Fuzheng Huayu recipe and vitamin E reverse renal interstitial fibrosis through counteracting TGF-β1-induced epithelial-to-mesenchymal transition

Wang, Qinglan; Yuan, Jianmin; Yue, Tao; Zhang, Yue; Liu, Ping; Liu, Chenghai

doi:10.1016/j.jep.2009.12.011

Cited by 37 publications

(32 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…HgCl 2 per os in Sprague-Dawley rats once a day for 9 weeks led to renal interstitial fibrosis with an increased amount of collagen. The effect of HgCl 2 is characterized by the activation of renal fibroblasts, the overproduction and deposition of ECM, increased renal lipid peroxidation (49), elevated NFĸB activity (50), renal necrosis and tubular dysfunction in rats (51).…”

Section: Mercuric Chloride (Hgcl 2 )mentioning

confidence: 99%

“…This action is probably potentiated, at least in part, by reducing SMAD2/3 phosphorylation (49). Indeed, it appears that in rats, vitamin E has a protective effect on HgCl 2 -induced renal interstitial fibrosis (49,50). However, it is worth noting that a meta-analysis of 136,000 subjects in 19 clinical trials indicated that a high dosage (400 IU/day) of vitamin E supplements increased all-cause mortality in humans, limiting the efficacy of this treatment in humans (96).…”

Section: Effective Treatments and New Perspectives Of Researchmentioning

confidence: 99%

See 1 more Smart Citation

Pathophysiological Mechanisms of Renal Fibrosis: A Review of Animal Models and Therapeutic Strategies

2017

View full text Add to dashboard Cite

Abstract. Chronic kidney disease (CKD) is a long-term condition in which theChronic kidney disease (CKD) represents a serious hazard to human health, and has a high prevalence. In developed countries, it is estimated that more than 10% of adults present some degree of CKD (1). Despite a varied initial evolution, which is related to the diversity of its aetiologies -namely genetics, autoimmune-related infections, environmental factors, diet, and drugs -progressive renal disease frequently results in renal fibrosis and finally in renal failure. The mechanisms implicated in renal fibrosis are still poorly understood, and existing therapies are ineffective or only slightly successful, hence it is essential to understand the pathophysiological mechanisms underlying the usual development of CKD, and to discover and better understand new strategies for treating this disease. In order to study the biopathology of this disease and to evaluate new treatments, animal models are required. The perfect animal model for renal disease research should have human-like renal anatomy, haemodynamics and physiology, as well as enabling the determination of relevant renal, biochemical and haemodynamic parameters. In all probability, no species can consistently meet all these requirements, and the experimental plan and other constraints often determine the choice of animal models for particular research applications. With this in mind, this review aims to describe and analyze animal models of renal fibrosis and suggest new areas of research. Renal Fibrosis: Aetiology and PathophysiologyDiabetes and hypertension are currently the two principal causes of CKD (2), among other causes such as infectious glomerulonephritis, renal vasculitis, ureteral obstruction, genetic alterations, autoimmune diseases (1) and drugs (3, 4). In general, diabetes causes glomerular hypertension by reducing the afferent arteriolar resistance while stimulating the efferent arterioles (2). Thus, elevated glomerular capillary pressure is one of the major factors in progressive renal sclerosis (5). Diabetes and hypertension gradually lead to glomerular expansion, which causes endothelial dysfunction and haemodynamic changes: loss of the glomerular basement membrane electric charge and its thickening, a decreased number of podocytes, foot-process effacement and mesangial distension have been shown to 1

show abstract

Section: Mercuric Chloride (Hgcl 2 )mentioning

confidence: 99%

Section: Effective Treatments and New Perspectives Of Researchmentioning

confidence: 99%

Pathophysiological Mechanisms of Renal Fibrosis: A Review of Animal Models and Therapeutic Strategies

2017

View full text Add to dashboard Cite

show abstract

“…Vitamin E is also a powerful antioxidant that maintains the permeability of fluidity of biological membranes and prevents them from demolition (19). Vitamin E may increase the expression of E-cadherin in kidney tissue and renal tubular basal membrane degradation can be improved (20). Factors such as carboxyethyl hydroxychromans (CEHC) are water-soluble metabolites of vitamin E that have anti-inflammatory and antioxidant properties.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Vitamin E on Formaldehyde-Induced Injuries in the Rat Kidney

et al. 2014

View full text Add to dashboard Cite

Background: Formaldehyde (F) is a chemical component that has an extensive usage on fixation of tissues and produces different types of reactive oxygen species (ROS) in our body. Studies have shown that long exposure to F damages the eyes, nose and throat; in addition it has adverse effects on body organs such as the urinary system. Vitamins can reduce free ROS. Objectives: The aim of this study was evaluating the protective effect of vitamin E on the kidney damaged by formaldehyde. Materials and Methods: Male adult wistar rats were divided into three groups. Group A (control): rats received vehicle (normal saline) for two weeks. Group E1 (formaldehyde): rats received formaldehyde (10 mg/kg) for two weeks. Group E2 (formaldehyde + vitamin E): rats received formaldehyde (10 mg/kg) and vitamin E (30 mg/kg) for two weeks. After two weeks, all rats were killed, and the kidneys were dissected and processed for routine histological staining. Results: Comparison of the control and formaldehyde groups with the vitamin E group revealed that there were significant differences in lumen size and nuclear color of proximal tubules in rats treated by vitamin E (P < 0.05). Cell degeneration, lumen size, number and size of nucleus of distal tubules were statistically different among the three groups. In the vitamin E treated group observed histological changes were improved compared to the formaldehyde group. Conclusions: According to the results of this study, vitamin E probably improves the harmful effects of formaldehyde on rat kidney tissue.

show abstract

“…Contents lists available at SciVerse ScienceDirect journal homepage: www.elsevier.com/locate/jep Pharmacological studies and clinical trials have demonstrated that FZHY is an effective antagonist of liver fibrosis and that many of the effects are attributable to the pharmacological actions of the herbs chemicals (Wang et al, 2010). Mechanistic studies have shown that FZHY decreases a-SMA protein expression in fibrotic livers, as examined by Western blot and immunohistochemical stain, and also attenuates ECM deposition in the liver ).…”

Section: Introductionmentioning

confidence: 99%

Fuzheng Huayu inhibits carbon tetrachloride-induced liver fibrosis in mice through activating hepatic NK cells

Cheng

Chen

et al. 2013

Journal of Ethnopharmacology

View full text Add to dashboard Cite

Fuzheng Huayu recipe and vitamin E reverse renal interstitial fibrosis through counteracting TGF-β1-induced epithelial-to-mesenchymal transition

Cited by 37 publications

References 28 publications

Pathophysiological Mechanisms of Renal Fibrosis: A Review of Animal Models and Therapeutic Strategies

Pathophysiological Mechanisms of Renal Fibrosis: A Review of Animal Models and Therapeutic Strategies

Protective Effect of Vitamin E on Formaldehyde-Induced Injuries in the Rat Kidney

Fuzheng Huayu inhibits carbon tetrachloride-induced liver fibrosis in mice through activating hepatic NK cells

Contact Info

Product

Resources

About