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Mechanisms renal damage diabetes

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https://www.readbyqxmd.com/read/29926663/-effects-of-centella-asiatica-granule-on-the-expression-of-tgf-%C3%AE-1-and-related-down-stream-signals-in-rats-with-early-diabetic-nephropathy
#1
Ji-Wei Ma, Hong-Tian Wang, Hao-Fei Liu, Yuan Ding, Ji-Qiong Bai, Zhu Zhang
OBJECTIVE: To investigate the effects of centella asiatica (CA) granule on the expression of transform growth factor-β1 (TGF-β1 ) and related down-stream signals in rats with early diabetic nephropathy(DN) and to clarify the molecular mechanisms of CA molecular mechanism of on preventing and curing early diabetic kidney disease DN by studying the effects of centella asiatica on TGF-β1 expression and related down-stream signals. METHODS: Sixty male SD rats were divided into control group( n =10) and DN model group( n =50)...
January 8, 2018: Chinese Journal of Applied Physiology
https://www.readbyqxmd.com/read/29901130/grape-seed-proanthocyanidins-protect-against-streptozotocin%C3%A2-induced-diabetic-nephropathy-by-attenuating-endoplasmic-reticulum-stress%C3%A2-induced-apoptosis
#2
Zhaoli Gao, Guangyi Liu, Zhao Hu, Weiwei Shi, Binbin Chen, Peimei Zou, Xianhua Li
Diabetic nephropathy (DN) is by far the most common cause of end‑stage renal disease (ESRD) in industrial countries, accounting for ~45% of all new ESRD cases in the United States. Grape seed proanthocyanidin extracts (GSPE) are powerful antioxidants, with an antioxidant ability 50‑fold greater than that of vitamin E and 20‑fold greater than that of vitamin C. The present study investigated whether GSPE can protect against streptozotocin (STZ)‑induced DN and aimed to elucidate a possible mechanism...
June 6, 2018: Molecular Medicine Reports
https://www.readbyqxmd.com/read/29897845/renal-mitochondrial-oxidative-stress-is-enhanced-by-the-reduction-of-sirt3-activity-in-zucker-diabetic-fatty-rats
#3
Yoshio Ogura, Munehiro Kitada, Itaru Monno, Keizo Kanasaki, Ai Watanabe, Daisuke Koya
OBJECTIVES: Mitochondrial oxidative stress is involved in the pathogenesis of diabetic kidney disease. The objective of our study is to identify the mechanisms of renal mitochondrial oxidative stress, focusing on Sirt3, which is nicotinamide adenine dinucleotide (NAD+ ; oxidized NAD)-dependent deacetylase in mitochondria. METHODS: Renal mitochondrial oxidative stress and Sirt3 activity, using Zucker diabetic fatty rats (ZDFRs) and cultured proximal tubular cells under high-glucose condition were evaluated...
December 2018: Redox Report: Communications in Free Radical Research
https://www.readbyqxmd.com/read/29888290/vitamin-d-binding-protein-clearance-ratio-is-significantly-associated-with-glycemic-status-and-diabetes-complications-in-a-predominantly-vitamin-d-deficient-population
#4
Nabila A Abdella, Olusegun A Mojiminiyi
Introduction: Studies have shown increased urine excretion of vitamin D-binding protein (VDBP) in patients with diabetic nephropathy (DN) resulting from postulated mechanisms linked to renal tubular damage. In this study, we evaluate the utility of VDBP clearance ratio as a novel determinant of glycemic status, DN, and other diabetes-associated complications. Methods: Levels of vitamin D, HbA1c, serum, urine concentrations of VDBP, and creatinine were measured in 309 subjects...
