KKL 顾客使用本产品发表的 19 篇科研文献

Diphenyleneiodonium chloride is a NADPH oxidase (NOX) inhibitor and also functions as a TRPA1 activator with an EC₅₀ of 1 to 3 μM. Diphenyleneiodonium chloride selectively inhibits intracellular reactive oxygen species.

Diphenyleneiodonium chloride is a NADPH oxidase (NOX) inhibitor and also functions as a TRPA1 activator with an EC₅₀ of 1 to 3 μM. Application of Diphenyleneiodonium chloride to HEK-TRPA1 cells at a concentration ranges of 0.03 to 10 μM effectively induces a Ca response. However, Diphenyleneiodonium chloride fails to evoke a Ca response in control HEK cells, even at a relatively high dose of 10 μM. When Diphenyleneiodonium chloride is included in the co-cultures, lipopolysaccharide (LPS)-induced preOL apoptosis is significantly inhibited. Treatment with Diphenyleneiodonium chloride is found to significantly attenuate the LPS-induced O₂ production by 2.0-fold, reducing it to within 27% of the controls.

Intraplantar injection of 2 mM Diphenyleneiodonium chloride to the hindpaw causes licking or biting behavior. Diphenyleneiodonium chloride treatment immediately or 24 h after lipopolysaccharide (LPS) injection significantly attenuates the LPS-induced loss of O4 positive cells. Treatment with Diphenyleneiodonium chloride either immediately or 24 h after LPS injection significantly ameliorates the LPS-induced disorganization of the white matter nerve fibers. However, treatment with DPI 48 h after LPS injection does not appear to correct the LPS-induced white matter damage. DPI treatment either immediately or 24 h after LPS injection significantly reduces the accumulation of both gp91phox and p67phox in the membrane fraction.

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