M Ito

Meijo University, Nagoya-shi, Aichi-ken, Japan

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Publications (43)15.89 Total impact

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    ABSTRACT: In the present study, we investigated the susceptibility to restraint plus water-immersion stress (RWIS) in rats with daunomycin-induced nephrosis in comparison to that in normal rats. The severity of RWIS-induced gastric lesions was significantly less in nephrotic rats on the 20th and 40th days after a single i.v. injection of daunomycin (12 mg/kg) than in the respective control rats. Acid secretion in pylorus-ligated rats significantly decreased under the 3-h stress. On the 20th day after treatment with daunomycin, acid secretion was significantly less in nephrotic rats than in control rats under both stress and unstressed conditions. Pretreatment of normal rats with methylene blue, a guanylate cyclase inhibitor, or phenylephrine, a vasoconstrictor, significantly prevented the stress-induced gastric lesions and decreased acid secretion. N(omega)-Nitro-L-arginine methyl ester, a nitric oxide (NO) synthase inhibitor, prevented the stress-induced gastric lesion formation only. These results indicate that nephrotic rats are more resistant to RWIS-induced gastric lesions than normal rats. In addition, these results suggest that the decrease in acid secretion related to the decrease in the release of NO from endothelial cells may contribute, at least in part, to the prevention of the stress-induced gastric lesion formation in nephrotic rats.
    The Japanese Journal of Pharmacology 11/1999; 81(2):230-6.
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    ABSTRACT: When free radical-scavenging activities of quercetin, alpha-tocopherol, nifedipine and tetracycline were measured by an electron spin resonance technique, all test compounds (10(-5) to 10(-3) M) scavenged both superoxide anions and hydroxyl radicals. The oral administration of quercetin (50 and 100 mg/kg), alpha-tocopherol (8 and 16 mg/kg), nifedipine (20 and 40 mg/kg) or tetracycline (10 and 20 mg/kg) markedly prevented the HCl plus ethanol-induced gastric mucosal injury and the increase in the content of thiobarbituric acid-reactive substances in the injured mucosa in rats. In addition, quercetin (25, 50 and 100 mg/kg), alpha-tocopherol (4, 8 and 16 mg/kg), nifedipine (10, 20 and 40 mg/kg) and tetracycline (5, 10 and 20 mg/kg), given orally, twice daily for 14 consecutive days from the day after acetic acid injection, dose-dependently promoted the ulcer healing and inhibited the increase in the content of thiobarbituric acid-reactive substances in the ulcerated mucosa. These results indicate that quercetin, alpha-tocopherol, nifedipine and tetracycline possess gastric cytoprotective and gastric ulcer healing-promoting actions. In addition, the free radical-scavenging properties of these compounds may be partly related to their anti-ulcer effects.
    The Japanese Journal of Pharmacology 01/1999; 78(4):435-41.
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    ABSTRACT: This study was performed to evaluate the effect of nephrosis on gastric lesions in the rats. A single i.v. injection of daunomycin (12 mg/kg) into rats produced severe proteinuria and hypercholesterolemia on the 20th and 40th days after the administration. The severity of HCl-ethanol-induced gastric lesions was significantly greater in nephrotic rats than in control animals on the 20th and 40th days. The gastric mucosal blood flow on the 40th day was significantly lower in nephrotic rats. Pretreatment of normal rats with N(ω)-nitro-l-arginine or N(ω)-nitro-l-arginine methyl ester, a nitric oxide (NO) synthase inhibitor, methylene blue, a guanylate cyclase inhibitor, or phenylephrine, a vasoconstrictor, significantly aggravated the HCl-ethanol-induced gastric lesions and reduced the blood flow. When N(ω)-nitro-l-arginine methyl ester was given to nephrotic rats on the 40th day, it further increased the aggravation of the gastric lesions caused by nephrosis. These results suggest that the aggravation of HCl-ethanol-induced gastric lesions observed in nephrotic rats may be, at least in part, related to the decrease in the release of NO from endothelial cells.
