scholarly journals Ethanol Extract of Detam 1 Soybean Seed (Glycine Max L. Merr) for Chronic Kidney Disease Therapy by In Vitro Study

2019 ◽  
Vol 24 (3) ◽  
pp. 160
Author(s):  
Sijani Prahastuti ◽  
Meilinah Hidayat ◽  
Stella Tinia Hasiana ◽  
Wahyu Widowati ◽  
Annisa Amalia ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Transforming Growth Factor ◽  
Mesangial Cells ◽  
Soybean Seed ◽  
In Vitro Study ◽  
Ethanol Extract ◽  
Vitro Study ◽  
Tgf Β1

Chronic Kidney Disease (CKD) has increased incidence and prevalence in developing nations. In this in vitro study, we evaluated the cells proliferative effects, fibronectin (FN), transforming growth factor β (TGF-β1), and Reactive oxygen species (ROS) - level inhibition potential of ethanol extract of detam 1 soybean seed (EEDS) on glucose-induced kidney mesangial cells (SV40 MES 13). The cells proliferation assay used 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)2H-tetrazolium (MTS) assay. FN and TGF-β1 level were measured using ELISA assay kit and ROS level using flow cytometry. Level of   FN, TGF-β1 and ROS, on CKD cells model (5 mM, 10 mM glucose-induced mesangial cell) treated with EEDS 6.25 µg/mL were lower significantly compared to positive control,  EEDS improve cells viability and decrease FN, TGF-β1 and ROS level in glucose-induced kidney mesangial cells as CKD cells model.

scholarly journals Telocinobufagin, a Novel Cardiotonic Steroid, Promotes Renal Fibrosis via Na+/K+-ATPase Profibrotic Signaling Pathways

2018 ◽  
Vol 19 (9) ◽  
pp. 2566 ◽  
Author(s):  
David Kennedy ◽  
Fatimah Khalaf ◽  
Brendan Sheehy ◽  
Malory Weber ◽  
Brendan Agatisa-Boyle ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Growth Factor ◽  
Kidney Disease ◽  
Renal Dysfunction ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Mesangial Cells ◽  
Src Kinase ◽  
Tissue Growth

Cardiotonic steroids (CTS) are Na+/K+-ATPase (NKA) ligands that are elevated in volume-expanded states and associated with cardiac and renal dysfunction in both clinical and experimental settings. We test the hypothesis that the CTS telocinobufagin (TCB) promotes renal dysfunction in a process involving signaling through the NKA α-1 in the following studies. First, we infuse TCB (4 weeks at 0.1 µg/g/day) or a vehicle into mice expressing wild-type (WT) NKA α-1, as well as mice with a genetic reduction (~40%) of NKA α-1 (NKA α-1+/−). Continuous TCB infusion results in increased proteinuria and cystatin C in WT mice which are significantly attenuated in NKA α-1+/− mice (all p < 0.05), despite similar increases in blood pressure. In a series of in vitro experiments, 24-h treatment of HK2 renal proximal tubular cells with TCB results in significant dose-dependent increases in both Collagens 1 and 3 mRNA (2-fold increases at 10 nM, 5-fold increases at 100 nM, p < 0.05). Similar effects are seen in primary human renal mesangial cells. TCB treatment (100 nM) of SYF fibroblasts reconstituted with cSrc results in a 1.5-fold increase in Collagens 1 and 3 mRNA (p < 0.05), as well as increases in both Transforming Growth factor beta (TGFb, 1.5 fold, p < 0.05) and Connective Tissue Growth Factor (CTGF, 2 fold, p < 0.05), while these effects are absent in SYF cells without Src kinase. In a patient study of subjects with chronic kidney disease, TCB is elevated compared to healthy volunteers. These studies suggest that the pro-fibrotic effects of TCB in the kidney are mediated though the NKA-Src kinase signaling pathway and may have relevance to volume-overloaded conditions, such as chronic kidney disease where TCB is elevated.

scholarly journals Periadventitial Delivery of Simvastatin‐Loaded Microparticles Attenuate Venous Neointimal Hyperplasia Associated With Arteriovenous Fistula

2020 ◽  
Vol 9 (24) ◽  
Author(s):  
Chenglei Zhao ◽  
Sean T. Zuckerman ◽  
Chuanqi Cai ◽  
Sreenivasulu Kilari ◽  
Avishek Singh ◽  
...  
Keyword(s):  
Gene Expression ◽  
Chronic Kidney Disease ◽  
Growth Factor ◽  
Kidney Disease ◽  
Arteriovenous Fistula ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Neointimal Hyperplasia ◽  
Systemic Delivery ◽  
Tgf Β1

