scholarly journals Absence of Dipeptidyl Peptidase 3 Increases Oxidative Stress and Causes Bone Loss

2019 ◽  
Vol 34 (11) ◽  
pp. 2133-2148 ◽  
Author(s):  
Ciro Menale ◽  
Lisa J Robinson ◽  
Eleonora Palagano ◽  
Rosita Rigoni ◽  
Marco Erreni ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Bone Loss ◽  
Dipeptidyl Peptidase ◽  
Dipeptidyl Peptidase 3

Radix Dipsaci extract protects against Rosiglitazone induced bone loss

2021 ◽  
Vol 8 (9) ◽  
pp. 15-21
Author(s):  
Khalid A Asseri ◽  
◽  
Yahya I Asiri ◽  
Ali Alqahtani ◽  
Krishnaraju Venkatesan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Bone Loss ◽  
Bone Fractures ◽  
Scientific Evidence ◽  
Streptozotocin Diabetes ◽  
Diabetic Control ◽  
Albino Rats ◽  
Protective Effects ◽  
Diabetes Group ◽  
Diabetic Osteoporosis

The dried root of Dipsacus asperoides is known as Radix Dipsaci extract(RDE). It's a kidney-toning herbal medication with a lengthy track record of safe usage in the treatment of bone fractures and joint disorders. The drug rosiglitazone (RSG) causes an imbalance in bone remodelling, which results in increased apoptotic death of osteogenic cells and decreased bone production. The goal of this study was to investigate the effects of RDE on RSGinduced bone loss in diabetic rats in a systematic way. Five groups of six Wistar albino rats were studied: control (vehicle therapy), Streptozotocin (diabetes) group, RDE group, Rosiglitazone, and Rosiglitazone +RDE group. Insulin, oxidative stress, and bone turnover markers in the blood were all detected using ELISA tests. When compared to diabetic control rats, RDE therapy significantly raised insulin and osteocalcin levels. RDE may be able to prevent diabetic osteoporosis by boosting osteogenesis and lowering oxidative stress in the bone.These findings support the use of RDE as a bone loss inhibiting in diabetics. Well-designed clinical trials are likely to yield further scientific evidence on its bone-protective effects and safety. Keywords: Radix Dipsaci, Diabetic osteoporosis, Rosiglitazone.

scholarly journals Effect of Dipeptidyl-Peptidase 4 Inhibitors on Circulating Oxidative Stress Biomarkers in Patients with Type 2 Diabetes Mellitus

Antioxidants ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 233
Author(s):  
Elisabetta Bigagli ◽  
Cristina Luceri ◽  
Ilaria Dicembrini ◽  
Lorenzo Tatti ◽  
Francesca Scavone ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Propensity Score ◽  
Oxidative Damage ◽  
Dipeptidyl Peptidase ◽  
Dipeptidyl Peptidase 4 ◽  
Dipeptidyl Peptidase 4 Inhibitors

Pre-clinical studies suggested potential cardiovascular benefits of dipeptidyl peptidase-4 inhibitors (DPP4i), however, clinical trials showed neither beneficial nor detrimental effects in patients with type 2 diabetes mellitus (T2DM). We examined the effects of DPP4i on several circulating oxidative stress markers in a cohort of 32 T2DM patients (21 males and 11 post-menopausal females), who were already on routine antidiabetic treatment. Propensity score matching was used to adjust demographic and clinical characteristics between patients who received and who did not receive DPP4i. Whole-blood reactive oxygen species (ROS), plasma advanced glycation end products (AGEs), advanced oxidation protein products (AOPP), carbonyl residues, as well as ferric reducing ability of plasma (FRAP) and leukocyte DNA oxidative damage (Fpg sites), were evaluated. With the exception of Fpg sites, that showed a borderline increase in DPP4i users compared to non-users (p = 0.0507), none of the biomarkers measured was affected by DPP4i treatment. An inverse correlation between estimated glomerular filtration rate and AGEs (p < 0.0001) and Fpg sites (p < 0.05) was also observed. This study does not show any major effect of DPP4i on oxidative stress, assessed by several circulating biomarkers of oxidative damage, in propensity score-matched cohorts of T2DM patients.

