tranilast has been researched along with Nephritis--Interstitial* in 2 studies
2 other study(ies) available for tranilast and Nephritis--Interstitial
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Tranilast attenuates the up-regulation of thioredoxin-interacting protein and oxidative stress in an experimental model of diabetic nephropathy.
Diabetic nephropathy is the leading cause of kidney failure in the developed world. Tranilast has been reported to not only act as an anti-inflammatory and anti-fibrotic compound, but it also exerts anti-oxidative stress effects in diabetic nephropathy. Thioredoxin-interacting protein (Txnip) is the endogenous inhibitor of the anti-oxidant thioredoxin and is highly up-regulated in diabetic nephropathy, leading to oxidative stress and fibrosis. In this study, we aimed to investigate whether tranilast exerts its anti-oxidant properties through the inhibition of Txnip.. Heterozygous Ren-2 rats were rendered diabetic with streptozotocin. Another group of rats were injected with citrate buffer alone and treated as non-diabetic controls. After 6 weeks of diabetes, diabetic rats were divided into two groups: one group gavaged with tranilast at 200 mg/kg/day and another group with vehicle.. Diabetic rats had a significant increase in albuminuria, tubulointerstitial fibrosis, peritubular collagen IV accumulation, reactive oxygen species (ROS) and macrophage infiltration (all P < 0.05). These changes were associated with an increase in Txnip mRNA and protein expression in the tubules and glomeruli of diabetic kidney. Treatment with tranilast for 4 weeks significantly attenuated Txnip up-regulation in diabetic rats and this was associated with a reduction in ROS, fibrosis and macrophage infiltration (all P < 0.05).. This is the first study to demonstrate that tranilast not only has anti-inflammatory and anti-fibrotic effects as previously reported but also attenuates the up-regulation of Txnip and oxidative stress in diabetic nephropathy. Topics: Albuminuria; Animals; Anti-Inflammatory Agents, Non-Steroidal; Antioxidants; Carrier Proteins; Cell Cycle Proteins; Collagen Type IV; Diabetes Mellitus, Type 1; Diabetic Nephropathies; Disease Models, Animal; Female; Fibrosis; Immunoenzyme Techniques; In Situ Hybridization; Luminescence; Macrophages; Nephritis, Interstitial; ortho-Aminobenzoates; Oxidative Stress; Rats; Reactive Oxygen Species; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Up-Regulation | 2011 |
Mast cell, a promising therapeutic target in tubulointerstitial fibrosis.
Tubulointerstitial fibrosis is a final common pathway to the eventual structural desolation of kidneys. However, the mechanism involved in this phenomenon is still poorly understood, and current therapies are ineffective or only marginally effective. Mast cell has a variety of physiological and pathological functions through the production of heparin, histamine, neutrophil chemoattractants, immunoregulatory cytokines, and mast cell-specific serine proteases tryptase and chymase. The survival and proliferation of mast cell are dependent upon stem cell factor. Presently, mast cells are known to participate in the pathogenesis of tubulointerstitial fibrosis in many kidney diseases. Several therapeutic approaches to inhibit mast cell activation have already demonstrated some clinical utility in tissue fibrosis or inflammatory diseases such as the use of mast cell stabilizers, inhibitors of tryptase or chymase, blockade of stem cell factor and anti-IgE therapy. We hypothesize that mast cell has a significant role in the progression of tubulointerstitial fibrosis, thus the treatment strategies based on mast cell appear to be promising in these conditions. Development of these novel therapeutic approaches will enable us to target any types of renal disease. Topics: Anti-Inflammatory Agents; Anti-Inflammatory Agents, Non-Steroidal; Drug Delivery Systems; Fibrosis; Humans; Mast Cells; Nephritis, Interstitial; ortho-Aminobenzoates | 2007 |