6-ketoprostaglandin-f1-alpha and Glomerulonephritis--Membranous

To clucidate the mechanism of the therapeutic effect of Yiqi Huoxue (YQHX) serial recipes on membranous nephritis.. Forty-nine New Zealand male rabbits were made to menbranous nephritis model by cation bovine serum albumin and divided into 5 groups, the group A (treated by Qingre Moshen granule), B (treated by Bushen Moshen granule), C (treated by steroid), D (the control group) and E (the normal group). Twenty-four hours' urinary protein content of the animals was determined every week, and plasma albumin, blood lipid, renal function and prostaglandins were tested by the end of experiment. And pathological changes of basement membrane were observed by using light, electronic and immunofluorescent microscopy with polyethylene imine stain.. The 24 hours urinary protein content, plasma albumin and blood lipid in the group A and B were lower than those in the control group significantly, P < 0.01 or 0.05, while those in the group C and the D were similar, P > 0.05. In comparing the group A and B with the group C, the difference was also significant, P < 0.05. Light, electronic and immunofluorescent microscopic examination all showed that the pathologic changes in the group A, B and C were lesser than that of the control, the effect was in the order A > B > C.. YQHX serial recipes can reduce urinary protein content, elevate plasma albumin level, restore the charge barrier effect of and attenuate the immune complex deposition on the basement membrane of glomeruli.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Basement Membrane; Drugs, Chinese Herbal; Glomerulonephritis, Membranous; Male; Proteinuria; Rabbits; Random Allocation; Serum Albumin; Thromboxane B2

The antinephritic effect of lipo-prostaglandin E1, prostaglandin E1 ((1R,2R,3R)-3-hydroxy-2-[(E)-(3S)-3-hydroxy-1-octenyl]-5-oxocyclopent ane heptanoic acid) incorporated in lipid microspheres was investigated using an experimental model of nephritis, crescentic-type anti-glomerular basement membrane nephritis. Lipo-prostaglandin E1 was given i.v. twice a day at 20, 40 and 80 microg/kg and azathioprine, an immunosuppressive agent, at 20 mg/kg was given p.o. once daily from the autologous phase, in which glomerulonephritis was fully developed (the 21 st day after injection of the anti-glomerular basement membrane serum), to the 50th day. Lipo-prostaglandin E1 (40 and 80 microg/kg x 2 per day) significantly inhibited the development of glomerular alterations as well as the elevation of proteinuria and plasma creatinine. Lipo-prostaglandin E1 (20 microg/kg x 2 per day) and azathioprine (20 mg/kg per day) significantly inhibited only the glomerular histopathological changes. Lipo-prostaglandin E1 at three doses significantly decreased the deposition of both rabbit immunoglobulin G and rat immunoglobulin G on the glomerular basement membrane in nephritic rats, but azathioprine apparently inhibited only the deposition of rat immunoglobulin G. A single administration of lipo-prostaglandin E1 inhibited the elevation of platelet aggregation and restored the decrease in renal tissue blood flow in nephritic rats. In addition, a single administration of lipo-prostaglandin E1 inhibited the elevation of glomerular thromboxane B2 and 6-keto prostaglandin F1alpha production in nephritic rats. These results suggest that lipo-prostaglandin E1 may be an effective agent for the treatment of glomerulonephritis. Its antinephritic effect may be due to the inhibition of platelet aggregation, an increase in renal tissue blood flow, a decrease in rabbit and rat immunoglobulin G deposition, and amelioration of the abnormal metabolism of arachidonic acid.

Topics: 6-Ketoprostaglandin F1 alpha; Alprostadil; Animals; Basement Membrane; Creatinine; Glomerulonephritis, Membranous; Immunoenzyme Techniques; Kidney; Liposomes; Male; Proteinuria; Rats; Rats, Sprague-Dawley; Thromboxane B2