scholarly journals Intervention Effect of Compatibility of Salvianolic Acid A & B on PDGF-C/PDGFR-α Signaling Pathway in Renal Fibrosis

2015 ◽  
Vol 4 (2) ◽  
pp. 13
Author(s):  
Bin Yu
Keyword(s):  
Signaling Pathway ◽  
Renal Fibrosis ◽  
Kidney Tissue ◽  
Renal Tissue ◽  
Salvianolic Acid B ◽  
Control Group ◽  
Salvianolic Acid ◽  
Salvianolic Acid A ◽  
Drug Compatibility ◽  
Renal Tubular

<strong>Objective</strong>: To explore the effect of salvianolic acid A &amp; B component molecules of drug compatibility on PDGF-c/PDGFR-α signaling pathway in renal fibrosis of rats. <strong>Methods</strong>: 40 male SPF SD rats were randomly divided into four groups: control group, salvianolic acid A group, salvianolic acid B group and salvianolic acid A + B group, with 10 rats in each group. Each group was treated for two weeks. After the intervention, samples were collected. And scores of HE and Masson was compared. The expression of PDGF-c/PDGFR-α in rental tissue in them was also tested and compared.<strong> Results</strong>: Compared with the control group, the score of HE and Masson in intervention groups was markedly decreased, and scores in salvianolic acid B group and salvianolic acid A + B group were reduced significantly (<em>p </em>&lt; 0.05); Compared with the control group, the expression of PDGF-c/PDGFR-α in rental tissue in intervention groups was lower(<em>p </em>&lt; 0.05), especially in salvianolic acid B group and salvianolic acid A + B group (<em>p </em>&lt; 0.05).<strong>Conclusion</strong>: salvianolic acid A &amp; B component molecules of drug compatibility could significantly improve the pathological changes in the kidney tissue of rats, suppress the expression of PDGF-c/PDGFR-α in renal tissue, and improve the renal function, renal tubular function and renal pathology.

scholarly journals Effect of tripterine on Notch signaling pathway in IgA nephropathy rats

2018 ◽  
Vol 2 (6) ◽  
Author(s):  
Dan Liu
Keyword(s):  
Notch Signaling ◽  
Iga Nephropathy ◽  
Signaling Pathway ◽  
Intervention Group ◽  
Kidney Tissue ◽  
Renal Tissue ◽  
Notch Signaling Pathway ◽  
Male Rats ◽  
Control Group ◽  
Model Group

Abstract: Objective: To investigate the effect of tripterine on Notch signaling pathway in renal tissue of IgA nephropathy rats. Methods: SD male rats were divided into the control group, IgAN nephropathy model group, benazepril group, 1mg/kg/d tripterine intervention group and 10mg/kg/d tripterine intervention group according to the random number table method, with 10 rats in each group. The urinary sediment and 24-hour urinary protein quantity were detected by conventional methods. The expressions of Notch1, Jagged1, Hes1 and Hey1 in renal tissue of rats were detected by real-time fluorescent quantitative PCR. Results: IgA nephropathy model was successfully established. The hematuria and proteinuria in model group were higher than those of control group (P<0.05). The expressions of Notch1, Jagged1, Hes1 and hey1 in kidney tissue of IgA nephropathy rats were significantly increased (P<0.05). Compared with the model group, hematuria and proteinuria in tripterine intervention group were alleviated. The expressions of Notch1, Jagged1, Hes1 and Hey1 in rat renal tissue were decreased (P<0.05). Moreover, the expressions of Notch1, Jagged1, Hes1 and Hey1 in renal tissue of rats in 10mg/kg/d tripterine intervention group were decreased (P<0.05). Conclusion: Tripterine can decrease the levels of hematuria and proteinuria in IgA nephropathy rats. The expression of Notch signaling pathway in IgA nephropathy rats is increased by the down-regulation of tripterine, suggesting that tripterine has a certain therapeutic effect on IgA nephropathy rat. And its role may be realized through this signal pathway so as to provide the new mentality for the diagnosis and treatment of IgA nephropathy.

