Inhibitory Effect Of Tranilast Research Articles

Crosstalk between cancer-associated fibroblasts and immune cells in peritoneal metastasis: inhibition in the migration of M2 macrophages and mast cells by Tranilast

BackgroundThe role of tumor–stroma interactions in tumor immune microenvironment (TME) is attracting attention. We have previously reported that cancer-associated fibroblasts (CAFs) contribute to the progression of peritoneal metastasis (PM) in gastric cancer (GC), and M2 macrophages and mast cells also contribute to TME of PM. To elucidate the role of CAFs in TME, we established an immunocompetent mouse PM model with fibrosis, which reflects clinical features of TME. However, the involvement of CAFs in the immunosuppressive microenvironment remains unclear. In this study, we investigated the efficacy of Tranilast at modifying this immune tolerance by suppressing CAFs.MethodsThe interaction between mouse myofibroblast cell line LmcMF and mouse GC cell line YTN16 on M2 macrophage migration was investigated, and the inhibitory effect of Tranilast was examined in vitro. Using C57BL/6J mouse PM model established using YTN16 with co-inoculation of LmcMF, TME of resected PM treated with or without Tranilast was analyzed by immunohistochemistry.ResultsThe addition of YTN16 cell-conditioned medium to LmcMF cells enhanced CXCL12 expression and stimulated M2 macrophage migration, whereas Tranilast inhibited the migration ability of M2 macrophages by suppressing CXCL12 secretion from LmcMF. In PM model, Tranilast inhibited tumor growth and fibrosis, M2 macrophage, and mast cell infiltration and significantly promoted CD8 + lymphocyte infiltration into the tumor, leading to apoptosis of cancer cells by an immune response.ConclusionTranilast improved the immunosuppressive microenvironment by inhibiting CAF function in a mouse PM model. Tranilast is thus a promising candidate for the treatment of PM.

Tranilast-loaded tubular scaffold and surgical suture for suppression of stenosis after tracheal prosthesis transplantation

Most tracheal prosthesis implantation fail because of restenosis at the anastomotic site. Tranilast, which is approved as an anti-allergic drug, has been found to inhibit the proliferation of fibroblasts. In this study, use of a tracheal scaffold and surgical suture loaded with tranilast was proposed. A three-dimensionally printed tubular scaffold was designed as an artificial tracheal implant, both ends of which were fixed with surgical sutures. The formation of granulation tissue at both ends of the scaffold were compared among four animal groups that were transplanted with a drug-loaded or bare scaffold and sutured with drug-loaded or bare thread. In animal models with a tracheal defect, the inhibitory effect of tranilast on stenosis at an anastomotic site was observed to be synergistically enhanced when both the scaffold and suture were loaded with tranilast, allowing for better survival after tracheal implantation. Histologic evaluation also revealed that more M2 phenotype macrophages, which are known to be responsible for anti-inflammation and tissue regeneration, were recruited around the scaffold than pro-inflammatory M1 macrophages that otherwise would stimulate fibrosis. Therefore, these results suggest that tracheal implantation using a tubular scaffold and suture, both loaded with tranilast, is a promising strategy for suppression of tracheal stenosis.

Inhibitory effect of tranilast on the myofibroblast differentiation of rat mesenchymal stem cells induced by transforming growth factor‑β1 invitro.

Mesenchymal stem cell (MSC) transplantation is able to attenuate organ fibrosis; however, increasing evidence has indicated that MSCs may be an important cell source of myofibroblasts, which are vital pathogenic cells in fibrotic diseases. The results of the present study revealed that co‑culturing with exogenous transforming growth factor (TGF)‑β1 can induce the transdifferentiation of cultured rat MSCs into myofibroblasts invitro. Treatment of the MSCs with tranilast [N‑(3',4'‑dimethoxycinnamoyl)‑anthranilic acid] attenuated this fibrotic process. Immunocytochemical staining, western blot analysis, reverse transcription‑quantitative polymerase chain reaction analysis and cell viability assays were performed in order to evaluate the molecular mechanisms underlying the effects of tranilast on TGF‑β1‑mediated MSC‑to‑myofibroblast activation. The results demonstrated that TGF‑β1 upregulated the expression of α‑smooth muscle actin (α‑SMA) and collagen type I, and increased the phosphorylation of mothers against decapentaplegic homolog3 (Smad3) and extracellular signal‑regulated kinase1/2 (ERK1/2) in the rat MSCs; by contrast, tranilast pretreatment downregulated their expression. Furthermore, the proliferation of MSCs induced by TGF‑β1 was decreased by pretreatment with tranilast. In conclusion, the results of the present study demonstrated that tranilast treatment markedly suppressed the TGF‑β1‑induced differentiation of cultured rat MSCs into myofibroblasts, potentially by inhibiting the Smad3 and ERK1/2 signaling pathways. Therefore, this may be a potential antifibrotic therapeutic strategy, serving as an adjuvant treatment following transplantation of MSCs.

