Triptoquinone A
Triptoquinone A may be a useful candidate for the development of a drug as a potent inhibitor of iNOS gene over-expression. Triptoquinone A has anti-inflammatory activity, it prevents ndotoxin-or interleukin-1 beta-promoted induction of nitric oxide synthase in vascular smooth muscle, thus inhibiting development of L-arginine-induced vasorelaxation.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to
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Biochem Biophys Res Commun. 1996 Jul 16;224(2):579-85.
Suppression of inducible nitric oxide synthase mRNA expression by tryptoquinone A.[Pubmed:
8702429 ]
Triptoquinone A (TQA), which is an anti-inflammatory constituent in plants, was studied for its suppressive effect on nitric oxide production by LPS.
METHODS AND RESULTS:
TQA significantly suppressed smooth muscle relaxation and increase in cyclic GMP levels by nitric oxide (NO) in an L-arginine-induced relaxation experiment. The mechanistic studies showed that TQA did not directly inhibit NO radicals and inducible nitric oxide synthase (iNOS) enzyme but suppressed IL-1 beta and iNOS mRNA expression by LPS. The suppression level of iNOS gene expression by TQA was comparable to that by dexamethasone.
CONCLUSIONS:
TQA may be a useful candidate for the development of a drug as a potent inhibitor of iNOS gene over-expression.
Life Sci. 1996;59(3):PL49-54.
Inhibition by triptoquinone-A of LPS- and IL-1 beta-primed induction of NO synthase in rat thoracic aorta.[Pubmed:
8699928]
METHODS AND RESULTS:
We investigated the effect of Triptoquinone A (TQA), an active principal of Triptergium wilfordii, on the induction of nitric oxide synthase (NOS) promoted by endotoxin (LPS) and interleukin-1 beta (IL-1 beta). Prophylactic application of TQA selectively prevented LPS-primed initiation of L-arginine (Arg)-induced relaxation, and cGMP formation of rat thoracic aorta, and LPS-stimulated nitrite production by cultured aortic smooth muscle cells, which appear to be mediated by NOS expressed by LPS in vascular smooth muscle. TQA also prevented IL-1 beta-triggered initiation of Arg-induced relaxation and nitrite accumulation.
CONCLUSIONS:
These results suggest that TQA prevents LPS-or IL-1 beta-promoted induction of NOS in vascular smooth muscle, thus inhibiting development of Arg-induced vasorelaxation.