The Effect of High Salt Diet in Renal Fibrosis Through CHOP Protein Stimulated Apoptosis in Rat Model

2021 ◽  
Author(s):  
Darya Ghadimi ◽  
Tooka Khadive ◽  
Mina Hemmati ◽  
Hannaneh Golshahi ◽  
Meysam Ehtesham
Keyword(s):  
Renal Fibrosis ◽  
Salt Intake ◽  
Mrna Level ◽  
Renal Tissue ◽  
High Salt ◽  
Control Group ◽  
High Salt Diet ◽  
Salt Diet ◽  
Male Wistar Rats ◽  
Renal Tubular

Abstract І. Background: Prolonged excessive salt intake is an important risk factor for development of renal fibrosis. In the onset of renal tubular destruction, KIM-1 appears in urine. CHOP is an important apoptosis stimulator protein. The aim of present study was to investigate the effect of high salt diet in development of renal fibrosis through apoptosis.ІІ. Methods and results: The 25 male Wistar rats were divided randomly into five groups and treated with 0%, 0.5%, 1%, 1.2%, 1.5% of NaCl dissolved in distilled water for 8 weeks. For confirmation of renal tubular destruction, the urinary KIM-1 was measured. The slides of renal tissue were prepared and stained with Hematoxylin and Eosin and Masson´s Trichrome for fibrosis detection. To investigate the role of CHOP protein in development of renal tubulointerstitial destruction, the relative gene expression of CHOP in renal tissue was analyzed using qRT-PCR method.There was no significant differences in urea, creatinine and total protein concentration of rats received different concentrations of NaCl compared to the control group. Urinary KIM-1 and mRNA level of CHOP was found to be increased significantly in rats treated with 1.5% NaCl compared to the control group. Mild renal fibrosis was observed in the same group too.III. Conclusion: Excessive salt intake can lead to fibrosis through increasing the expression of apoptotic CHOP gene in renal tissue. KIM-1 can be detectable in urine long before the development of renal fibrosis.

scholarly journals Retraction: Salvianolic acid B inhibits inflammatory response and cell apoptosis via the PI3K/Akt signaling pathway in IL-1β-induced osteoarthritis chondrocytes

RSC Advances ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 4441-4441
Author(s):  
Laura Fisher
Keyword(s):  
Inflammatory Response ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Akt Signaling ◽  
Salvianolic Acid B ◽  
Signalling Pathway ◽  
Akt Signaling Pathway ◽  
Salvianolic Acid ◽  
Osteoarthritis Chondrocytes

Retraction of ‘Salvianolic acid B inhibits inflammatory response and cell apoptosis via the PI3K/Akt signalling pathway in IL-1β-induced osteoarthritis chondrocytes’ by Bin Zhu et al., RSC Adv., 2018, 8, 36422–36429, DOI: 10.1039/C8RA02418A.

scholarly journals Extracellular vesicles as immune mediators in response to kidney injury

2018 ◽  
Vol 314 (1) ◽  
pp. F9-F21 ◽  
Author(s):  
Eva Feigerlová ◽  
Shyue-Fang Battaglia-Hsu ◽  
Thierry Hauet ◽  
Jean-Louis Guéant
Keyword(s):  
Extracellular Vesicles ◽  
Therapeutic Potential ◽  
Kidney Tissue ◽  
Kidney Injury ◽  
Renal Tissue ◽  
Bioactive Molecules ◽  
Renal Diseases ◽  
Cytokine Signaling ◽  
Renal Tubular ◽  
Tissue Recovery

Important progress has been made on cytokine signaling in response to kidney injury in the past decade, especially cytokine signaling mediated by extracellular vesicles (EVs). For example, EVs released by injured renal tubular epithelial cells (TECs) can regulate intercellular communications and influence tissue recovery via both regulating the expression and transferring cytokines, growth factors, as well as other bioactive molecules at the site of injury. The effects of EVs on kidney tissue seem to vary depending on the sources of EVs; however, the literature data are often inconsistent. For example, in rodents EVs derived from mesenchymal stem cells (MSC-EVs) and endothelial progenitor cells (EPC-EVs) can have both beneficial and harmful effects on injured renal tissue. Caution is thus needed in the interpretation of these data as contradictory findings on EVs may not only be related to the origin of EVs, they can also be caused by the different methods used for EV isolation and the physiological and pathological states of the tissues/cells under which they were obtained. Here, we review and discuss our current understanding related to the immunomodulatory function of EVs in renal tubular repair in the hope of encouraging further investigations on mechanisms related to their antiinflammatory and reparative role to better define the therapeutic potential of EVs in renal diseases.

