scholarly journals Tyrosine and Tryptophan vibrational bands as markers of kidney injury: a renocardiac syndrome induced by renal ischemia and reperfusion study

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Gabrielle Nepomuceno ◽  
Carolina Victoria Cruz Junho ◽  
Marcela Sorelli Carneiro-Ramos ◽  
Herculano da Silva Martinho
Keyword(s):  
Raman Spectroscopy ◽  
Kidney Injury ◽  
Cardiorenal Syndrome ◽  
Renal Ischemia ◽  
Ischemia And Reperfusion ◽  
Collagen Iii ◽  
Ft Raman Spectroscopy ◽  
Ft Raman

AbstractRenal injury caused by renal ischemia and reperfusion strongly influences heart morphology, electrophysiology, and redox unbalance. The so-called cardiorenal syndrome is an important class of dysfunction since heart and kidneys are responsible for hemodynamic stability and organ perfusion through a complex network. In the present work we investigate the vibrational spectral features probed by Fourier-Transform Raman (FT-Raman) spectroscopy due to physiological alterations induced by renal ischemic reperfusion aiming to detect molecular markers related to progression of acute to chronic kidney injury and mortality predictors as well. C57BL/6J mice were subjected to unilateral occlusion of the renal pedicle for 60 min and reperfusion for 5, 8, and 15 days. Biopsies of heart and kidney tissues were analyzed. Our findings indicated that cysteine/cystine, fatty acids, methyl groups of Collagen, α-form of proteins, Tyrosine, and Tryptophan were modulated during renal ischemia and reperfusion process. These changes are consistent with fibroblast growth factors and Collagen III contents changes. Interestingly, Tyrosine and Tryptophan, precursor molecules for the formation of uremic toxins such as indoxyl sulfate and p-cresyl sulfate were also modulated. They are markers of kidney injury and their increase is strongly correlated to cardiovascular mortality. Regarding this aspect, we notice that monitoring the Tyrosine and Tryptophan bands at 1558, 1616, and 1625 cm−1 is a viable and and advantageous way to predict fatality in cardiovascular diseases both “in vivo” or “in vitro”, using the real-time, multiplexing, and minimally invasive advantages of FT-Raman spectroscopy.

scholarly journals Penetration mechanism of dimethyl sulfoxide in human and pig ear skin: An ATR–FTIR and near-FT Raman spectroscopicin vivoandin vitrostudy

2008 ◽  
Vol 22 (5) ◽  
pp. 405-417 ◽  
Author(s):  
Tanja M. Greve ◽  
Kristine B. Andersen ◽  
Ole F. Nielsen
Keyword(s):  
Dimethyl Sulfoxide ◽  
Conformational Changes ◽  
Bound Water ◽  
Free Water ◽  
Skin Barrier ◽  
Ft Raman Spectroscopy ◽  
Penetration Mechanism ◽  
Ft Raman

The penetration mechanism of dimethyl sulfoxide (DMSO) in human skinin vivoandin vitroand pig ear skin in vitro was studied using attenuated total reflectance (ATR) Fourier transform (FT) infrared (IR) and near-FT-Raman spectroscopy. The results showed changes in the conformation of the skin keratins from an α-helical to a β-sheet conformation. These changes were proved to depend on the concentration of free water in the sample as DMSO tended to bind to free water before the protein-bound water was replaced and the protein conformational changes were induced. The induced conformational changes were shown to be completely reversible as the proteins are returned to their original state within 20 h after the treatment with DMSO. The penetration depth of DMSO was shown to depend on the time of exposure – however, after only 15 min DMSO has penetrated thestratum corneum, which is the skin barrier.