Tranilast inhibits TGF-β-induced collagen gel contraction mediated by human corneal fibroblasts.

To determine if tranilast affects human corneal fibroblast (HCFs) contraction. HCFs cultured in a three-dimensional type I collagen gel were treated with or without transforming growth factor beta (TGF-β) or tranilast. Gel diameter was measured as an indicator for collagen contraction. Immunoblot was performed to evaluate myosin light chain (MLC) and paxillin phosphorylation. Confocal microscopy was employed to examine the focal adhesions and actin stress fiber formation. Immunoblot analysis and gelatin zymography were performed to detect tissue inhibitors of metalloproteinases and matrix metalloproteinases (MMPs) in supernatant. The inhibitory effect of tranilast on HCFs-mediated collagen gel contraction induced by TGF-β was dose-dependent. The significant effect of tranilast was started from 100 µmol/L and maximized at 300 µmol/L. The peak effect of 300 µmol/L tranilast also relied on the duration of treatment, which showed statistical significance from day 2. TGF-β-induced paxillin and MLC phosphorylation, stress fiber formation, focal adhesions, and MMP-1, MMP-2, and MMP-3 secretion in HCFs were also inhibited by tranilast. Tranilast suppresses the HCFs-cultured collagen gel contraction induced by TGF-β. It attenuates actin stress fibers formation, focal adhesions, and the secretion of MMPs, with these actions likely contributing to the inhibitory effect on HCF contractility. By attenuating the contractility of corneal fibroblasts, tranilast treatment may inhibit corneal scarring.

Inhibitory Effects of Tranilast on Cytokine, Chemokine, Adhesion Molecule, and Matrix Metalloproteinase Expression in Human Corneal Fibroblasts Exposed to Poly(I:C)

ABSTRACTPurpose/Aim: Viral infection of the cornea can result in inflammation and scarring and eventually cause blindness. Polyinosinic–polycytidylic acid [poly(I:C)], an analog of viral double-stranded RNA, induces the synthesis of various cytokines, chemokines, adhesion molecules, and matrix metalloproteinases (MMPs) in corneal fibroblasts. The effects of tranilast on the expression of these molecules in human corneal fibroblasts were examined.Materials and methods: Human corneal fibroblasts were cultured with or without poly(I:C) or tranilast. The release of the proinflammatory cytokine interleukin (IL)-6 and of the chemokines IL-8 and monocyte chemotactic protein-1 (MCP-1) was measured with enzyme-linked immunosorbent assays. The expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), MMP-1, and MMP-3 was evaluated by immunoblot or immunofluorescence analysis. The phosphorylation of mitogen-activated protein kinases (MAPKs), c-Jun (a component of the transcription factor AP-1), and IκB-α (an endogenous inhibitor of the transcription factor NF-κB) was examined by immunoblot analysis.Results: Tranilast inhibited in a concentration- and time-dependent manner the production of IL-6, IL-8, MCP-1, ICAM-1, VCAM-1, MMP-1, and MMP-3 by corneal fibroblasts exposed to poly(I:C). It also inhibited the poly(I:C)-induced phosphorylation of c-Jun and the MAPK JNK without affecting that of IκB-α or the MAPKs ERK and p38.Conclusions: Tranilast inhibited proinflammatory cytokine, chemokine, adhesion molecule, and MMP expression in human corneal fibroblasts exposed to poly(I:C), with these effects likely being mediated by attenuation of JNK-AP-1 signaling. Tranilast might therefore be expected to limit immune cell infiltration and stromal degradation associated with viral infection of the cornea.

Inhibitory Effect of Tranilast on Transforming Growth Factor-Beta-Induced Protein in Granular Corneal Dystrophy Type 2 Corneal Fibroblasts.