    Environmental Toxicology and Pharmacology 04/1996; 1(2):117-22. · 2.01 Impact Factor
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    ABSTRACT: It is known that adhesion molecules play a crucial role in the development of glomerulonephritis. Therefore, we investigated the effects of acteoside on the expression of intercellular adhesion molecule-1 (ICAM-1) in nephritic glomeruli, in vivo, and human umbilical vein endothelial cells (HUVECs) and rat mesangial cells, in vitro. Aceteoside treatment significantly decreased the up-regulation of ICAM-1 expression in nephritic glomeruli. Acteoside prevented the up-regulation of ICAM-1 expression mediated by inflammatory cytokines or phorbol 12-myristate 13-acetate on HUVECs and rat mesangial cells. Adhesion of neutrophils and macrophages to acteoside-treated HUVECs was suppressed to one half of that in untreated HUVECs. These data support the finding that acteoside inhibits the up-regulation of ICAM-1 in the nephritic glomeruli. Additionally, it is suggested that the antinephritic action of acteoside is due to the inhibition of intraglomerular accumulation of leukocytes through the prevention of the up-regulation of ICAM-1. This is the first paper demonstrating that the up-regulation of ICAM-1 in nephritic glomeruli is inhibited by a natural product, acteoside.
    The Japanese Journal of Pharmacology 03/1996; 70(2):157-68.
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    ABSTRACT: The possibility that hyperlipidemia and an increase of mononuclear cells in the glomeruli could participate in the pathogenesis of minimal change glomerulopathy was evaluated in puromycin aminonucleoside (PAN) nephrosis in rats. Significant increases in intraglomerular CD4-, IL-2-receptor (R)- and ED-1-positive cells were found in PAN rats. Urinary protein excretion and mononuclear cells in the glomeruli of 1% cholesterol diet-fed rats significantly increased, compared with standard diet feeding. Moreover, administration of a subnephrogenic dose of PAN in cholesterol diet-fed rats substantially increased urinary protein excretion and mononuclear cells in the glomeruli. Additionally, antihyperlipidemia agents and immunosuppressive agents prevented urinary protein excretion and increases of CD4-, IL-2R- and ED-1-positive cells in the glomeruli of PAN nephrotic rats. Monoclonal antibodies directed against these cells also prevented urinary protein excretion. These results suggest that CD4-, IL-2R- and ED-1-positive cells and hyperlipidemia are involved in the progression, but not the pathogenesis, of PAN.
    The Japanese Journal of Pharmacology 02/1996; 70(1):25-33.
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    ABSTRACT: The effect of FK506 (tacrolims hydrate), an immunosuppressive agent produced by Streptomyces tsukubaensis, on crescentic-type anti-glomerular basement membrane (GBM) nephritis in rats was investigated. When rats were treated with FK506 from 1 or 20 days after the anti-GBM serum injection, FK506 inhibited the increase in urinary protein excretion. Histological observation demonstrated that FK506 suppressed glomerular alterations. In the FK506-treated rats, antibody production and rat-IgG and C3 deposits on the GBM were significantly less than those in the nephritic control group. FK506 treatment suppressed the accumulation of ED-1-positive cells, CD4-positive cells, CD8-positive cells, interleukin-2 (IL-2)-receptor-positive cells, leukocyte-function-associated antigen-1 (LFA-1)-positive cells and intercellular adhesion molecule-1 (ICAM-1)-expression in nephritic glomeruli. However, in the in vitro study, FK506 failed to inhibit the up-regulated ICAM-1 expression on endothelial cells in response to tumor necrosis factor (TNF)-alpha. On the other hand, IL-2 production from the spleen cells isolated from nephritic rats treated with FK506 was lower than that in the nephritic control rats. These results suggest that FK506 is effective against crescentic-type anti-GBM nephritis and that the antinephritic mechanisms of FK506 is due to the inhibition of intraglomerular accumulation and activation of leukocytes through the suppression of ICAM-1 expression and IL-2 production.
    The Japanese Journal of Pharmacology 02/1996; 70(1):43-54.
