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KMID : 0386519960040020335
Research Institute of Korean Medicone
1996 Volume.4 No. 2 p.335 ~ p.336
The effect of artemisinin on the rabbit IgG accelerated nephrotoxic serum glomerulonephritis in mice


Abstract
Artemisinin, anew antimalarial to treat patients infected with strains of plasmodium falciparum, derived from the plant Artemisia annua Linn, has immunopharmacologic acitons such as enhence the PHA-induced lymphocyte transformation rate,
increased
the
weight of spleen but reduced the weight of thymus, reduced phagocytic function of peritoneal macrophage, renmarkably reduced the level of serum IgG and hemolysin forming capacity(sentitized with SRBC), inhibited the activity of Ts cells of donor
mice by
supraoptimal immunuization(SOI), but enhenced activity of Ts cells of recipient mice by SOI. These results suggested that Ts Cells may be the target cells of artemisinin. To the serum complement C3 level of plasmodium berghei-infeted mice,
artemisinin
(i. m.) could remarkly increase it. The artemisinin also obviously reduced the prostaglandin E(PGE) in the mouse hind paw swelling induced by carrageenin. Numerous studies have demonstrated that pharmacologic doses of PGE attenuate the
development
of
immunocomplex nephritis. Some autologous immune mechanisms may be invoolved in the pathogenisis of some types of glmurulonephritis. Glomerular abnormalities can be induced in animals by variety of immunological manipulations. The resulting
disorder
has
many clinical and pathogical similarities to the disease in human. Our purpose was therefore to test the ability of the artemisinin to lessen the severity of rabbit IgG accelerated nephrotoxic serum glomerulonephritis in mice model.
Mice which had treated with rabbit IgG and NTS, administrated with saline, showed Significant increase of urinary protein, cholesterol level, and decrease of serum albumin in NS group. On the contrary, By i.g. adminstration of artemisinin at dose
of
12.5, 25 and 50 mg/kg for 14 days after NTS injection, shown that artemisinin inhibied the nephritic changes in some parameters by means of urinary protein(P<0.05, p<0.01) and serum choleterol(p<0.05, p<0.01) and albumin (p<0.05, p<0.01), blood
urea
nitrogen(p<0.05, p<0.01), serum albumin(p<0.05, p<0.01); Cyclophosphamide(i.p. 10mg/kg for 14d) and almost same effect as the artemisinin had.
Morphological studies shown that the picture of kidney from the mouse with NTS-nephritis accerated with rabbit IgG, treated with i.g. saline as the control, the mesangiocapillary were enlarged and proliferated; There were inflammatory cells
infiltrating
around the glomeruli; The ethelial cell were proliferated in the wall of Bowman's capsule.
Histopathological picture of kidney from the NTS-nephritis accerated with rabbit IgG mouse treated with i.p. 10mg/kg cyclophosphamide as the positive control. No significant histopathological evidence were found. Treated with i.p. 12.5mg/kg
artemisinine, the picture shown that mesangiocapillary were lightly proliferated; There were inflammatory cells infiltrating around the glomeruli; Treatded with i.p. 25mg/kg artemisinine, The picture shown that the mesangiocapillary were lightly
proliferated; Treated with i.p. 50mg/kg artemisinine, The picture shown that both the mesangiocapillary proliferated and the inflammatory cells infiltrating around the glomeruli are less than treated with saline, 12.5 and 25 mg/kg artemisinine.
On the basis of these studies we conclude that the artemisinin can relieve pathological change caused by NTS-nephritis aacerated with rabbit IgG.
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