To investigate the effects of tranilast, an inhibitor of chemical mediators and fibroblast proliferation, on the expression of transforming growth factor-beta (TGF-β)-induced protein (TGFBIp) in wild-type (WT) and homozygous (HO) granular corneal dystrophy type 2 corneal fibroblasts. Cell proliferation and cytotoxicity were measured by Cell Counting Kit-8 and lactate dehydrogenase assay. Western blotting and real-time polymerase chain reaction were used to determine changes in the expression of TGFBIp and TGFBI mRNA. We determined the effects of tranilast on phosphorylated Smad2 (pSmad2) and pSmad3, wound-healing, and expression of alpha-smooth muscle actin (α-SMA), type I collagen, and integrins. High concentrations of tranilast decreased proliferation of corneal fibroblasts but did not cause elevation of lactate dehydrogenase, except at 1.0 mM tranilast. TGF-β increased the expression of TGFBIp and TGFBI mRNA in WT and HO corneal fibroblasts. Cotreatment of corneal fibroblasts with tranilast and TGF-β reduced the levels of TGFBIp and TGFBI mRNA. In addition, application of tranilast reduced pSmad2 in WT and HO corneal fibroblasts and pSmad3 in HO corneal fibroblasts, both of which were increased initially by TGF-β. Tranilast delayed wound healing and reduced the expression of α-SMA, type I collagen, and some of integrins in WT and HO corneal fibroblasts. Application of tranilast in WT and HO corneal fibroblasts inhibited the expression of TGFBIp by blocking TGF-β signaling. Thus, tranilast may be useful in delaying or preventing the recurrence of corneal opacity in TGFBI-linked corneal dystrophies if clinical studies confirm these findings.

The Effectiveness of Tranilast in the Prevention of Posterior Capsular Opacity

Purpose: To evaluate the inhibitory effect of tranilast on the formation of posterior capsular opacity (PCO) after a cataract operation ex vivo and in a rabbit model. Methods: A human lens epithelial cell line (B3) was treated with 0.005-0.1 mM tranilast. Cytotoxicity assessment and effective dosage determination of tranilast were performed using MTT assays. B3 cell lines were cultured in Eagle's minimal essential medium (EMEM) containing 20% FBS with different concentrationsof tranilast, and morphological differences were observed. To investigate the effect of tranilast on cytokine production in B3 cell lines, cells were treated with 0.01 mM tranilast and expression profiles of cytokines were analyzed by RT-PCR. After performing phacoemulsification and intraocular lens implantation in 10 white rabbits, 0.5% tranilast eye drops were given 4 times per day, and the severity of PCO was evaluated bi-weekly using POCOman for 8 weeks after the operation. Results: Cell death was observed in the 0.05 mM tranilast-treated B3 cell lines, and inhibition of epithelial- mesenchymal transition (EMT) was also observed in the 0.01 mM tranilast-treated B3 cell lines. TGF-β1/2, IL-18, and CDK7 mRNA expression decreased in the 0.01 mM tranilast-treated B3 cell lines. Significant suppression of PCO formation was observed in rabbits treated with 0.5% tranilast eye drops 5 weeks post operative (p

Suppressive Effects of Tranilast on Eotaxin-1 Production from Cultured Conjunctival Fibroblasts

Purpose: Eotaxin, a CC-chemokine with selective chemotactic effects for eosinophils, has been reported to play an important role in allergic conjunctival diseases. We previously reported that eotaxin is produced by conjunctival fibroblasts and keratocytes on stimulation with Th2 cytokines. Tranilast is known to have anti-allergic properties. In this study, we examined the inhibitory effect of tranilast, an anti-allergic drug, on eotaxin-1 production from cultured conjunctival fibroblasts. Methods:Conjunctival fibroblasts obtained from normal patients were cultured in DMEM/F12 medium. On the fifth passage, the cells were transferred to a 96-well plate and, after starvation for 24 hr, TNF-α, IL-4, and tranilast or dexamethasone were added. After 48 hr, the concentrations of eotaxin-1 in the supernatants were measured by ELISA, and the cells were tested for eotaxin-1 expression by real-time PCR. Results:Eotaxin-1 production was observed on simultaneous stimulation with TNF-α and IL-4. This production was inhibited by both tranilast and dexamethasone. Inhibition of eotaxin-1 expression was also observed by real-time PCR. Conclusions: Eotaxin-1 production from conjunctival fiboblasts was inhibited by both tranilast and dexamethasone. These results suggest that the anti-allergic effect of tranilast may be partly due to the inhibition of eotaxin-1 production from conjunctival fibroblasts.

