The effect of
triptolide, which is isolated from Tripterygium Wilfordii, on induction and development of murine
AA amyloidosis was studied. In the first experiment, we examined the ability of
triptolide to inhibit initiation of
amyloidosis. Oral or intraperitoneal administration of 480 microg/kg/day
triptolide inhibited splenic
amyloid deposition in both rapid and chronic induction models of mouse
AA amyloidosis. Moreover,
serum amyloid A (SAA) and
interleukin (IL)-6 levels were also suppressed remarkably.
Triptolide also immediately decreased SAA levels and reduced the incidence of
amyloidosis even under conditions of high SAA levels. In the second experiment, we evaluated the influence of
triptolide on development and resorption of
amyloid deposition.
Amyloid deposition was induced in mice by 28 daily
injections of
casein. After splenic and hepatic biopsies to confirm the presence of
amyloid deposits, the mice immediately started to receive daily
injections of 480 microg/kg/day
triptolide with or without
casein. Treatment with
triptolide for 35 days and 105 days prevented deposition of
amyloid and promoted resorption of splenic
amyloid deposits. In conclusion, we show for the first time that
triptolide inhibits induction and development of experimental murine
amyloidosis. These results suggest that through suppression of
IL-6,
triptolide can reduce production of SAA.
Amyloid deposition is prevented when levels of the
amyloid-forming precursor
protein SAA are decreased significantly.