Studies on the Antinephritic Effects of Plant Components (6): Antinephritic Effects and Mechanisms of Phellodendrine (OB-5) on Crescentic-Type Anti-GBM Nephritis in Rats (2).

Abstract

ABSTRACT-Effects of phellodendrine (OB-5) on crescentic-type anti-GBM nephritis in rats and the cell number of the various leukocyte subpopulations in the glomeruli of the nephritic rats were investi gated. OB-5 at 25, 50 and 100 mg/kg/day, p.o. prevented the urinary protein excretion by the 19th day after i.v.-injection of anti-GBM serum. In the OB-5-treated rats, plasma cholesterol and creatinine con tents were lower than those of the control rats throughout the 40-day experimental period. Histopatho logical observations demonstrated that OB-5 inhibited the incidence of crescent formation, adhesion and fibrinoid necrosis in the glomeruli by the 41st day. OB-5 did not affect the plasma antibody titer against rabbit gamma globulin. The increases in total leukocytes, macrophages, cytotoxic/suppressor T cells, la positive cells, and IL-2 receptor positive cells in the glomeruli in OB-5, 100 mg/kg-treated rats as well as those of the animals treated with azathioprine or cyclosporin A were lower than those of the anti-GBM nephritic control. These results indicate that OB-5 was effective in crescentic-type anti-GBM nephritis and the antinephritic mechanisms of this agent may be due to its ability to inhibit the prolifera tion or the migration of macrophages and cytotoxic T lymphocytes in the glomeruli.

Acteoside, a Component of Stachys Sieboldii MIQ, May Be a Promising Antinephritic Agent (2): Effect of Acteoside on Leukocyte Accumulation in the Glomeruli of Nephritic Rats

“…Renal tissues for immunoperoxidase staining were fixed in paraformaldehyde-lysine-periodate, and serial cryostat sections (4 pm) were labeled with monoclonal antibodies (mAbs) as previously reported (9). The monoclonal antibodies used in this study were as follows: OX-1 (leukocyte common antigen, total leukocyte), W3/25 (CD4, helper/inducer T cells), OX-8 (CD8, cytotoxic/suppressor T cells), ED-1 (most macrophage and some dendritic cells), OX-39 (interleukin-2 (IL-2) receptor, activated T cells) and OX-18 (MHC class II, la positive cell).…”

“…Labeling cryostat tissue sections with each mAbs were analyzed as regards to the number of cells in the leukocyte subpopula tion in the glomeruli. Cells labeled by each of the mAbs within each glomerulus were counted with an image analyzer (Toyobo Image analyzer V1, Toyobo Co., Ltd., Tokyo), and the results were expressed as the number of cells per glomerular cross section (9).…”

“…More recently, Hattori et al (9) reported that the progression of crescentic-type anti-GBM nephritis in rats …”

Acteoside, a Component of Stachys Sieboldii MIQ, May Be a Promising Antinephritic Agent: Effect of Acteoside on Crescentic-Type Anti-GBM Nephritis in Rats.

“…Moreover, Neild et al (6) reported that suppression of T cell function by cyclosporin A (CyA) blocked the subse quent development of glomerular lesions in acute sickness nephritis. We reported that mizoribin (7), azathioprine (7), CyA (8), methylprednisolone (9) and some plant com ponents (10) that have immunosuppressive action showed a salutary effect on anti-GBM nephritis. Although these immunosuppressive agents exert antinephritic action, it is difficult to use them in clinical trials because of their side effects (11).…”

Saireito and Saikosaponin D Prevent Urinary Protein Excretion via Glucocorticoid Receptor in Adrenalectomized WKY Rats with Heterologous-Phase Anti-GBM Nephritis

“…There is evidence that glucocorticoids inhibit IL-2 and IL-10 production stimulated by anti-CD3, LPS, or PHA [21, 22]. Moreover, it is known that increases in the IL-2 level in the glomeruli in nephritis induced by heterogeneous antibody injection and suppression of IL-2 function, particularly local suppression in the kidney, lead to improvement of nephritis [23, 24]. The mechanisms by which Th1 cytokines affect the consequent inflammatory cascade that is caused by glomerular injury, such as proteinuria or histopathological changes, remain unclear.…”