High-wavenumber FT-Raman spectroscopy for in vivo and ex vivo measurements of breast cancer

2011 ◽  
Vol 130 (4-6) ◽  
pp. 1231-1238 ◽  
Author(s):  
A. F. García-Flores ◽  
L. Raniero ◽  
R. A. Canevari ◽  
K. J. Jalkanen ◽  
R. A. Bitar ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Raman Spectroscopy ◽  
Ex Vivo ◽  
Ft Raman Spectroscopy ◽  
Ft Raman

A naturally occurring FXR agonist, alisol B 23-acetate, protects against renal ischemia-reperfusion injury

2021 ◽  
Author(s):  
Zhi-Lin Luan ◽  
Wen-Hua Ming ◽  
Xiao-Wan Sun ◽  
Cong Zhang ◽  
Yang Zhou ◽  
...  
Keyword(s):  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Renal Ischemia ◽  
Farnesoid X Receptor ◽  
Site Directed Mutagenesis ◽  
Luciferase Assay ◽  
Naturally Occurring

The ligand-activated nuclear receptor, farnesoid X receptor (FXR), plays a pivotal role in regulating renal function. Activation of FXR by its specific agonists exerts renoprotective action in animals with acute kidney injury (AKI). In the present study, we aimed to identify naturally occurring agonists of FXR with potential as therapeutic agents in renal ischemia-perfusion injury (IRI). In vitro and in vivo FXR activation was determined by dual-luciferase assay, docking analysis, site-directed mutagenesis, and whole kidney transcriptome analysis. Wild-type (WT) and FXR knockout (FXR-/-) mice were used to determine the effect of potential FXR agonist on renal IRI. We found that alisol B 23-acetate (ABA), a major active triterpenoid extracted from Alismatis Rhizoma, a well-known traditional Chinese medicine, can activate renal FXR and induce FXR downstream gene expression in mouse kidney. ABA treatment significantly attenuated renal IR-induced AKI in WT mice but not in FXR-/- mice. Our results demonstrate that ABA can activate renal FXR to exert renoprotection against IRI-induced AKI. Therefore, ABA may represent a potential therapeutic agent in the treatment of ischemic AKI.

Trehalose attenuates renal ischemia-reperfusion injury by enhancing autophagy and inhibiting oxidative stress and inflammation

2020 ◽  
Vol 318 (4) ◽  
pp. F994-F1005
Author(s):  
Suwen Liu ◽  
Yunwen Yang ◽  
Huiping Gao ◽  
Ning Zhou ◽  
Peipei Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Renal Function ◽  
Renal Injury ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Renal Ischemia ◽  
Renal Histology ◽  
Hypoxia Reoxygenation

Renal ischemia-reperfusion (IR) injury is one of the most common acute kidney injuries, but there is still a lack of effective treatment in the clinical setting. Trehalose (Tre), a natural disaccharide, has been demonstrated to protect against oxidative stress, inflammation, and apoptosis. However, whether it could protect against IR-induced renal injury needs to be investigated. In an in vivo experiment, C57BL/6J mice were pretreated with or without Tre (2 g/kg) through a daily single intraperitoneal injection from 3 days before renal IR surgery. Renal function, apoptosis, oxidative stress, and inflammation were analyzed to evaluate kidney injury. In an in vitro experiment, mouse proximal tubular cells were treated with or without Tre under a hypoxia/reoxygenation condition. Western blot analysis, autophagy flux detection, and apoptosis assay were performed to evaluate the level of autophagy and antiapoptotic effect of Tre. The in vivo results showed that the renal damage induced by IR was ameliorated by Tre treatment, as renal histology and renal function were improved and the enhanced protein levels of kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin were blocked. Moreover, autophagy was activated by Tre pretreatment along with inhibition of the IR injury-induced apoptosis, oxidative stress, and inflammation. The in vitro results showed that Tre treatment activated autophagy and protected against hypoxia/reoxygenation-induced tubular cell apoptosis and oxidative stress. Our results demonstrated that Tre protects against IR-induced renal injury, possibly by enhancing autophagy and blocking oxidative stress, inflammation, and apoptosis, suggesting its potential use for the clinical treatment of renal IR injury.

scholarly journals Mouse model of ischemic acute kidney injury: technical notes and tricks