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    T Segami, Y Suzuki, M Ito
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    ABSTRACT: We investigated the effects of cimetidine, omeprazole and atropine, antisecretory anti-ulcer agents, on the healing of gastric and duodenal ulcers simultaneously induced in the same rats. Furthermore, we examined the effect of histamine, an acid secretory agent, on the healing of both ulcers. When the effects of test drugs were assessed on the 15th day after local application of acetic acid, repeated oral administration of cimetidine (50 and 100 mg/kg twice daily) or omeprazole (25 and 50 mg/kg once daily) markedly accelerated the healing of both gastric and duodenal ulcers. Atropine (10 mg/kg twice daily, p.o.) showed a healing effect on duodenal ulcers only. The repeated subcutaneous administration of histamine (30 mg/kg 3 times daily) apparently delayed the healing of duodenal ulcers but not gastric ulcers. In conclusion, this experimental chronic ulcer model in rats is useful for directly comparing the effects of anti-ulcer drugs on the healing of gastric and duodenal ulcers. In addition, the increase in acid secretion appears to have a greater influence on the delay of ulcer healing in the duodenum than in the stomach.
    Biological & Pharmaceutical Bulletin 02/1996; 19(1):53-6. · 1.85 Impact Factor
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    ABSTRACT: This study was performed to evaluate the effect of nephrosis on gastric lesions in the rats. A single i.v. injection of daunomycin (12 mg/kg) into rats produced severe proteinuria and hypercholesterolemia on the 20th and 40th days after the administration. The severity of HCl-ethanol-induced gastric lesions was significantly greater in nephrotic rats than in control animals on the 20th and 40th days. The gastric mucosal blood flow on the 40th day was significantly lower in nephrotic rats. Pretreatment of normal rats withN -nitro-l-arginine or N-nitro-l-arginine methyl ester, a nitric oxide (NO) synthase inhibitor, methylene blue, a guanylate cyclase inhibitor, or phenylephrine, a vasoconstrictor, significantly aggravated the HCl-ethanol-induced gastric lesions and reduced the blood flow. WhenN -nitro-l-arginine methyl ester was given to nephrotic rats on the 40th day, it further increased the aggravation of the gastric lesions caused by nephrosis. These results suggest that the aggravation of HCl-ethanol-induced gastric lesions observed in nephrotic rats may be, at least in part, related to the decrease in the release of NO from endothelial cells.
    Environmental Toxicology and Pharmacology 01/1996; 1(2). · 2.01 Impact Factor
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    ABSTRACT: We investigated the effect of the zinc-cimetidine complex on the healing of acetic acid-induced gastric ulcers in rats. When the effects of test drugs were assessed on the 15th day after acetic acid injection, the zinc-cimetidine complex at oral doses of 15.0 (11.4 mg as cimetidine), 30.0 and 60.0 mg/kg twice daily promoted the ulcer healing in a dose-dependent manner. Cimetidine was effective at oral doses of over 45.4 mg/kg twice daily. ZnCl2 was ineffective on all ulcer parameters. The effect of the combination of cimetidine and ZnCl2 was similar to that of cimetidine alone. The zinc-cimetidine complex had already inhibited the increase in thiobarbituric acid reactants in the ulcerated region before the ulcer-healing effect of this compound was recognized. A single oral administration of the complex at 15 and 30 mg/kg to normal rats was ineffective in inhibiting acid secretion and in increasing serum gastrin levels, although cimetidine was markedly effective on both parameters. These results indicate that the zinc-cimetidine complex at about 1/4 the dose of cimetidine was as effective as cimetidine when the ulcer-healing effects of both compounds were compared with the same dose of cimetidine. In addition, the ulcer-healing effect of this complex may be due, at least in part, to the inhibition of lipid peroxidation but not due to the inhibition of acid secretion or the trophic effect of gastrin.
    The Japanese Journal of Pharmacology 08/1995; 68(3):287-95.