The inhibitory effect of tranilast on transforming growth factor-beta(2) expression in cultured human trabecular meshwork cells

To investigate the effect of tranilast on transforming growth factor-beta(2) (TGF-beta(2)) expression in cultured human trabecular meshwork cells. TGF-beta(2) expression in cultured 3-5 passage human trabecular meshwork cells was measured by semi-quantitative RT-PCR after treated with 0.0 micro g/ml (control), 12.5, 25.0 and 50.0 mg/L tranilast for 48 h. The value of TGF-beta(2)/G3PDH of cells treated with 12.5, 25.0 and 50.0 mg/L tranilast was 1.85 +/- 0.35, 1.66 +/- 0.42, 1.16 +/- 0.24, respectively. The difference between these treated groups and that of the control group (3.82 +/- 0.56) was statistically significant (q' = 10.77, 11.80, 14.54, P < 0.01), respectively. The value of TGF-beta(2)/G3PDH in the tranilast treated trabecular meshwork cells decreased in a dose-dependent manner. Tranilast could inhibit TGF-beta(2) expression in cultured human trabecular meshwork cells. It is worth to study the using of tranilast in the treatment of primary open-angle glaucoma.

Anti-allergic Drugs Inhibit the Proliferation of Bovine Lens Epithelial Cells in Culture

To examine the inhibitory effects of tranilast, ketotifen fumarate, and disodium cromoglycate which are used clinically as anti-allergic agents, on the growth of bovine lens epithelial cells (LE) in culture. LE was grown in Dulbecco's modified Eagle's medium(DMEM) with 10% fetal calf serum and growth was measured with 3-[4,5-dimethylthiazole-2-yl]-2,5-diphenyltetrazolium bromide(MTT) and 5-bromo-2'deoxy-uridine(BrdU). Production of collagen, transforming growth factor-beta 1(TGF-beta 1), and basic-fibroblast growth factor(b-FGF) were measured with corresponding enzyme-linked immunosorbent assay(ELISA). Apoptotic cell death was detected by TdT-mediated dUTP-biotin nick end labelling method(TUNEL technique) and the DNA ladder method. Both ketotifen and tranilast inhibited the growth of LE, and half-inhibitory concentrations were 200 microM and 1,000 microM, respectively. Disodium cromoglycate did not inhibit LE proliferation significantly. Ketotifen and tranilast decreased the synthesis of collagen but had no obvious effect on TGF-beta 1 and b-FGF production. Apoptotic cell death was detected in LE treated with ketotifen or tranilast. Ketotifen and tranilast may be clinically useful for the prevention of aftercataract. Apoptotic cell death may be involved in the process.

Inhibitory effects of tranilast on the proliferation and functions of human pterygium-derived fibroblasts.

We studied the possibility that tranilast, an antiallergic and antiproliferative drug, may be beneficial for the treatment of pterygium. Pterygium-derived cells were identified by immunohistochemical methods. Growth rate of pterygium-derived cells was determined by using a hemocytometer. Chemotaxis was determined in a microchemotaxis chamber. Pterygium-derived cells were cultured on floating collagen gel, and the contracted diameter was measured. Collagen synthesis by pterygium-derived cells was determined by the collagenase digestive method. Tranilast was added to the culture medium at final concentrations of 0, 12.5, 25, 50, and 100 microg/ml. Pterygium-derived cells were stained with anti-prolylhydroxylase and anti-alpha-smooth muscle actin, and identified as fibroblasts. Tranilast inhibited the proliferation and chemotaxis of pterygium-derived fibroblasts, and the collagen-gel contraction induced by these cells, but it exerted no inhibitory action on collagen synthesis by pterygium-derived fibroblasts. Tranilast may be useful for suppressing the recurrence and, possibly, the development of pterygium.