2018: Journal of Diabetes Research
https://www.readbyqxmd.com/read/29887266/intracellular-organelles-in-health-and-kidney-disease
#5
Fateme Shamekhi Amiri
Subcellular organelles consist of smaller substructures called supramolecular assemblies and these in turn consist of macromolecules. Various subcellular organelles have critical functions that consist of genetic disorders of organelle biogenesis and several metabolic disturbances that occur during non-genetic diseases e.g. infection, intoxication and drug treatments. Mitochondrial damage can cause renal dysfunction as ischemic acute renal injury, chronic kidney disease progression. Moreover, mitochondrial dysfunction is an early event in aldosterone-induced podocyte injury and cardiovascular disease due to oxidative stress in chronic kidney disease...
June 7, 2018: Néphrologie & Thérapeutique
https://www.readbyqxmd.com/read/29861832/the-role-of-tlr4-on-pgc-1-%C3%AE-mediated-oxidative-stress-in-tubular-cell-in-diabetic-kidney-disease
#6
Shuguang Yuan, Xuemei Liu, Xuejing Zhu, Zhong Qu, Zailiang Gong, Jun Li, Li Xiao, Yuan Yang, Hong Liu, Lin Sun, Fuyou Liu
The role and precise mechanism of TLR4 in mitochondria-related oxidative damage and apoptosis of renal tubules in diabetic kidney disease (DKD) remain unclear. We examined the expression of TLR4 in renal biopsy tissues. Db/db diabetic mice and HK-2 cells cultured under high glucose (HG) were used as in vivo and vitro models. Real-time RT-PCR, Western blot, and immunohistochemistry were performed to examine the mRNA and protein levels of TLR4, NF- κ Β, PGC-1 α , cytochrome C, and cleaved caspase-3. ATP level, activity of electron transport chain complex III, and antioxidant enzymes were investigated for mitochondrial function...
2018: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/29852492/a-review-of-podocyte-biology
#7
Puneet Garg
BACKGROUND: Podocyte biology is a developing science that promises to help improve understanding of the mechanistic nature of multiple diseases associated with proteinuria. Proteinuria in nephrotic syndrome has been linked to mechanistic dysfunctions in the renal glomerulus involving the function of podocyte epithelial cells, including podocyte foot process effacement. SUMMARY: Developments in imaging technology are improving knowledge of the detailed structure of the human renal glomerulus and cortex...
2018: American Journal of Nephrology
https://www.readbyqxmd.com/read/29849705/renoprotective-effect-of-danhong-injection-on-streptozotocin-induced-diabetic-rats-through-a-peroxisome-proliferator-activated-receptor-%C3%AE-mediated-pathway
#8
Xue Yang, Xiang Xiao, Hailian Wang, Yi Li, Li Wang, Guisen Li, Shaoping Deng
The aim of the study was to investigate the protective effect of Danhong injection (DHI) on diabetic kidney disease and explore the potential mechanisms. Diabetic kidney disease was induced by unilateral nephrectomy, high-fat diet, and streptozotocin. After DHI administration, the renal function deterioration, 24-hour total urine protein excretion, and elevated serum lipid levels were reversed to some extent, and the renal pathological damage was also ameliorated. The KEGG pathway enrichment analysis demonstrated that the PPAR γ signal pathway was significantly upregulated in DH group...
2018: Evidence-based Complementary and Alternative Medicine: ECAM
https://www.readbyqxmd.com/read/29848325/role-of-p53-mir-155-5p-sirt1-loop-in-renal-tubular-injury-of-diabetic-kidney-disease
#9
Yue Wang, Zong-Ji Zheng, Yi-Jie Jia, Yan-Lin Yang, Yao-Ming Xue
BACKGROUND: Diabetic kidney disease is a renal microvascular disease caused by diabetes, known as one of the most serious and lethal complications of diabetes. Early renal hypertrophy is the main pathological feature, which gradually leads to the deposition of glomerular extracellular matrix and tubulointerstitial fibrosis, eventually developing irreversible structural damage to the kidneys. Autophagy is a cell self-homeostatic mechanism that is activated under stress conditions and may serve as a protective response to the survival of renal fibrogenic cells...
