Comparative Improvement in Function of Isolated Rat Langerhans Islets by Various Phosphodiesterase 3, 4 and 5 Inhibitors

Mohammadi, Mojdeh; Atashpour, Shekoufeh; Pourkhalil, Nazila; Nili-Ahmad, A.; Baeeri, Maryam; Mohammadir, Azadeh; Hassani, Shokoufeh; Nikfar, Shekoufeh; Abdollahi, Mohammad

doi:10.3923/ajava.2011.1233.1240

Cited by 22 publications

(8 citation statements)

References 17 publications

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“…2 To overwhelm oxidative stress during islet transplantation, various antioxidants like vitamin supplements, trace elements and drugs have been widely examined. 2 –4 On the basis of evidences, we recently hypothesized that the combination of cerium oxide (CeO 2 ) and yttrium oxide (Y 2 O 3 ) nanoparticles with a potential free radical scavenger behavior should be useful to make isolated islets survive until transplanted. 5 Therefore, in the present work, we studied the protective effects of this combination in isolated islets by measuring the biomarkers involved in the survival of islets in an ex vivo model.…”

Section: Introductionmentioning

confidence: 99%

Antiapoptotic effects of cerium oxide and yttrium oxide nanoparticles in isolated rat pancreatic islets

et al. 2013

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Type I diabetes mellitus is a metabolic disease caused by the impairment of pancreatic β-cells mainly mediated through oxidative stress and related apoptosis. Islets transplantation seems a promising treatment for these patients, but during islets transplant, various types of stresses related to the isolation and transplantation procedure compromise the function and viability of islets. We recently hypothesized that the combination of cerium oxide (CeO2) and yttrium oxide (Y2O3) nanoparticles with a potential free radical scavenger behavior should be useful to make isolated islets survive until transplanted. In the present study, oxidative stress-induced apoptosis in isolated rat pancreatic islets exposed to hydrogen peroxide (H2O2) and the protective effects of CeO2 and Y2O3 nanoparticles were investigated. Exposure of islets to H2O2 (50 µm, 2 h) increased intracellular oxidant formation such as reactive oxygen species and subsequently apoptosis and decreased viability, glucose-induced adenosine triphosphate (ATP) production and glucose-stimulated insulin secretion. Pretreatment with CeO2 and/or Y2O3 nanoparticles reduced the oxidant formation and apoptosis and increased viability, glucose-induced ATP production and glucose-stimulated insulin secretion. These results suggest that this combination may protect β-cell apoptosis by improving the oxidative stress-mediated apoptotic pathway.

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Section: Introductionmentioning

confidence: 99%

Antiapoptotic effects of cerium oxide and yttrium oxide nanoparticles in isolated rat pancreatic islets

et al. 2013

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“…[ 51 ] In this regard, free radicals lead to LPO and produce active aldehydes such as malondialdehyde. [ 52 ] These by‐products are used as diagnostic biomarkers to assess the severity of oxidative damage. [ 53 ] In the current study, the administration of PQ significantly increased the LPO level and decreased the antioxidant capacity of the lung tissue, confirming the findings of Hosseini et al [ 5 ] and Gohari‐Piran et al [ 54 ] It appears that the quaternary nitrogens in the molecular structure of PQ and their interference with the electron transfer cycle of cells are responsible for the formation of free radicals and subsequently lipid and protein oxidation.…”

Section: Discussionmentioning

confidence: 99%

Chlorogenic acid protective effects on paraquat‐induced pulmonary oxidative damage and fibrosis in rats