scholarly journals Salvianolic Acid B Improves Postresuscitation Myocardial and Cerebral Outcomes in a Murine Model of Cardiac Arrest: Involvement of Nrf2 Signaling Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-17
Author(s):  
Qing-Qi Ji ◽  
Yan-Jie Li ◽  
Ying-Hua Wang ◽  
Zi Wang ◽  
Liang Fang ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Signaling Pathway ◽  
Murine Model ◽  
Nuclear Translocation ◽  
Salvia Miltiorrhiza ◽  
Left Ventricular ◽  
Salvianolic Acid B ◽  
Mitochondrial Morphology ◽  
Salvianolic Acid ◽  
Nrf2 Signaling Pathway

Survival and outcome of cardiac arrest (CA) are dismal despite improvements in cardiopulmonary resuscitation (CPR). Salvianolic acid B (Sal B), extracted from Salvia miltiorrhiza, has been investigated for its cardioprotective properties in cardiac remodeling and ischemic heart disease, but less is known about its role in CA. The aim of this study was to learn whether Sal B improves cardiac and neurologic outcomes after CA/CPR in mice. Female C57BL/6 mice were subjected to eight minutes of CA induced by an intravenous injection of potassium chloride (KCl), followed by CPR. After 30 seconds of CPR, mice were blindly randomized to receive either Sal B (20 mg/kg) or vehicle (normal saline) intravenously. Hemodynamic variables and indices of left ventricular function were determined before CA and within three hours after CPR, the early postresuscitation period. Sal B administration resulted in a remarkable decrease in the time required for the return of spontaneous circulation (ROSC) in animals that successfully resuscitated compared to the vehicle-treated mice. Myocardial performance, including cardiac output and left ventricular systolic (dp/dtmax) and diastolic (dp/dtmin) function, was clearly ameliorated within three hours of ROSC in the Sal B-treated mice. Moreover, Sal B inhibited CA/CPR-induced cardiomyocyte apoptosis and preserved mitochondrial morphology and function. Mechanistically, Sal B dramatically promoted Nrf2 nuclear translocation through the downregulation of Keap1, which resulted in the expression of antioxidant enzymes, including HO-1 and NQO1, thereby counteracted the oxidative damage in response to CA/CPR. The aforementioned antiapoptotic and antioxidant effects of Sal B were impaired in the setting of gene silencing of Nrf2 with siRNA in vitro model. These improvements were associated with better neurological function and increased survival rate (75% vs. 40%, p<0.05) up to 72 hours postresuscitation. Our findings suggest that the administration of Sal B improved cardiac function and neurological outcomes in a murine model of CA via activating the Nrf2 antioxidant signaling pathway, which may represent a novel therapeutic strategy for the treatment of CA.

MDM2 inhibition improves cisplatin-induced renal injury in mice via inactivation of Notch/hes1 signaling pathway

2020 ◽  
pp. 096032712095215
Author(s):  
X Luo ◽  
L Zhang ◽  
G-D Han ◽  
P Lu ◽  
Y Zhang
Keyword(s):  
Signaling Pathway ◽  
Renal Injury ◽  
Cell Apoptosis ◽  
Renal Tissue ◽  
Tunel Staining ◽  
Acute Renal Injury ◽  
Renal Tubular ◽  
Injury Models