May 30, 2018: Journal of Translational Medicine
https://www.readbyqxmd.com/read/29844451/blockade-of-hmgb1-attenuates-diabetic-nephropathy-in-mice
#10
Xiaochen Chen, Jin Ma, Tony Kwan, Elisabeth G D Stribos, A Lianne Messchendorp, Yik W Loh, Xiaoyu Wang, Moumita Paul, Eithne C Cunningham, Miriam Habib, Ian E Alexander, Alexandra F Sharland, Steven J Chadban, Huiling Wu
Activation of TLR2 or TLR4 by endogenous ligands such as high mobility group box 1 (HMGB1) may mediate inflammation causing diabetic kidney injury. We determined whether blockade of HMGB1 signaling by: (1) supra-physiological production of endogenous secretory Receptor for Advanced Glycation End-products (esRAGE), a receptor for HMGB1; (2) administration of HMGB1 A Box, a specific competitive antagonist, would inhibit development of streptozotocin induced diabetic nephropathy (DN). Wild-type diabetic mice developed albuminuria, glomerular injuries, interstitial fibrosis and renal inflammation...
May 29, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29806072/deregulation-of-autophagy-under-hyperglycemic-conditions-is-dependent-on-increased-lysin63-ubiquitination-a-candidate-mechanism-in-the-progression-of-diabetic-nephropathy
#11
Paola Pontrelli, Annarita Oranger, Mariagrazia Barozzino, Chiara Divella, Francesca Conserva, Maria Grazia Fiore, Roberta Rossi, Massimo Papale, Giuseppe Castellano, Simona Simone, Luigi Laviola, Francesco Giorgino, Domenico Piscitelli, Anna Gallone, Loreto Gesualdo
Diabetic nephropathy patients (DN) are characterized by increased lysine63 ubiquitination (Lys63-Ub) at the tubular level. Autophagy is deregulated under diabetic conditions, even though the molecular mechanisms and the consequences of this alteration need to be elucidated. The aim of this study was to investigate the link between Lys63-Ub and autophagy in DN and the involvement of these two processes in tubular cell fate. Immunohistochemistry of beclin-1, LC3, and p62 on kidney biopsies highlighted increased protein expression of all these autophagic factors at the tubular level in DN compared to other nephritis...
May 27, 2018: Journal of Molecular Medicine: Official Organ of the "Gesellschaft Deutscher Naturforscher und Ärzte"
https://www.readbyqxmd.com/read/29793963/a-nox4-trpc6-pathway-in-podocyte-calcium-regulation-and-renal-damage-in-diabetic-kidney-disease
#12
Daria V Ilatovskaya, Gregory Blass, Oleg Palygin, Vladislav Levchenko, Tengis S Pavlov, Michael N Grzybowski, Kristen Winsor, Leonid S Shuyskiy, Aron M Geurts, Allen W Cowley, Lutz Birnbaumer, Alexander Staruschenko
Background Loss of glomerular podocytes is an indicator of diabetic kidney disease (DKD). The damage to these cells has been attributed in part to elevated intrarenal oxidative stress. The primary source of the renal reactive oxygen species, particularly H2 O2 , is NADPH oxidase 4 (NOX4). We hypothesized that NOX4-derived H2 O2 contributes to podocyte damage in DKD via elevation of podocyte calcium. Methods We used Dahl salt-sensitive (SS) rats with a null mutation for the Nox4 gene (SSNox4-/- ) and mice with knockout of the nonselective calcium channel TRPC6 or double knockout of TRPC5 and TRPC6...
