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 Ca²⁺ response. However, Diphenyleneiodonium chloride fails to evoke a Ca²⁺ 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.

西域 has not independently confirmed the accuracy of these methods. They are for reference only.

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.

西域 has not independently confirmed the accuracy of these methods. They are for reference only.

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.

西域 has not independently confirmed the accuracy of these methods. They are for reference only.

• . Suzuki H, et al. The NADPH oxidase inhibitor diphenyleneiodonium activates the human TRPA1 nociceptor. Am J Physiol Cell Physiol. 2014 Aug 15;307(4):C384-94.  [Content Brief]

  . He YF, et al. Diphenyleneiodonium protects preoligodendrocytes against endotoxin-activated microglial NADPH oxidase-generated peroxynitrite in a neonatal rat model of periventricular leukomalacia. Brain Res. 2013 Jan 25;1492:108-21.  [Content Brief]