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Dibutyryl-cGMP sodium

CAS No. : 51116-00-8

MCE 国际站：Dibutyryl-cGMP sodium

产品活性：Dibutyryl-cGMP sodium (Bt2cGMP sodium) 是细胞可渗透的 cGMP 类似物，可优先激活 cGMP 依赖性蛋白激酶 (PKG)。Dibutyryl-cGMP sodium 抑制 γ 凝血酶刺激的人血小板中 [³H]-花生四烯酸的释放。Dibutyryl-cGMP sodium 可通过激活ATP 敏感的 K⁺ 通道而具有缓解疼痛作用。

研究领域：Membrane Transporter/Ion Channel

作用靶点：Potassium Channel

In Vitro: Dibutyryl-cGMP is able to induce process elongation and branching in astrocytes resulting from a rapid, reversible and concentration-dependent redistribution of glial fibrillary acidic protein (GFAP) and actin filaments without significant change in protein levels.
When cells are co-incubated with Dibutyryl-cGMP (100 μM) stress fibre formation is prevented and cells acquired a stellate morphology in cerebellar astrocytes.
In cells treated with Dibutyryl-cGMP (100 μM, 2 h) the particulate fraction is nearly devoid of RhoA protein. Dibutyryl-cGMP prevents RhoA-membrane association.
Using the scratchwound model, the size of the wound is significantly smaller in cells treated with Dibutyryl-cGMP after the wound indicating that dbcGMP accelerates wound closure.

In Vivo: Dibutyryl-cGMP (50-200 μg/paw; subcutaneous injection; male Wistar rats) treatment antagonizes the hyperalgesic effect of PGE2 in a dose-dependent manner. Maximal antinociceptive effect of DbcGMP is at 1 h after administration and last for plus 2 h.

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