May 23, 2018: Journal of the American Society of Nephrology: JASN
https://www.readbyqxmd.com/read/29778909/n-acetylcysteine-protects-against-diabetic-nephropathy-through-control-of-oxidative-and-nitrosative-stress-by-recovery-of-nitric-oxide-in-rats
#13
Guilherme B Nogueira, Giovana R Punaro, Clemerson S Oliveira, Fabiane R Maciel, Thamires O Fernandes, Deyse Y Lima, Adelson M Rodrigues, Margaret G Mouro, Sergio R R Araujo, Elisa M S Higa
The diabetes mellitus (DM) induces several changes, with substantial increase of reactive oxygen species (ROS). The ROS cause damage to systemic and renal microvasculature, which could be one of the mechanisms involved in the development of diabetic nephropathy (DN). The ROS modulate other substances like the nitric oxide (NO), a vasodilator with important role in the renal function. N-acetylcysteine (NAC) is an antioxidant that acts replenishing intracellular cysteine levels, which is essential for glutathione formation...
May 17, 2018: Nitric Oxide: Biology and Chemistry
https://www.readbyqxmd.com/read/29761900/fenofibrate-improves-renal-function-by-amelioration-of-nox-4-il-18-and-p53-expression-in-an-experimental-model-of-diabetic-nephropathy
#14
Habib Yaribeygi, Mohammad T Mohammadi, Ramin Rezaee, Amirhossein Sahebkar
Among several pathological mechanisms involved in diabetic nephropathy, oxidative stress, inflammation, and apoptosis play a prominent role. Fenofibrate, a peroxisome proliferator-activated receptor-α (PPAR-α) agonist, has markedly improved oxidative stress and inflammatory responses, but there is no evidence about its effects on interleukin-18 (IL-18), NADPH oxidase type 4 (NOX-4), and p53 expression in diabetic kidneys. The aim of this study was to evaluate possible effects of fenofibrate on improving the underlying mechanisms of diabetic nephropathy...
May 15, 2018: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/29737200/human-peripheral-blood-mononuclear-cells-incubated-in-vasculogenic-conditioning-medium-dramatically-improve-ischemia-reperfusion-acute-kidney-injury-in-mice
#15
Takayasu Ohtake, Shuzo Kobayashi, Shimon Slavin, Yasuhiro Mochida, Kunihiro Ishioka, Hidekazu Moriya, Sumi Hidaka, Ryo Matsuura, Maki Sumida, Daisuke Katagiri, Eisei Noiri, Kayoko Okada, Hiroshi Mizuno, Rica Tanaka
Acute kidney injury (AKI) is a major clinical problem that still has no established treatment. We investigated the efficacy of cultured human peripheral blood mononuclear cells (PBMNCs) for AKI. Ischemia/reperfusion injury (IRI) was used to induce AKI in male nonobese diabetic (NOD/severe combined immunodeficiency) mice aged 7 to 8 wk. PBMNCs were isolated from healthy volunteers and were subjected to quality and quantity controlled (QQc) culture for 7 d in medium containing stem cell factor, thrombopoietin, Flt-3 ligand, vascular endothelial growth factor, and interleukin 6...
January 1, 2018: Cell Transplantation
https://www.readbyqxmd.com/read/29723228/divergent-antioxidant-capacity-of-human-islet-cell-subsets-a-potential-cause-of-beta-cell-vulnerability-in-diabetes-and-islet-transplantation
#16
Atsushi Miki, Camillo Ricordi, Yasunaru Sakuma, Toshiyuki Yamamoto, Ryosuke Misawa, Atsuyoshi Mita, Ruth D Molano, Nosratola D Vaziri, Antonello Pileggi, Hirohito Ichii
BACKGROUND: Type 1 and Type 2 diabetes mellitus (T1DM and T2DM) are caused by beta(β)-cell loss and functional impairment. Identification of mechanisms of β-cell death and therapeutic interventions to enhance β-cell survival are essential for prevention and treatment of diabetes. Oxidative stress is a common feature of both T1DM and T2DM; elevated biomarkers of oxidative stress are detected in blood, urine and tissues including pancreas of patients with DM. Islet transplantation is a promising treatment for diabetes...
