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      Sarpogrelate hydrochloride ameliorates diabetic nephropathy associated with inhibition of macrophage activity and inflammatory reaction in db/db mice

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          Abstract

          The aim of this study was to evaluate the effects of sarpogrelate hydrochloride (SH), a selective serotonin 2A receptor antagonist, on diabetic nephropathy in a type 2 diabetes mouse model. We treated db/m and db/db mice with SH (30 mg/kg/day) for 12 weeks. Rat renal proximal tubule cells (NRK-52E) and mouse macrophages (Raw 264.7) were stimulated by high glucose (30 mM glucose) or LPS (100 ng/ml) with or without SH (20 μM). We found that SH treatment increased serum adiponectin level and decreased urinary albumin, macrophage infiltration to glomeruli, and renal inflammatory and fibrosis signals, which were highly expressed in diabetic mice. Proximal tubule cells treated with high glucose (30 mM) also showed increased inflammatory and fibrosis signals. However, SH (20 μM) treatment reduced these changes. Moreover, SH treatment inhibited LPS-stimulated macrophage migration and activation. These findings suggest that SH ameliorates diabetic nephropathy not only by suppressing macrophage infiltration, but also by anti-inflammatory and anti-fibrotic effects.

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          Plasma concentrations of a novel, adipose-specific protein, adiponectin, in type 2 diabetic patients.

          Kikuko Hotta, Tohru Funahashi, Yukio Arita … (2000)
          Adiponectin is a novel, adipose-specific protein abundantly present in the circulation, and it has antiatherogenic properties. We analyzed the plasma adiponectin concentrations in age- and body mass index (BMI)-matched nondiabetic and type 2 diabetic subjects with and without coronary artery disease (CAD). Plasma levels of adiponectin in the diabetic subjects without CAD were lower than those in nondiabetic subjects (6.6+/-0.4 versus 7.9+/-0.5 microg/mL in men, 7.6+/-0.7 versus 11.7+/-1.0 microg/mL in women; P<0.001). The plasma adiponectin concentrations of diabetic patients with CAD were lower than those of diabetic patients without CAD (4.0+/-0.4 versus 6.6+/-0.4 microg/mL, P<0.001 in men; 6.3+/-0.8 versus 7.6+/-0. 7 microg/mL in women). In contrast, plasma levels of leptin did not differ between diabetic patients with and without CAD. The presence of microangiopathy did not affect the plasma adiponectin levels in diabetic patients. Significant, univariate, inverse correlations were observed between adiponectin levels and fasting plasma insulin (r=-0.18, P<0.01) and glucose (r=-0.26, P<0.001) levels. In multivariate analysis, plasma insulin did not independently affect the plasma adiponectin levels. BMI, serum triglyceride concentration, and the presence of diabetes or CAD remained significantly related to plasma adiponectin concentrations. Weight reduction significantly elevated plasma adiponectin levels in the diabetic subjects as well as the nondiabetic subjects. These results suggest that the decreased plasma adiponectin concentrations in diabetes may be an indicator of macroangiopathy.
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            Inflammation in Diabetic Nephropathy

            Andy K. H. Lim, Gregory Tesch (2012)
            Diabetic nephropathy is the leading cause of end-stage kidney disease worldwide but current treatments remain suboptimal. This review examines the evidence for inflammation in the development and progression of diabetic nephropathy in both experimental and human diabetes, and provides an update on recent novel experimental approaches targeting inflammation and the lessons we have learned from these approaches. We highlight the important role of inflammatory cells in the kidney, particularly infiltrating macrophages, T-lymphocytes and the subpopulation of regulatory T cells. The possible link between immune deposition and diabetic nephropathy is explored, along with the recently described immune complexes of anti-oxidized low-density lipoproteins. We also briefly discuss some of the major inflammatory cytokines involved in the pathogenesis of diabetic nephropathy, including the role of adipokines. Lastly, we present the latest data on the pathogenic role of the stress-activated protein kinases in diabetic nephropathy, from studies on the p38 mitogen activated protein kinase and the c-Jun amino terminal kinase cell signalling pathways. The genetic and pharmacological approaches which reduce inflammation in diabetic nephropathy have not only enhanced our understanding of the pathophysiology of the disease but shown promise as potential therapeutic strategies.
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              Adiponectin increases fatty acid oxidation in skeletal muscle cells by sequential activation of AMP-activated protein kinase, p38 mitogen-activated protein kinase, and peroxisome proliferator-activated receptor alpha.