HIGH GLUCOSE INDUCED BONE LOSS VIA ATTENUATING THE PROLIFERATION AND OSTEOBLASTOGENESIS AND ENHANCING ADIPOGENESIS OF BONE MARROW MESENCHYMAL STEM CELLS

2013 ◽  
Vol 25 (05) ◽  
pp. 1340010 ◽  
Author(s):  
Wen-Tyng Li ◽  
Wen-Kai Hu ◽  
Feng-Ming Ho
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Bone Loss ◽  
High Glucose ◽  
Chromatin Condensation ◽  
Diabetic Rats ◽  
Peroxisome Proliferator ◽  
Bone Marrow Mscs

Diabetes mellitus (DM) is associated with bone loss and leads to osteopenia and osteoporosis. This study was undertaken to investigate whether the impaired functions of mesenchymal stem cells (MSCs) derived from bone marrow play a role in pathogenesis of DM-associated bone loss. Bone marrow MSCs were taken from the alloxan-induced diabetic rats and normal rats. Bone mineral densities of tibias and femurs in diabetic rats decreased compared to those of normal rats as shown by dual energy X-ray absorptiometry. MSCs from diabetic rats exhibited reduced colony formation activity. The in vitro effects of high glucose (HG) (20 or 33 mM) on the growth, oxidative stress, apoptosis, and differentiation MSCs were next assessed. The viability and proliferation of MSCs derived from diabetic rats decreased significantly compared with that from normal rats. HG further suppressed the proliferation and viability of MSCs from both diabetic and normal rats. HG was associated with 38–40% increase in reactive oxygen species level and had significantly downregulated the activities of superoxide dismutase (SOD) and catalase (CAT) which could be recovered by the addition of L-ascorbic acid. The phenomena of apoptosis such as chromatin condensation and DNA fragmentation were found in cells cultured under HG conditions. As compared with 5.5 mM glucose, exposure of MSCs to HG enhanced adipogenic induction of triacylglycerol accumulation and inhibited osteogenic induction of alkaline phosphatase activity. HG increased peroxisome proliferator-activated receptor gamma expression during adipogenesis and reduced RUNX2 expression during osteoblastogenesis. These results indicate that MSCs derived from diabetic rats exhibited the inhibitory effects on cell growth and osteogenic ability. The oxidative stress, apoptosis, and adipogenic capability of MSCs were increased by HG. Furthermore, it is suggested that HG induces bone loss via attenuating the proliferation and osteoblastogenesis and enhancing adipogenesis mediated by the oxidative stress in rat bone marrow MSCs.

MnTBAP inhibits bone loss in ovariectomized rats by reducing mitochondrial oxidative stress in osteoblasts

2019 ◽  
Vol 38 (1) ◽  
pp. 27-37 ◽  
Author(s):  
Xiangchang Cao ◽  
Deqing Luo ◽  
Teng Li ◽  
Zunxian Huang ◽  
Weitao Zou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Bone Loss ◽  
Ovariectomized Rats ◽  
Mitochondrial Oxidative Stress

Functional tyrosine residue in the active center of human dipeptidyl peptidase III

2008 ◽  
Vol 389 (2) ◽  
pp. 163-167 ◽  
Author(s):  
Branka Salopek-Sondi ◽  
Bojana Vukelić ◽  
Jasminka Špoljarić ◽  
Šumski Šimaga ◽  
Dušica Vujaklija ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Transition State ◽  
Active Site ◽  
Functional Role ◽  
Dipeptidyl Peptidase ◽  
Site Directed Mutagenesis ◽  
Directed Mutagenesis ◽  
Tyrosine Residue ◽  
Transition State Stabilization ◽  
Endogenous Defense