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    ABSTRACT: The current studies were designed to identify which mononuclear leukocytes have an important role in the development of glomerular injury using rats with original-type (mild injury) and crescentic-type (severe injury) anti-glomerular basement membrane (GBM) nephritis. 1) Proteinuria was persistent in crescentic-type anti-GBM nephritis compared with original-type anti-GBM nephritis. Macrophages/monocytes (ED-1), cytotoxic/suppressor T cells (CD-8), interleukin-2-receptor (CD-25)-positive cells and Ia-positive cells accumulated remarkably and persisted for longer in crescentic-type nephritic glomeruli. 2) We then performed investigations using immunosuppressants. Cyclosporin A abrogated proteinuria more effectively than azathioprine in crescentic-type nephritis. However, plasma antibody titer and glomerular rat IgG deposition were equally reduced by both azathioprine and cyclosporin A. The increase in the numbers of ED-1-, CD-8- and CD-25-positive cells in nephritic glomeruli was completely inhibited by cyclosporin A, but inhibited only slightly by azathioprine. 3) There was a correlation between the degree of proteinuria and the number of ED-1- and CD-8-positive cells. It is likely that these cells are leukocytes that lead to glomerular injury in nephritis. 4) In additional experiments using monoclonal antibodies against macrophages/monocytes and cytotoxic/suppressor T cells, urinary protein excretion and accumulation of these cells were blunted in nephritic rats treated with these antibodies. These results suggest that ED-1- and CD-8-positive cells are involved in the development of crescentic-type anti-GBM nephritis.
    Nippon Jinzo Gakkai shi 12/1994; 36(11):1228-39.
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    ABSTRACT: The effects of cimetidine, omeprazole and atropine sulfate on the healing of acetic acid-induced gastric ulcers in rats with limited food intake time (9:00-10:00 a.m. and 5:00-6:00 p.m.) were evaluated 15 days after the acid injection. Oral repeated administration of cimetidine (25-100 mg/kg twice daily) or omeprazole (10-50 mg/kg once daily) dose dependently accelerated ulcer healing. Atropine sulfate (10 mg/kg twice daily, p.o.) was ineffective. A single oral administration of omeprazole (50 mg/kg) or cimetidine (100 mg/kg) resulted in potent and long-lasting anti-acid secretory and gastrin-releasing actions. The degree and duration of anti-acid secretion by atropine sulfate were equal to those of cimetidine, but the elevation of gastrin release by atropine sulfate was weak and temporary. These results indicate that the gastric ulcers of rats with a limited food intake time are useful for evaluating the healing effects of cimetidine and omeprazole on gastric ulcers. In addition, the effects of both drugs may be related to the increased gastrin release rather than to the reduced acid secretion.
    European Journal of Pharmacology 11/1994; 263(3):245-51. · 2.59 Impact Factor
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    ABSTRACT: Daily oral administration of cimetidine or omeprazole markedly accelerated the healing of acetic acid-induced gastric ulcers in rats with a limited food intake time. The increased gastric acid secretion induced by daily treatment with histamine affected neither the spontaneous healing of the ulcers nor the healing-promoting actions of both agents. Pretreatment of rats with ulcers with 6-hydroxydopamine significantly inhibited the increase in the antrum gastrin cells, serum gastrin levels and corpus mucosal thickness elicited by repeated administration of cimetidine or omeprazole. Pretreatment with 6-hydroxydopamine did not affect the inhibitory actions of cimetidine and omeprazole on acid secretion, but completely abolished the ulcer healing-promoting actions of both drugs. Daily intraperitoneal administration of pentagastrin accelerated ulcer healing. These results suggest that cimetidine and omeprazole mainly accelerate the healing of gastric ulcers by the trophic action of gastrin via the increase in gastrin secretion, while the inhibition of acid secretion may play a minor role in ulcer healing.