Inhibitory effects of tranilast on expression of transforming growth factor- β isoforms and receptors in injured arteries

Tranilast (N(3,4-dimethoxycinnamoyl)anthranilic acid), an agent which in cell culture inhibits transforming growth factor- β (TGF- β) secretion and antagonises the effects of TGF- β and platelet-derived growth factor (PDGF) on cell migration and proliferation, has been reported to reduce the incidence of restenosis after angioplasty in angiographically validated human clinical trials. We investigated in a rat model of balloon angioplasty whether tranilast's effects in vivo could be attributed to inhibition of expression of TGF- β and/or its receptor types. Using a standardised reverse transcriptase-polymerase chain reaction (RT-PCR) assay, we examined the effects of three doses of tranilast (25, 50 and 100 mg/kg) on the expression of two TGF- β isoforms, the types I and II TGF- β receptors and two putative TGF- β responses, induction of integrins α v and β 3 mRNA, 2 h after oral administration and 26 h after vessel injury. Tranilast attenuated in a dose-dependent and reversible manner the injury-induced increases in mRNA levels encoding TGF- β 1, TGF- β 3, two type I TGF- β receptors ALK-5 and ALK-2, and the type II receptor T βRII. At the highest dose mRNA levels encoding TGF- β 1 and T βRII were attenuated to levels approaching or below those observed in uninjured vessels. Messenger RNAs encoding TGF- β 3, ALK-5 and ALK-2 were all attenuated by between 70 and 74% (all P<0.05). Tranilast also attenuated in a reversible manner the elevations in mRNA levels for integrins α v and β 3 observed after vessel injury, by 90 and 72%, respectively. We also investigated, in cultured smooth muscle cells derived from injured carotid arteries, the extent to which tranilast (300 mg/l) attenuated any increases in expression of type I and type II receptors stimulated by PDGF-BB and TGF- β 1, growth factors implicated in smooth muscle cell migration and proliferation in injured vessels. Increases in mRNA levels of the type I receptors ALK-5 and ALK-2 induced by PDGF-BB and TGF- β 1 were almost completely prevented by tranilast. Tranilast also prevented the PDGF-BB induced increases in T βRII but only partially inhibited the TGF- β 1 induced upregulation of T βRII. We conclude that tranilast can inhibit transcriptional mechanisms associated with the upregulation of TGF- β and its receptor types in balloon catheter injured vessels. It is possible that these mechanisms contribute to its ability to reduce the frequency of restenosis after angioplasty.

Inhibitory Effect of Tranilast on Hypertrophic Collagen Production in the Spontaneously Hypertensive Rat Heart

Tranilast, N-(3,4-dimethoxycinnamoyl) anthranilic acid, a widely used antiallergy drug in Japan, has been shown to inhibit transforming growth factor-β1 release from fibroblasts and reduce collagen synthesis in keloid cells. In the present study, we have investigated the effect of this drug on cardiac hypertrophy in spontaneously hypertensive rats (SHR), with a focus on the cardiac collagen matrix, which is associated with myocardial stiffness. Twenty-four-week-old SHRs and Wistar Kyoto rats (WKYs) were administered tranilast (300 mg/kg) orally once a day for 4 weeks. This treatment significantly suppressed increases in left ventricular collagen concentration (P<0.05) and the left ventricular weight / body weights ratios (P<0.05) in SHRs, and tranilast was ineffective on collagen concentration and ventricular weight / body weights ratios in WKYs. Tranilast did not affect systolic or diastolic blood pressure, end-diastolic left ventricular pressure and heart rate in both SHRs and WKYs, and the agent did not change positive dp/dt or cardiac output in SHRs. The pressure-volume relationship curve was shifted to the left by the drug; the slope (k) of the logarithm of the pressure-volume relationship curve was significantly increased (P<0.05) in SHRs. It is concluded that the suppression of increases in cardiac collagen and left ventricular mass by tranilast results in a corresponding prevention of cardiac stiffness as studied in the SHR.

Inhibition of proliferation of MCF-7 breast cancer cells by a blocker of Ca 2+-permeable channel

In MCF-7 breast cancer cells, insulin-like growth factor-1 (IGF-1) increased the calcium-permeability of the cells by activating a voltage-independent calcium-permeable channel. IGF-1 also induced oscillatory elevation of cytoplasmic free calcium concentration in these cells. An anti-allergic compound, tranilast, reduced the calcium-permeability augmented by IGF-1 in a dose-dependent manner and blocked the oscillatory elevation of cytoplasmic free calcium concentration. Tranilast did not affect early intracellular signals activated by IGF-1, including receptor autophosphorylation, activations of Ras, mitogen-activated protein kinase and phosphatidylinositol 3-kinase. Tranilast inhibited increases in [ 3H]-thymidine incorporation, DNA content and cell number induced by IGF-1. The ID 50 for [ 3H]-thymidine incorporation and DNA content were about 10 μM. The inhibitory effect of tranilast was reversible, and cell viability was not affected. Treatment with tranilast increased the number of cells in the G 1 phase suggesting that this compound induced G 1 arrest. Tranilast also reduced the phosphorylation of the retinoblastoma protein. These results indicate that tranilast inhibits the IGF-1-induced cell growth in MCF-7 cells by blocking calcium entry.