Abstract Human dipeptidyl peptidase III (DPP III) is a member of the metallopeptidase family M49 with an implied role in the pain-modulatory system and endogenous defense against oxidative stress. Here, we report the heterologous expression of human DPP III and the site-directed mutagenesis results which demonstrate a functional role for Tyr318 at the active site of this enzyme. The substitution of Tyr318 to Phe decreased k cat by two orders of magnitude without altering the binding affinity of substrate, or of a competitive hydroxamate inhibitor designed to interact with S1 and S2 subsites. The results indicate that the conserved tyrosine could be involved in transition state stabilization during the catalytic action of M49 peptidases.

scholarly journals Identification of dipeptidyl peptidase 3 as the Angiotensin-(1–7) degrading peptidase in human HK-2 renal epithelial cells

Peptides ◽  
2016 ◽  
Vol 83 ◽  
pp. 29-37 ◽  
Author(s):  
Nildris Cruz-Diaz ◽  
Bryan A. Wilson ◽  
Nancy T. Pirro ◽  
K. Bridget Brosnihan ◽  
Allyson C. Marshall ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Dipeptidyl Peptidase ◽  
Renal Epithelial Cells ◽  
Dipeptidyl Peptidase 3

scholarly journals Stemodia maritima L. Extract Decreases Inflammation, Oxidative Stress, and Alveolar Bone Loss in an Experimental Periodontitis Rat Model

2017 ◽  
Vol 8 ◽  
Author(s):  
Alrieta H. Teixeira ◽  
Jordânia M. de Oliveira Freire ◽  
Luzia H. T. de Sousa ◽  
Antônia T. Parente ◽  
Nayara A. de Sousa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Bone Loss ◽  
Rat Model ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Experimental Periodontitis

scholarly journals Oxidative stress and gamma radiation-induced cancellous bone loss with musculoskeletal disuse

2010 ◽  
Vol 108 (1) ◽  
pp. 152-161 ◽  
Author(s):  
Hisataka Kondo ◽  
Kenji Yumoto ◽  
Joshua S. Alwood ◽  
Rose Mojarrab ◽  
Angela Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Bone Loss ◽  
Gamma Irradiation ◽  
Cancellous Bone ◽  
Lipoic Acid ◽  
Lumbar Vertebrae ◽  
Hindlimb Unloading ◽  
Oxygen Species ◽  
Radiation Induced

Exposure of astronauts in space to radiation during weightlessness may contribute to subsequent bone loss. Gamma irradiation of postpubertal mice rapidly increases the number of bone-resorbing osteoclasts and causes bone loss in cancellous tissue; similar changes occur in skeletal diseases associated with oxidative stress. Therefore, we hypothesized that increased oxidative stress mediates radiation-induced bone loss and that musculoskeletal disuse changes the sensitivity of cancellous tissue to radiation exposure. Musculoskeletal disuse by hindlimb unloading (1 or 2 wk) or total body gamma irradiation (1 or 2 Gy of 137Cs) of 4-mo-old, male C57BL/6 mice each decreased cancellous bone volume fraction in the proximal tibiae and lumbar vertebrae. The extent of radiation-induced acute cancellous bone loss in tibiae and lumbar vertebrae was similar in normally loaded and hindlimb-unloaded mice. Similarly, osteoclast surface in the tibiae increased 46% as a result of irradiation, 47% as a result of hindlimb unloading, and 64% as a result of irradiation + hindlimb unloading compared with normally loaded mice. Irradiation, but not hindlimb unloading, reduced viability and increased apoptosis of marrow cells and caused oxidative damage to lipids within mineralized tissue. Irradiation also stimulated generation of reactive oxygen species in marrow cells. Furthermore, injection of α-lipoic acid, an antioxidant, mitigated the acute bone loss caused by irradiation. Together, these results showed that disuse and gamma irradiation, alone or in combination, caused a similar degree of acute cancellous bone loss and shared a common cellular mechanism of increased bone resorption. Furthermore, irradiation, but not disuse, may increase the number of osteoclasts and the extent of acute bone loss via increased reactive oxygen species production and ensuing oxidative damage, implying different molecular mechanisms. The finding that α-lipoic acid protected cancellous tissue from the detrimental effects of irradiation has potential relevance to astronauts and radiotherapy patients.

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