2012 ◽  
Vol 303 (11) ◽  
pp. F1487-F1494 ◽  
Author(s):  
Qingqing Wei ◽  
Zheng Dong
Keyword(s):  
Acute Kidney Injury ◽  
Mouse Model ◽  
Drug Testing ◽  
Ischemia Reperfusion ◽  
Small Animal ◽  
Kidney Injury ◽  
Experimental Models ◽  
Renal Ischemia

Renal ischemia-reperfusion leads to acute kidney injury (AKI), a major kidney disease associated with an increasing prevalence and high mortality rates. A variety of experimental models, both in vitro and in vivo, have been used to study the pathogenic mechanisms of ischemic AKI and to test renoprotective strategies. Among them, the mouse model of renal clamping is popular, mainly due to the availability of transgenic models and the relatively small animal size for drug testing. However, the mouse model is generally less stable, resulting in notable variations in results. Here, we describe a detailed protocol of the mouse model of bilateral renal ischemia-reperfusion. We share the lessons and experiences gained from our laboratory in the past decade. We further discuss the technical issues that account for the variability of this model and offer relevant solutions, which may help other investigators to establish a well-controlled, reliable animal model of ischemic AKI.

In vivo toxicological evaluation and FT-Raman spectroscopy correlations on a photochemical melanoma model

2009 ◽  
Vol 189 ◽  
pp. S59
Author(s):  
Cristina Adriana Dehelean ◽  
Simona Cinta-Pinzaru ◽  
Daniela Ionescu ◽  
Codruta Soica ◽  
Camelia Peev
Keyword(s):  
Raman Spectroscopy ◽  
Toxicological Evaluation ◽  
Melanoma Model ◽  
Ft Raman Spectroscopy ◽  
Ft Raman

Increased progression to kidney fibrosis after erythropoietin is used as a treatment for acute kidney injury

2014 ◽  
Vol 306 (6) ◽  
pp. F681-F692 ◽  
Author(s):  
Glenda C. Gobe ◽  
Nigel C. Bennett ◽  
Malcolm West ◽  
Paul Colditz ◽  
Lindsay Brown ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Renal Function ◽  
Kidney Disease ◽  
Kidney Injury ◽  
Renal Ischemia ◽  
Acute Injury

Treatment of renal ischemia-reperfusion (IR) injury with recombinant human erythropoietin (rhEPO) reduces acute kidney injury and improves function. We aimed to investigate whether progression to chronic kidney disease associated with acute injury was also reduced by rhEPO treatment, using in vivo and in vitro models. Rats were subjected to bilateral 40-min renal ischemia, and kidneys were studied at 4, 7, and 28 days postreperfusion for renal function, tubular injury and repair, inflammation, and fibrosis. Acute injury was modulated using rhEPO (1,000 or 5,000 IU/kg, intraperitoneally) at the time of reperfusion. Renal tubular epithelial cells or fibroblasts in culture were subjected to hypoxia or oxidative stress, with or without rhEPO (200 IU/ml), and fibrogenesis was studied. The results of the in vivo model confirmed functional and structural improvement with rhEPO at 4 days post-IR ( P < 0.05). At 7 days post-IR, fibrosis and myofibroblast stimulation were increased with IR with and without rhEPO ( P < 0.01). However, at 28 days post-IR, renal fibrosis and myofibroblast numbers were significantly greater with IR plus rhEPO ( P < 0.01) compared with IR only. Mechanistically, rhEPO stimulated profibrotic transforming growth factor-β, oxidative stress (marker 8-hydroxy-deoxyguanosine), and phosphorylation of the signal transduction protein extracellular signal-regulated kinase. In vitro, rhEPO protected tubular epithelium from apoptosis but stimulated epithelial-to-mesenchymal transition and also protected and activated fibroblasts, particularly with oxidative stress. In summary, although rhEPO was protective of renal function and structure in acute kidney injury, the supraphysiological dose needed for renoprotection contributed to fibrogenesis and stimulated chronic kidney disease in the long term.

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