2018: PloS One
https://www.readbyqxmd.com/read/29702558/a-low-protein-diet-for-diabetic-kidney-disease-its-effect-and-molecular-mechanism-an-approach-from-animal-studies
#17
REVIEW
Munehiro Kitada, Yoshio Ogura, Itaru Monno, Daisuke Koya
A low-protein diet (LPD) can be expected to retard renal function decline in advanced stages of chronic kidney disease (CKD), including diabetic kidney disease (DKD), and is recommended in a clinical setting. Regarding the molecular mechanisms of an LPD against DKD, previous animal studies have shown that an LPD exerts reno-protection through mainly the improvement of glomerular hyperfiltration/hypertension due to the reduction of intraglomerular pressure. On the other hand, we have demonstrated that an LPD, particularly a very-LPD (VLPD), improved tubulo-interstitial damage, inflammation and fibrosis, through the restoration of autophagy via the reduction of a mammalian target of rapamycin complex 1 (mTORC1) activity in type 2 diabetes and obesity animal models...
April 27, 2018: Nutrients
https://www.readbyqxmd.com/read/29701296/repression-of-microrna-382-inhibits-glomerular-mesangial-cell-proliferation-and-extracellular-matrix-accumulation-via-foxo1-in-mice-with-diabetic-nephropathy
#18
Shan Wang, Xin Wen, Xin-Rui Han, Yong-Jian Wang, Min Shen, Shao-Hua Fan, Juan Zhuang, Zi-Feng Zhang, Qun Shan, Meng-Qiu Li, Bin Hu, Chun-Hui Sun, Dong-Mei Wu, Jun Lu, Yuan-Lin Zheng
OBJECTIVES: Diabetic nephropathy (DN) is a nerve damaging disorder, characterized by glomerular mesangial cell expansion and accumulation of extracellular matrix (ECM) proteins. In this study, we aimed to investigate mesangial cell proliferation and ECM accumulation when promoting or suppressing endogenous miR-382 in glomerular mesangial cells of DN. MATERIALS AND METHODS: Model establishment consisted of DN induction by streptozotocin (STZ) in mice. The underlying regulatory mechanisms of miR-382 were analysed in concert with the treatment of miR-382 mimics, miR-382 inhibitors or siRNA against FoxO1 in cultured glomerular mesangial cells isolated from DN mice...
April 27, 2018: Cell Proliferation
https://www.readbyqxmd.com/read/29669962/renal-protective-effect-of-paeoniflorin-by-inhibition-of-jak2-stat3-signaling-pathway-in-diabetic-mice
#19
Xinyu Li, Yan Wang, Kun Wang, Yonggui Wu
Paeoniflorin is the main bioactive components of the root of P.lactiflora Pall., and has been widely used as an anti-inflammation and immunomodulatory agent. However, the effect and mechanisms of Paeoniflorin in diabetic nephropathy (DN) remains to be elucidated. In the present study, streptozotocin (STZ)-induced type 1 diabetic mice model was used to investigate the protective effect of Paeoniflorin and the role of the Janus kinase (JAK) 2/signal transducer (STAT) 3 signaling pathway on DN. After treatment with Paeoniflorin at a dose of 25, 50 and 100 mg/kg once a day for 12 weeks, both the functional and histological damage to diabetic mice kidney had been attenuated significantly...
May 13, 2018: Bioscience Trends
https://www.readbyqxmd.com/read/29623210/new-onset-insulin-dependent-diabetes-due-to-nivolumab
#20
Ali A Zaied, Halis K Akturk, Richard W Joseph, Augustine S Lee
Nivolumab, a monoclonal antibody against programmed cell death-1 receptor, is increasingly used in advanced cancers. While nivolumab use enhances cancer therapy, it is associated with increased immune-related adverse events. We describe an elderly man who presented in ketoacidosis after receiving nivolumab for metastatic renal cell carcinoma. On presentation, he was hyperpneic and laboratory analyses showed hyperglycemia and anion-gapped metabolic acidosis consistent with diabetic ketoacidosis. No other precipitating factors, besides nivolumab, were identified...
2018: Endocrinology, Diabetes & Metabolism Case Reports
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