels of IFN-γ were produced under this co-culture condition. We explored the modulatory roles of histamine on IFN-γ production and found that several histamine receptor antagonists, such as pyrilamine, diphenhydramine, JNJ7777120, and thioperamide, could significantly suppress IFN-γ production. However, suppression of IFN-γ production by these antagonists was also found when splenocytes were derived from the Hdc−/− BALB/c mice. Suppressive effects of these antagonists were found on IFN-γ production induced by concanavalin A or the combination of an anti-CD3 antibody and an anti-CD28 antibody in a histamine-independent manner. Murine splenocytes were found to express H1 and H2 receptors, but not H3 and H4 receptors. IFN-γ production in the Hh1r−/− splenocytes induced by the combination of an anti-CD3 antibody and an anti-CD28 antibody was significantly suppressed by these antagonists. These findings suggest that pyrilamine, diphenhydramine, JNJ7777120, and thioperamide can suppress IFN-γ production in activated splenocytes in a histamine-independent manner.
Accumulating evidence suggests that histamine synthesis induced in several types of tumor tissues should modulate tumor immunity. We found that a transient histamine synthesis was induced in CD11b+Gr-1+splenocytes derived from BALB/c mice transplanted with a syngeneic colon carcinoma, CT-26, when they were co-cultured with CT-26 cells. Significant levels of IFN-γ were produced under this co-culture condition. We explored the modulatory roles of histamine on IFN-γ production and found that several histamine receptor antagonists, such as pyrilamine, diphenhydramine, JNJ7777120, and thioperamide, could significantly suppress IFN-γ production. However, suppression of IFN-γ production by these antagonists was also found when splenocytes were derived from the Hdc-/- BALB/c mice. Suppressive effects of these antagonists were found on IFN-γ production induced by concanavalin A or the combination of an anti-CD3 antibody and an anti-CD28 antibody in a histamine-independent manner. Murine splenocytes were found to express H1 and H2 receptors, but not H3 and H4 receptors. IFN-γ production in the Hh1r-/- splenocytes induced by the combination of an anti-CD3 antibody and an anti-CD28 antibody was significantly suppressed by these antagonists. These findings suggest that pyrilamine, diphenhydramine, JNJ7777120, and thioperamide could suppress IFN-γ production in activated splenocytes in histamine-independent manner.
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