    European Journal of Pharmacology 11/1994; 263(3):253-9. · 2.59 Impact Factor
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    ABSTRACT: We investigated the effect of acteoside in comparison with that of cyclosporin A on leukocyte accumulation in the glomeruli of rats with crescentic-type anti-glomerular basement membrane (GBM) nephritis. Acteoside given p.o. at a dose of 30 mg/kg once a day for 15 consecutive days after treatment with anti-GBM serum markedly suppressed the urinary protein as well as glomerular histological changes. Acteoside given p.o. for 5 or 15 consecutive days markedly suppressed the accumulation of total leukocytes, ED-1-positive cells (monocytes/macrophages), CD4-positive cells, CD8-positive cells, interleukin-2-receptor-positive cells (activated T cells) and Ia-positive cells in the glomeruli. These effects of cyclosporin A (20 mg/kg/day, p.o.) were also as potent as those of acteoside (30 mg/kg/day, p.o.). Cyclosporin A also strongly suppressed the elevation of plasma antibody level against rabbit gamma-globulin. However, in this dose, acteoside did not significantly suppress the antibody formation. It can be concluded from these results that acetoside may exert its antinephritic action by suppressing the accumulation of leukocytes in the glomeruli.
    The Japanese Journal of Pharmacology 10/1994; 66(1):47-52.
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    ABSTRACT: The antinephritic effect of DP-1904 [6-(1-imidazolylmethyl)-5,6,7,8-tetrahydronaphthalene-2-carboxylic acid hydrochloride], a thromboxane A2 synthetase inhibitor, was compared with that of OKY-046, using an experimental model of nephritis, crescentic-type anti-glomerular basement membrane nephritis. Test drugs were given p.o. once daily from the day after the the development of glomerular alteration as well as the elevation of proteinuria and plasma cholesterol. On the other hand, OKY-046 (20 mg/kg per day), a thromboxane A2 synthetase inhibitor, significantly inhibited only deterioration in the glomeruli. DP-1904 and OKY-046 inhibited glomerular thromboxane B2 production and increased glomerular prostaglandin E2 and 6-keto prostaglandin F1 alpha production in normal and nephritic rats. Both drugs inhibited the increase in platelet aggregability, restored decreased renal tissue blood flow to a near-normal level and decreased the deposition of rat immunoglobulin G on glomerular basement membrane in nephritic rats. These results suggest that DP-1904 may be an effective agent for the treatment of proliferative glomerulonephritis.
    European Journal of Pharmacology 08/1994; 259(3):233-42. · 2.59 Impact Factor
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    ABSTRACT: Effects of acetoside (ACT) on crescentic-type anti-GBM nephritis in rats were investigated. When rats were treated with ACT from the 1st day after i.v. injection of anti-GBM serum, ACT inhibited the elevation of protein excretion into urine. In the ACT-treated rats, cholesterol and creatinine contents and antibody production against rabbit gamma-globulin in the plasmas were lower than those of the nephritic control rats. Histological observation demonstrated that this agent suppressed hypercellularity and the incidence of crescent formation, adhesion of capillary wall to Bowman's capsule and fibrinoid necrosis in the glomeruli. Furthermore, rat-IgG and C3 deposits on the GBM were significantly less in the ACT-treated group than in the control nephritic group. When the treatment was started from the 20th day after i.v. injection of anti-GBM serum, by which the disease had been established, ACT resulted in a similar effect on the nephritic rats as stated above. These results suggest that ACT may be a useful medicine against rapidly progressive glomerulonephritis, which is characterized by severe glomerular lesions with diffuse crescents.
    The Japanese Journal of Pharmacology 07/1994; 65(2):143-51.
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    ABSTRACT: To establish the regimen for beneficial prolonged treatment with glucocorticoids on nephritis, we investigated the antinephritic effect of methylprednisolone suleptanate (MPS) and its influence on adrenal function by intermittent administration (IA) in comparison with daily administration (DA) in crescentic-type anti-GBM nephritic rats. In IA, MPS (0.25, 1.0 and 3.0 mg/kg) was injected for 3 successive days followed by a 3-day withdrawal during a 40-day period. MPS inhibited the elevation of urinary protein and serum cholesterol and glomerular alterations by both IA and DA. The effect of MPS on these parameters was more potent by IA than by DA. MPS significantly suppressed the increment of the number of ED-1(+) cells and TH-1(+) cells in nephritic glomeruli. DA, but not IA, caused atrophy of the adrenal glands. IA prevented the remarkable decrease in corticosterone level provoked in nephritic rats. In conclusion, for the treatment of nephritis, IA seems to be a better regimen for the administration of MPS. MPS may exert an antinephritic action by inhibiting mesangial cell proliferation and infiltration of monocytes/macrophages into glomeruli in addition inhibiting antibody production.
