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      The Structure and Nephroprotective Activity of Oligo-Porphyran on Glycerol-Induced Acute Renal Failure in Rats

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          Abstract

          Porphyran is a sulfate galactan in the cell wall of Porphyra. Its acid hydrolysis product, oligo-porphyran (OP), was prepared and the structure studied by electrospray ionization time-of-flight mass spectrometry (ESI-TOF-MS). This oligosaccharide was mainly composed of monosulfate-oligo-galactan, disufate-oligo-galactan, trisulfate-oligo-galactan, trisulfate oligo-methyl-galactan, and 3,6-anhydrogalactose with the degree of polymerization ranging from 1 to 8. The effects of OP were investigated in the glycerol-induced acute renal failure (ARF) model. Compared with the normal group, rats from the glycerol-induced group exhibited collecting duct and medullary ascending limb dilation and casts. The OP-treated group exerted a protective effect against glycerol-induced changes. The results showed that the administration of OP markedly decreased mortality in female ARF rats. For male ARF rats, all of which survived, OP significantly decreased the blood urea nitrogen and serum creatinine levels. Ion levels in plasma and urine were significantly changed in ARF rats, whereas OP treatment almost recovered ion levels back to normal. This study showed a noticeable renal morphologic and functional protection by OP in glycerol-induced ARF rats.

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          Pathophysiology of acute kidney injury.

          David P Basile, Melissa Anderson, Timothy A. Sutton (2012)
          Acute kidney injury (AKI) is the leading cause of nephrology consultation and is associated with high mortality rates. The primary causes of AKI include ischemia, hypoxia, or nephrotoxicity. An underlying feature is a rapid decline in glomerular filtration rate (GFR) usually associated with decreases in renal blood flow. Inflammation represents an important additional component of AKI leading to the extension phase of injury, which may be associated with insensitivity to vasodilator therapy. It is suggested that targeting the extension phase represents an area potential of treatment with the greatest possible impact. The underlying basis of renal injury appears to be impaired energetics of the highly metabolically active nephron segments (i.e., proximal tubules and thick ascending limb) in the renal outer medulla, which can trigger conversion from transient hypoxia to intrinsic renal failure. Injury to kidney cells can be lethal or sublethal. Sublethal injury represents an important component in AKI, as it may profoundly influence GFR and renal blood flow. The nature of the recovery response is mediated by the degree to which sublethal cells can restore normal function and promote regeneration. The successful recovery from AKI depends on the degree to which these repair processes ensue and these may be compromised in elderly or chronic kidney disease (CKD) patients. Recent data suggest that AKI represents a potential link to CKD in surviving patients. Finally, earlier diagnosis of AKI represents an important area in treating patients with AKI that has spawned increased awareness of the potential that biomarkers of AKI may play in the future. © 2012 American Physiological Society. Compr Physiol 2:1303-1353, 2012.
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            Mechanisms of maladaptive repair after AKI leading to accelerated kidney ageing and CKD.

            David A Ferenbach, Joseph V. Bonventre (2015)
            Acute kidney injury is an increasingly common complication of hospital admission and is associated with high levels of morbidity and mortality. A hypotensive, septic, or toxic insult can initiate a cascade of events, resulting in impaired microcirculation, activation of inflammatory pathways and tubular cell injury or death. These processes ultimately result in acutely impaired kidney function and initiation of a repair response. This Review explores the various mechanisms responsible for the initiation and propagation of acute kidney injury, the prototypic mechanisms by which a substantially damaged kidney can regenerate its normal architecture, and how the adaptive processes of repair can become maladaptive. These mechanisms, which include G2/M cell-cycle arrest, cell senescence, profibrogenic cytokine production, and activation of pericytes and interstitial myofibroblasts, contribute to the development of progressive fibrotic kidney disease. The end result is a state that mimics accelerated kidney ageing. These mechanisms present important opportunities for the design of targeted therapeutic strategies to promote adaptive renal recovery and minimize progressive fibrosis and chronic kidney disease after acute insults.
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              Rhabdomyolysis and myohemoglobinuric acute renal failure.

              Richard Zager (1996)
              Article 0 comments Cited 107 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Keith B. Glaser: Role: Academic Editor
                Journal
                Journal ID (nlm-ta): Mar Drugs
                Journal ID (iso-abbrev): Mar Drugs
                Journal ID (publisher-id): marinedrugs
                Title: Marine Drugs
                Publisher: MDPI
                ISSN (Electronic): 1660-3397
                Publication date (Electronic): 09 May 2017
                Publication date Collection: May 2017
                Volume: 15
                Issue: 5
                Electronic Location Identifier: 135
                Affiliations
                [1 ]Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, Qingdao 266071, Shandong, China; jingwang@ 123456qdio.ac.cn (J.W.); houyun.china@ 123456gmail.com (Y.H.); dlduan@ 123456qdio.ac.cn (D.D.)
                [2 ]Laboratory for Marine Biology and Biotechnology, Qingdao National Laboratory for Marine Science and Technology, Qingdao 266071, China
                [3 ]Graduate University of the Chinese Academy of Sciences, Beijing 100049, China
                [4 ]State Key Lab of Seaweed Bioactive Substances, Qingdao 266500, China
                Author notes
                [* ]Correspondence: qbzhang@ 123456qdio.ac.cn ; Tel.: +86-532-8289-8708
                Article
                Publisher ID: marinedrugs-15-00135
                DOI: 10.3390/md15050135
                PMC ID: 5450541
                PubMed ID: 28486425
                SO-VID: 6f43793f-1fb8-4dd0-978f-d4d77d28c226
                Copyright © © 2017 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 01 February 2017
                Date accepted : 04 May 2017
                Categories
                Subject: Article

                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: sulfated galactan,oligo-porphyran,acute renal failure,gender difference
                Data availability:
                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: sulfated galactan, oligo-porphyran, acute renal failure, gender difference

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