              B Ahn, T. J. Kim, Christopher Hong … (2006)
              Adiponectin has recently received a great deal of attention due to its beneficial effects on insulin resistance and metabolic disorders. One of the mechanisms through which adiponectin exerts such effects involves an increase in fatty acid oxidation in muscle and liver. In the present study, we demonstrate that 5'-AMP-activated protein kinase (AMPK) and p38 mitogen-activated protein kinase (MAPK) are involved in the activation of peroxisome proliferator-activated receptor (PPAR)alpha by adiponectin in muscle cells. Adiponectin increases the transcriptional activity of PPARalpha and the expression of its target genes, including ACO, CPT1, and FABP3 in C2C12 myotubes. These effects were suppressed by the overexpression of a dominant-negative form of AMPK. Moreover, chemical inhibitors of AMPK and p38 MAPK potently repressed fatty acid oxidation and the induction of PPARalpha target gene expression by adiponectin. Interestingly, araA, an AMPK inhibitor, prevented the activation of p38 MAPK, whereas SB203580, a p38 MAPK inhibitor, did not affect AMPK activation, suggesting that p38 MAPK is a downstream signaling factor of AMPK. Taken together, these results suggest that adiponectin stimulates fatty acid oxidation in muscle cells by the sequential activation of AMPK, p38 MAPK, and PPARalpha.
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                Author and article information

                Contributors
                Rajesh Mohanraj: Role: Editor
                Journal
                Journal ID (nlm-ta): PLoS One
                Journal ID (iso-abbrev): PLoS ONE
                Journal ID (publisher-id): plos
                Journal ID (pmc): plosone
                Title: PLoS ONE
                Publisher: Public Library of Science (San Francisco, CA USA )
                ISSN (Electronic): 1932-6203
                Publication date (Electronic): 22 June 2017
                Publication date Collection: 2017
                Volume: 12
                Issue: 6
                Electronic Location Identifier: e0179221
                Affiliations
                [1 ]Department of Internal Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea
                [2 ]Department of Internal Medicine, Soonchunhyang University Cheonan Hospital, Cheonan, Korea
                Faculty of Medicine & Health Science, UNITED ARAB EMIRATES
                Author notes

                Competing Interests: The authors have declared that no competing interests exist.

                • Conceptualization: CHC ESL MYL.

                • Data curation: ESL MYL.

                • Formal analysis: ESL HMK YMK.

                • Funding acquisition: MYL EYL.

                • Investigation: ESL MYL CHC.

                • Methodology: ESL MYL M-HK HMK YMK.

                • Project administration: CHC ESL MYL.

                • Resources: MYL.

                • Software: ESL YMK.

                • Supervision: CHC.

                • Validation: CHC.

                • Visualization: CHC ESL.

                • Writing – original draft: ESL MYL.

                • Writing – review & editing: CHC M-HK HMK JSK EYL.

