Investigation of the inhibition by acetylshikonin of the respiratory burst in rat neutrophils

British Journal of Pharmacology
J P WangS C Kuo

Abstract

1. The ability of acetylshikonin to inhibit the respiratory burst in rat neutrophils was characterized and the underlying mechanism of action was also assessed in the present study. 2. Acetylshikonin caused an irreversible and a concentration-dependent inhibition of formylmethionylleucyl-phenylalanine (fMLP) plus dihydrocytochalasin B (CB)- and phorbol 12-myristate 13-acetate (PMA)-induced superoxide anion (O2.-) generation with IC50 values of 0.48 +/- 0.03 and 0.39 +/- 0.03 microM, respectively. Acetylshikonin also inhibited the O2 consumption in neutrophils in response to fMLP/CB as well as to PMA. 3. Acetylshikonin did not scavenge the generated O2.- in the xanthine-xanthine oxidase system or during dihydroxyfumaric acid (DHF) autoxidation but, on the contrary, acetylshikonin enhanced the O2.- generation in these cell-free oxygen radical generating systems. 4. Acetylshikonin inhibited the formation of inositol trisphosphate (IP3) (39.0 +/- 7.8% inhibition at 10 microM, P < 0.05) in neutrophils in response to fMLP. 5. Both the neutrophil cytosolic protein kinase C (PKC) activity and the PMA-induced PKC associated with the membrane were unaffected by acetylshikonin. 6. Acetylshikonin did not affect the porcine heart protein ki...Continue Reading

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Citations

Aug 8, 2002·Phytotherapy Research : PTR·Xin ChenM Zack Howard
May 15, 2002·Antioxidants & Redox Signaling·Claude A Piantadosi
May 15, 2002·Antioxidants & Redox Signaling·Gerald S MarksKanji Nakatsu
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Jul 14, 2007·The Journal of Sexual Medicine·M Talaat Abdel AzizSoheir Mahfouz
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