    The Japanese Journal of Pharmacology 03/1994; 64(2):79-88.
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    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 investigated. 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 contents were lower than those of the control rats throughout the 40-day experimental period. Histopathological 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, Ia 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 proliferation or the migration of macrophages and cytotoxic T lymphocytes in the glomeruli.
    The Japanese Journal of Pharmacology 12/1992; 60(3):187-95.
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    ABSTRACT: Z-103 at 1 to 25 mg/kg, p.o. prevented 100% ethanol-induced gastric mucosal lesions in a dose-dependent manner. Z-103 at 3 to 25 mg/kg, p.o. significantly elevated gastric mucosal superoxide dismutase (SOD)-like activity 1 hr after its administration to normal rats. In addition, Z-103 at doses (10 and 25 mg/kg, p.o.) which prevented 100% ethanol-induced gastric lesion further increased gastric mucosal SOD-like and glutathione peroxidase (GSH-px) activities elevated by 60% ethanol. Z-103 (10 and 25 mg/kg) significantly inhibited the increase in thiobarbituric acid-reactive substances in gastric mucosa injured by 60% ethanol. The combination with cycloheximide, a protein synthesis inhibitor, completely abolished the prevention of 60% ethanol-induced gastric mucosal lesions and the elevation of both free radical scavenging enzyme activities in the mucosa by Z-103 (10 mg/kg, p.o.). These results suggest that Z-103 may partly protect rat gastric mucosa against ethanol-induced damage by scavenging oxygen-derived free radicals via increases in the synthesis of SOD-like and GSH-px enzymes in the mucosa.
    The Japanese Journal of Pharmacology 08/1992; 59(3):267-74.
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    ABSTRACT: The present study was conducted to investigate the antinephritic effects of berberine and coptisine, which are contained in Coptidis rhizoma, on original-type anti-GBM nephritis in rats. Berberine and coptisine at the doses of 0.5, 1.0 and 5.0 mg/kg/day, i.p. were effective in inhibiting urinary protein excretion, elevation of serum cholesterol and creatinine contents as well as glomerular histopathological changes. In addition, berberine at 20 mg/kg/day, p.o. also inhibited urinary protein excretion throughout the experimental periods. Berberine and coptisine inhibited platelet aggregation in both in vitro and in vivo assays, and berberine inhibited the decline of renal blood flow. Although berberine inhibited an increase in thromboxane B2 formation, it increased the formation of 6-keto-prostaglandin F1 alpha in platelets and isolated glomeruli. These results indicate that the antinephritic effects of berberine and coptisine may be partly due to antiplatelet action and improved renal hemodynamics via changing prostanoid synthesis.
    The Japanese Journal of Pharmacology 07/1992; 59(2):159-69.
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    ABSTRACT: Effects of pherodendrin (OB-5) on anti-GBM nephritis were investigated. OB-5 (50 mg/kg/day, i.p.) prevented the urinary protein excretion in original and crescentic-type anti-GBM nephritis in rats. In addition, OB-5 also inhibited the elevation of serum creatinine, urea nitrogen and cholesterol contents in both models of nephritis. Histopathological observations indicated that OB-5 prevented the hypercellularity, crescent formation, adhesion and fibrinoid necrosis in the glomeruli of nephritic rats. OB-5 and cyclosporine A, a positive control drug, prevented the increase in the number of OX-1, CD8 and ED-1 positive cells in the glomeruli. These results indicated that OB-5 may be effective in human glomerulonephritis, and anti-nephritic mechanisms of OB-5 may be due to its inhibition of the activation of macrophages or cytotoxic T cells.
    Folia Pharmacologica Japonica 07/1992; 99(6):391-9.