                Article
                Publisher ID: PONE-D-16-45115
                DOI: 10.1371/journal.pone.0179221
                PMC ID: 5480859
                PubMed ID: 28640832
                SO-VID: 76d95594-77a1-4f34-80ed-a6e93290eae0
                Copyright © © 2017 Lee et al
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Date received : 13 November 2016
                Date accepted : 25 May 2017
                Page count
                Figures: 7, Tables: 2, Pages: 16
                Funding
                Funded by: funder-id http://dx.doi.org/10.13039/501100003725, National Research Foundation of Korea;
                Award ID: 2015R1D1A1A02060785
                Award Recipient :
                Funded by: funder-id http://dx.doi.org/10.13039/501100003725, National Research Foundation of Korea;
                Award ID: 2015R1A6A1A03032522
                Award Recipient :
                Funded by: Yonsei University Wonju College of Medicine (KR)
                Award ID: YUWCM-2009-23
                Award Recipient :
                This research was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (2015R1D1A1A02060785, 2015R1A6A1A03032522) to EYL, and the research grant from Yonsei University Wonju College of Medicine (YUWCM-2009-23) to MYL. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Subject: Research Article
                Subject: Biology and Life Sciences
                Subject: Cell Biology
                Subject: Cellular Types
                Subject: Animal Cells
                Subject: Blood Cells
                Subject: White Blood Cells
                Subject: Macrophages
                Subject: Biology and Life Sciences
                Subject: Cell Biology
                Subject: Cellular Types
                Subject: Animal Cells
                Subject: Immune Cells
                Subject: White Blood Cells
                Subject: Macrophages
                Subject: Biology and Life Sciences
                Subject: Immunology
                Subject: Immune Cells
                Subject: White Blood Cells
                Subject: Macrophages
                Subject: Medicine and Health Sciences
                Subject: Immunology
                Subject: Immune Cells
                Subject: White Blood Cells
                Subject: Macrophages
                Subject: Medicine and Health Sciences
                Subject: Endocrinology
                Subject: Endocrine Disorders
                Subject: Diabetes Mellitus
                Subject: Medicine and Health Sciences
                Subject: Metabolic Disorders
                Subject: Diabetes Mellitus
                Subject: Biology and Life Sciences
                Subject: Immunology
                Subject: Immune Response
                Subject: Inflammation
                Subject: Medicine and Health Sciences
                Subject: Immunology
                Subject: Immune Response
                Subject: Inflammation
                Subject: Medicine and Health Sciences
                Subject: Diagnostic Medicine
                Subject: Signs and Symptoms
                Subject: Inflammation
                Subject: Medicine and Health Sciences
                Subject: Pathology and Laboratory Medicine
                Subject: Signs and Symptoms
                Subject: Inflammation
                Subject: Biology and Life Sciences
                Subject: Anatomy
                Subject: Renal System
                Subject: Kidneys
                Subject: Medicine and Health Sciences
                Subject: Anatomy
                Subject: Renal System
                Subject: Kidneys
                Subject: Biology and Life Sciences
                Subject: Biochemistry
                Subject: Neurochemistry
                Subject: Neurotransmitters
                Subject: Biogenic Amines
                Subject: Serotonin
                Subject: Biology and Life Sciences
                Subject: Neuroscience
                Subject: Neurochemistry
                Subject: Neurotransmitters
                Subject: Biogenic Amines
                Subject: Serotonin
                Subject: Research and Analysis Methods
                Subject: Experimental Organism Systems
                Subject: Model Organisms
                Subject: Mouse Models
                Subject: Research and Analysis Methods
                Subject: Model Organisms
                Subject: Mouse Models
                Subject: Research and Analysis Methods
                Subject: Experimental Organism Systems
                Subject: Animal Models
                Subject: Mouse Models
                Subject: Biology and Life Sciences
                Subject: Physiology
                Subject: Immune Physiology
                Subject: Cytokines
                Subject: Adipokines
                Subject: Adiponectin
                Subject: Medicine and Health Sciences
                Subject: Physiology
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                Subject: Cytokines
                Subject: Adipokines
                Subject: Adiponectin
                Subject: Biology and Life Sciences
                Subject: Immunology
                Subject: Immune System
                Subject: Innate Immune System
                Subject: Cytokines
                Subject: Adipokines
                Subject: Adiponectin
                Subject: Medicine and Health Sciences
                Subject: Immunology
                Subject: Immune System
                Subject: Innate Immune System
                Subject: Cytokines
                Subject: Adipokines
                Subject: Adiponectin
                Subject: Biology and Life Sciences
                Subject: Developmental Biology
                Subject: Molecular Development
                Subject: Cytokines
                Subject: Adipokines
                Subject: Adiponectin
                Subject: Biology and Life Sciences
                Subject: Biochemistry
                Subject: Hormones
                Subject: Peptide Hormones
                Subject: Adiponectin
                Subject: Biology and Life Sciences
                Subject: Anatomy
                Subject: Renal System
                Subject: Kidneys
                Subject: Glomeruli
                Subject: Medicine and Health Sciences
                Subject: Anatomy
                Subject: Renal System
                Subject: Kidneys
                Subject: Glomeruli
                Custom metadata
                Data Availability All relevant data are within the paper and its Supporting Information files.

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