Objective: To explore the potential function of MDM2-mediated Notch/hes1 signaling pathway in cisplatin-induced renal injury. Methods: The acute renal injury models of mice after intraperitoneal injection of cisplatin in vivo, and the apoptotic models of human renal tubular epithelial (HK-2) cells induced by cisplatin in vitro, were conducted respectively. The renal function-related parameters were measured. The renal tissue pathological changes and apoptosis were observed by PAS staining and TUNEL staining, respectively. Cell viability and apoptosis were detected by MTT and flow cytometry. Notch/hes1 pathway-related proteins were tested by Western blotting. Results: After mice injected by cisplatin, the levels of Cr, BUN, urine cystatin C, urine NGAL and urine ACR were increased and GFR was decreased with the elevation of renal tubular injury scores, the upregulation of the expressions of MDM2, N1ICD, Hes1 and Cleaved caspase-3, as well as the enhancement of cell apoptosis accompanying decreased ratio of Bcl-2/Bax. However, these cisplatin-induced renal injuries of mice have been improved by MDM2 inhibition. Besides, the declined viability, increased cytotoxicity, and enhanced apoptosis were observed in cisplatin-induced HK-2 cells, with the activated Notch/hes1 pathway. Notably, the phenomenon was alleviated in cisplatin-induced HK-2 cells transfected with MDM2 shRNA, but was severer in those co-treated with AdMDM2. Moreover, Notch1 siRNA can reverse the injury of AdMDM2 on HK-2 cells. Conclusion: Inhibiting MDM2 could reduce cell apoptosis through blocking Notch/hes1 signaling pathway, thus alleviating the acute renal injury caused by cisplatin.

scholarly journals P0518VNN1 MEDIATES RENAL MALADAPTIVE REPAIR AFTER AKI BY INDUCING PREMATURE SENESCENCE OF RENAL TUBUAR CELLS

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Yani He ◽  
Kehong Chen ◽  
Jia Chen
Keyword(s):  
Renal Fibrosis ◽  
Sham Group ◽  
Renal Tissue ◽  
Premature Senescence ◽  
Wild Type ◽  
Injury Score ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Tubule Cells ◽  
Renal Tubular

Abstract Background and Aims Renal maladaptive repair after acute kidney injury (AKI) can easily progress to chronic kidney disease. Sustained renal interstitial damage caused by accelerated senescence of renal tubular cells leads to renal fibrosis. Vanin-1 (VNN1) is an extracellular enzyme with panthenylmethylaminease activity that indirectly reduces the synthesis of glutathione, causing oxidative stress. The purpose of this study was to investigate the expression and of VNN1 in renal tissue and to study its role in senescence of renal tubular cells after ischemia reperfusion (I/R). Method hirty male wild BALB/c mice were randomly divided into control group, sham group and I/R group. In the I/R group, the bilateral renal pedicle was ligatured for 35 min followed by reperfusion. The expression of VNN1 and aging markers (P16, P21, SA-b-gal) were detected. Furthermore, wild type mice and VNN1 knockout mice were used to compare the degree of renal tissue and functional damage and the senescence of renal tubular cells after I/R injury. Results Compared with sham group, Scr, BUN and renal injury score increased significantly in I/R group at the early stage (3d) of renal injury. Renal fibrosis was observed in the later stage (28-42d). The expression of VNN1 in renal tubular cells of I/R group increased after I/R injury. VNN1 was coexpressed with P16, suggesting that VNN1 might be related to cellular stress senescence. The SCr, BUN of VNN1 KO mice was significantly lower than that of wild type mice at 7-28 d after renal reperfusion. The renal interstitial injury score of VNN1 KO mice was significantly lower than that of wild type mice, and the renal interstitial fibrosis level was significantly higher than that of wild type mice at 42d after reperfusion. The results suggest that VNN1 KO promotes renal repair of AKI. The ratio of P16 positive tubule cells in VNN1 KO mice was significantly higher than that in wild-type mice at 7d after renal reperfusion, suggesting that VNN1 could promote the senescence of renal tubule cells during AKI repair. Conclusion VNN1 mediates renal maladaptive repair after AKI by inducing premature senescence of renal tubular cells.

Regulation of SIRT3/FOXO1 Signaling Pathway in Rats with Non-alcoholic Steatohepatitis by Salvianolic Acid B

2017 ◽  
Vol 48 (6) ◽  
pp. 506-512 ◽  
Author(s):  
Yingchun Wang ◽  
Juan Chen ◽  
Weizong Kong ◽  
Ruiping Zhu ◽  
Kai Liang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Salvianolic Acid B ◽  
Salvianolic Acid ◽  
Alcoholic Steatohepatitis
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