Inhibitory Effect of Tranilast on Activation and Transforming Growth Factor β1 Expression in Cultured Rat Stellate Cells

Stellate cells, the primary extracellular matrix-producing cells in the liver, undergo activation characterized by fibrogenesis, proliferation and smooth muscle α-actin expression, in hepatic fibrosis or when cultured on plastic. TGFβ1 is known to have a pivotal role in fibrogenesis. Tranilast, a drug used for allergic diseases with anti-inflammatory effects, is known to inhibit collagen synthesis by cultured fibroblasts. Thus, effects of tranilast on activation and TGFβ1 expression in stellate cells was investigatedin vitro.Tranilast reduced collagen synthesis in a dose-related manner up to 50.8% of the control. This effect was reversible after tranilast withdrawal. The mobility of procollagen on gel electrophoresis and the ratio of intracellular procollagen to extracellular collagen concentrations were not affected by tranilast. Tranilast decreased DNA synthesis and increased smooth muscle α-actin expression. mRNA expressions of procollagen and TGFβ1 were reduced by tranilast. Tranilast with anti-fibrogenic and anti-inflammatory actions merits consideration as a candidate for therapeutic agent of hepatic fibrosis.

Inhibitory effects of tranilast on proliferation, migration, and collagen synthesis of human vascular smooth muscle cells

The aim of this study was to examine the effects of tranilast (anti-allergic drug) on proliferation, migration, and collagen synthesis in cultures of human vascular smooth muscle cells. Tranilast at 100 and 300 microM had several inhibitory effects. One is the effect on vascular smooth muscle cell proliferation induced by fetal bovine serum and platelet-derived growth factor (PDGF)-BB. Second is the effect on PDGF-BB-induced migration. Third is the effect on c-myc expression after PDGF-BB stimulation. Lastly, tranilast reduced the spontaneous collagen synthesis without reducing total protein synthesis. These results suggest that tranilast may prevent restenosis after percutaneous transluminal coronary angioplasty via the inhibitory effects on proliferation, migration, c-myc gene expression, and collagen synthesis of vascular smooth muscle cells.

Inhibitory effects of tranilast on proliferation, migration, and collagen synthesis of human vascular smooth muscle cells

Inhibitory effects of tranilast on proliferation, migration, and collagen synthesis of human vascular smooth muscle cells

Inhibition of PDGF- and TGF-β1-induced collagen synthesis, migration and proliferation by tranilast in vascular smooth muscle cells from spontaneously hypertensive rats

Vascular smooth muscle cells (VSMC) from spontaneously hypertensive rats (SHR) proliferate faster and are more sensitive to transforming growth factor-/gb1 (TGF-/gb1) than those of normotensive Wistar-Kyoto rats. We studied the in vitro effects of tranilast, an anti-allergic drug, on the proliferation, migration and extracellular matrix synthesis in the SHR-VSMC. There were many inhibitory effects of tranilast (30–300 μM) on SHR-VSMC. One is the effect on the proliferation stimulated with fetal bovine serum (FBS), TGF-β1 and platelet-derived growth factor-BB (PDGF-BB). Another is the effect on the PDGF-BB-induced migration. Lastly, tranilast exhibited inhibitory effects on spontaneous collagen synthesis and TGF-β1-induced collagen and glycosaminoglycan synthesis. On the other hand, collagen induced the VSMC migration concentration-dependently. These results suggest that tranilast may prevent restenosis after percutaneous transluminal coronary angioplasty.

P1-202 - Inhibitory effect of tranilast on hypertrophic collagen production in the spontaneous hypertensive rat heart

P1-202 - Inhibitory effect of tranilast on hypertrophic collagen production in the spontaneous hypertensive rat heart

O-329 - Inhibitory effect of tranilast on femoral artery intima thickening in spontaneously hypertensive rats.

O-329 - Inhibitory effect of tranilast on femoral artery intima thickening in spontaneously hypertensive rats.