Background Venous neointimal hyperplasia and venous stenosis (VS) formation can result in a decrease in arteriovenous fistula (AVF) patency in patients with end‐stage renal disease. There are limited therapies that prevent VNH/VS. Systemic delivery of simvastatin has been shown to reduce VNH/VS but local delivery may help decrease the side effects associated with statin use. We determined if microparticles (MP) composed of cyclodextrins loaded with simvastatin (MP‐SV) could reduce VS/VNH using a murine arteriovenous fistula model with chronic kidney disease. Methods and Results Male C57BL/6J mice underwent nephrectomy to induce chronic kidney disease. Four weeks later, an arteriovenous fistula was placed and animals were randomized to 3 groups: 20 μL of PBS or 20 μL of PBS with 16.6 mg/mL of either MP or MP‐SV. Animals were euthanized 3 days later and the outflow veins were harvested for quantitative reverse transcriptase–polymerase chain reaction analysis and 28 days later for immunohistochemistical staining with morphometric analysis. Doppler ultrasound was performed weekly. Gene expression of vascular endothelial growth factor‐A ( Vegf‐A ), matrix metalloproteinase‐9 ( Mmp‐9 ), transforming growth factor beta 1 ( Tgf‐β1 ), and monocyte chemoattractant protein‐1 ( Mcp‐1 ) were significantly decreased in MP‐SV treated vessels compared with controls. There was a significant decrease in the neointimal area, cell proliferation, inflammation, and fibrosis, with an increase in apoptosis and peak velocity in MP‐SV treated outflow veins. MP‐SV treated fibroblasts when exposed to hypoxic injury had decreased gene expression of Vegf‐A and Mmp‐9 . Conclusions In experimental arteriovenous fistulas, periadventitial delivery of MP‐SV decreased gene expression of Vegf‐A , Mmp‐9 , Tgf‐β1 and Mcp‐1, VNH/VS, inflammation, and fibrosis.

scholarly journals THE EFFECT OF CURCUMA XANTHORRHIZA ETHANOL EXTRACT ON THE VIABILITY OF STREPTOCOCCUS MUTANS AND AGGREGATIBACTER ACTINOMYCETEMCOMITANS (DENTAL BIOFILM RESEARCH: IN VITRO STUDY)

2017 ◽  
Vol 10 (17) ◽  
pp. 30
Author(s):  
Royan Diana ◽  
Hedijanti Joenoes ◽  
Ariadna A Djais
Keyword(s):  
Streptococcus Mutans ◽  
In Vitro Study ◽  
Ethanol Extract ◽  
Single Species ◽  
Aggregatibacter Actinomycetemcomitans ◽  
Vitro Study ◽  
Dental Biofilm ◽  
Significant Difference ◽  
Curcuma Xanthorrhiza

Objective: This study aimed to compare the effect of Curcuma xanthrorrhiza ethanol extract to the viability of Streptococcus mutans and Aggregatibacter  actinomycetemcomitans using single- and dual-species biofilm at different phases of formation.Methods: Biofilm models were incubated for 4, 12, and 24 hrs, then exposed to the extract at a concentration of 0.525%.Results: The viability of the single-species S. mutans biofilm was low (p<0.05), and no significant difference (p>0.05) was found between singlespeciesA. actinomycetemcomitans and dual-species biofilm.Conclusions: Curcuma xanthorrhiza ethanol extract is more effective for decreasing the viability of single-species S. mutans biofilm.

In vitro study of nano-HA/PLLA composite scaffold for rabbit BMSC differentiation under TGF-β1 induction

2013 ◽  
Vol 50 (3) ◽  
pp. 214-220 ◽  
Author(s):  
Weimin Zhu ◽  
Kang Chen ◽  
Wei Lu ◽  
Qifeng Sun ◽  
Liangquan Peng ◽  
...  
Keyword(s):  
Composite Scaffold ◽  
In Vitro Study ◽  
Vitro Study ◽  
Tgf Β1

scholarly journals Secreted Frizzled-Related Protein 5 Ameliorates Vascular Calcification in a Rat Model of Chronic Kidney Disease through the Wnt/β-Catenin Pathway

2021 ◽  
pp. 1-10
Author(s):  
Dai Deng ◽  
Xue Han ◽  
Zongli Diao ◽  
Wenhu Liu
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vascular Calcification ◽  
Rat Model ◽  
In Vitro Study ◽  
Calcium Content ◽  
Control Group ◽  
Related Protein ◽  
High Phosphate

<b><i>Introduction:</i></b> Vascular calcification (VC) is highly prevalent and a major cardiovascular risk factor in chronic kidney disease (CKD) patients. Secreted frizzled-related protein 5 (SFRP5), an inhibitor of the Wnt pathway, is an adipokine with a positive effect on metabolic and cardiovascular diseases. Our previous in vitro study showed that SFRP5 attenuates high phosphate-induced calcification in vascular smooth muscle cells by inhibiting the Wnt/β-catenin pathway. Therefore, we hypothesized that SFRP5 may protect against CKD-associated VC (CKD-VC) through the same signalling. <b><i>Methods:</i></b> The rat model of CKD with VC was induced by 0.75% adenine combined with 1.8% high phosphate diet, which were administered with adenovirus vectors of SFRP5. We evaluated the SFRP5 effect on VC by von Kossa staining and calcium content analysis and osteogenic markers by immunohistochemistry and Western blot. The components of Wnt/ß-catenin signalling were also evaluated. <b><i>Results:</i></b> SFRP5 local and serum levels were significantly decreased in the CKD-VC rat model compared with the control group. Adenovirus-mediated overexpression of SFRP5 significantly inhibited VC, which was due to suppression of CKD-induced expression of calcification and osteoblastic markers. Additionally, SFRP5 abrogated activation of the Wnt/β-catenin pathway that plays a major role in the pathogenesis of VC. The specificity of SFRP5 for inhibition of VC was confirmed using an empty adenovirus as a control. <b><i>Conclusion:</i></b> Our results suggest that SFRP5 ameliorates VC of CKD rats by inhibiting the expression of calcification and osteoblastic markers as well as the Wnt/β-catenin pathway. Collectively, this study suggests that SFRP5 is a potential therapeutic target in CKD-VC.

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