Larki‐Harchegani

Fayazbakhsh

Nourian

et al. 2023

J Biochem & Molecular Tox

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Paraquat (PQ) is a widely used herbicide that can cause severe oxidative and fibrotic injuries in lung tissue. Due to the antioxidant and anti-inflammatory properties of chlorogenic acid (CGA), the present study investigated its effects on PQ-induced pulmonary toxicity. To this end, 30 male rats were randomly categorized into five groups of six. Initially, the first and third groups were treated intraperitoneally (IP) with normal saline and CGA (80 mg/kg) for 28 consecutive days, respectively.The second, fourth, and fifth groups were treated with normal saline and 20 and 80 mg/kg of CGA for 28 consecutive days, respectively, and received a single dose of PQ (IP, 20 mg/kg) on Day 7. Then, the animals were anesthetized with ketamine and xylazine, and lung tissue samples were collected for biochemical and histological examinations. The results showed that PQ significantly increased hydroxyproline (HP) and lipid peroxidation (LPO) and decreased the lung tissue antioxidant capacity.In addition, myeloperoxidase (MPO) activity increased significantly, while glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD) activity declined substantially. The administration of therapeutic doses of CGA could prevent the oxidative, fibrotic, and inflammatory effects of PQ-induced lung toxicity, and these changes were consistent with histological observations. In conclusion, CGA may improve the antioxidant defense of lung tissue and prevent the spread of inflammation and the development of PQ-induced fibrotic injuries by enhancing antioxidant enzymes and preventing inflammatory cell infiltration.

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“…In recent years, the antioxidant and anti-inflammatory properties of phosphodiesterase inhibitors have been considered in several studies [ 10 – 12 ]. For instance, Mohammadi et al (2011) showed that selective phosphodiesterase inhibitors could increase survival of Langerhans islets by preventing free radical formation [ 13 ]. Moreover, sildenafil, as phosphodiesterase 5-selective inhibitor, can have beneficial role in improvement of toxicities caused via cadmium [ 14 ] and lead acetate [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

Pentoxifylline Attenuates Arsenic Trioxide‐Induced Cardiac Oxidative Damage in Mice

Gholami

Ataei

Ahmadimoghaddam

et al. 2021

Oxidative Medicine and Cellular Longevity

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This study was undertaken to evaluate the therapeutic potential effect of pentoxifylline (PTX) against arsenic trioxide (ATO)-induced cardiac oxidative damage in mice. Thirty-six male albino mice were divided into six groups and treated intraperitoneally with normal saline (group 1), ATO (5 mg/kg; group 2), PTX (100 mg/kg; group 3), and different doses of PTX (25, 50, and 100 mg/kg; groups 4, 5, and 6, respectively) with ATO. After four weeks, the blood sample was collected for biochemical experiments. In addition, cardiac tissue was removed for assessment of oxidative stress markers and histopathological changes (such as hemorrhage, necrosis, infiltration of inflammatory cells, and myocardial degeneration). The findings showed that ATO caused a significant raise in serum biochemical markers such as lactate dehydrogenase (LDH), creatine phosphokinase (CPK) and troponin-I (cTnI), glucose, total cholesterol (TC), and triglyceride (TG) levels. In addition to histopathological changes in cardiac tissue, ATO led to the significant increase in cardiac lipid peroxidation (LPO) and nitric oxide (NO); remarkable decrease in the activity of cardiac antioxidant enzymes such as catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx); and the depletion of the total antioxidant capacity (TAC) and total thiol groups (TTGs). PTX was able to reduce the increased levels of serum cardiac markers (LDH, CPK, cTnI, TC, and TG), cardiac LPO, and improve antioxidant markers (TAC, TTGs, CAT, SOD, and GPx) alongside histopathologic changes. However, no significant changes were observed in elevated serum glucose and cardiac NO levels. In conclusion, the current study showed the potential therapeutic effect of PTX in the prevention of ATO-induced cardiotoxicity via reversing the oxidative stress.

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Comparative Improvement in Function of Isolated Rat Langerhans Islets by Various Phosphodiesterase 3, 4 and 5 Inhibitors

Cited by 22 publications

References 17 publications

Antiapoptotic effects of cerium oxide and yttrium oxide nanoparticles in isolated rat pancreatic islets

Antiapoptotic effects of cerium oxide and yttrium oxide nanoparticles in isolated rat pancreatic islets

Chlorogenic acid protective effects on paraquat‐induced pulmonary oxidative damage and fibrosis in rats

Pentoxifylline Attenuates Arsenic Trioxide‐Induced Cardiac Oxidative Damage in Mice

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