scholarly journals STAT3 and Nrf2 pathways modulate the protective effect of verapamil on lung injury of diabetic rats

2018 ◽  
Vol 52 (4) ◽  
pp. 192-198 ◽  
Author(s):  
Mervat Z. Mohamed ◽  
Heba M. Hafez ◽  
Hanaa H. Mohamed ◽  
Nagwa M. Zenhom
Keyword(s):  
Lung Injury ◽  
Lung Tissue ◽  
Protective Role ◽  
Diabetic Rats ◽  
Lung Damage ◽  
Male Rats ◽  
Channel Blockers ◽  
Inflammatory Infiltration ◽  
Necrosis Factor Alpha ◽  
Factor Alpha

AbstractObjective. We aimed to assess the protective role of verapamil, L-type calcium channel blockers, against early lung damage in diabetic rats. Lung injury has recently been recognized as a consequent complication of diabetes mellitus. Hyperglycemia induces inflammatory changes in lung tissue early in the disease. Methods. Twenty four adult male rats were grouped into control, diabetic, diabetic treated with verapamil, and verapamil control. Streptozotocin (STZ) was used to induce diabetes. Oxidative parameters and antioxidative mechanisms were assessed in lung homogenate. Tumor necrosis factor alpha (TNFα) protein was measured as a pro-inflammatory mediator. Signal transducer and activator of transcription 3 (STAT3) gene expression and nuclear erythroid factor 2 (Nrf2) immunoexpression were screened. Results. The lung showed oxidative damage and inflammatory infiltration in STZ diabetic rats early at 2 weeks. The parameters significantly improved in lung tissue treated with verapamil. Histopathology of the lung tissue confirmed the results. Inhibition of STAT3/TNFα pathway was involved in the protection offered by verapamil. Activation of Nrf2 together with an increasing antioxidant capacity of diabetic lung significantly ameliorates the injury induced by diabetes. Conclusions. Verapamil afforded protection in diabetic lung injury. The protection was mediated by the anti-inflammatory and antioxidant effects of verapamil.

scholarly journals Topiramate Reduces Aortic Cross-Clamping-Induced Lung Injury in Male Rats

2018 ◽  
Vol 61 (4) ◽  
pp. 144-149 ◽  
Author(s):  
Aysel Kurt ◽  
Yildiray Kalkan ◽  
Hasan Turut ◽  
Medine Cumhur Cure ◽  
Levent Tumkaya ◽  
...  
Keyword(s):  
Lung Tissue ◽  
Ischemia Reperfusion ◽  
Lung Damage ◽  
Male Rats ◽  
Albino Rats ◽  
Ros Generation ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Ros Formation ◽  
Wistar Albino Rats

Background: Topiramate (TPM) decreases cytokine release and generation of reactive oxygen species (ROS). Cytokine and endothelin-1 (ET-1) secretion and ROS formation play an important role in ischemia-reperfusion (I/R) injury. We aimed to evaluate whether TPM prevents damage occurring in lung tissue during I/R. Materials and Methods: A total of 27 Wistar albino rats were divided into three groups of nine. To the I/R group, two hours of ischemia via infrarenal abdominal aorta cross-ligation and then two hours of reperfusion process were applied. TPM (100 mg/kg/day) orally for seven days was administered in the TPM treatment group. After the last dose of TPM treatment, respectively, two hours of ischemia and two hours of reperfusion were applied in this group. Results: Tumor necrosis factor-alpha (TNF-α) (p < 0.05), malondialdehyde (MDA) (p < 0.05), myeloperoxidase (MPO) (p < 0.05) and ET-1 (p < 0.05) levels of TPM treatment group’s lung tissue were significantly lower than for the I/R group. Caspase-3 and histopathological damage were rather lower than that of the I/R group. Conclusions: During I/R, lung damage occurs due to excessive TNF-α and ET-1 release and ROS generation. TPM could well reduce development of lung damage by decreasing cytokine and ET-1 release and levels of ROS produced.

scholarly journals Antioxidant Potential ofSpirulina platensisMitigates Oxidative Stress and Reprotoxicity Induced by Sodium Arsenite in Male Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Samir A. E. Bashandy ◽  
Sally A. El Awdan ◽  
Hossam Ebaid ◽  
Ibrahim M. Alhazza
Keyword(s):  
Oxidative Stress ◽  
Sperm Count ◽  
Therapeutic Option ◽  
Testicular Tissue ◽  
Protective Role ◽  
Male Rats ◽  
Plasma Testosterone ◽  
Necrosis Factor Alpha ◽  
Sperm Abnormalities ◽  
Factor Alpha

The present study aimed to examine the protective role ofSpirulina platensis(S. platensis) against arsenic-induced testicular oxidative damage in rats. Arsenic (in the form of NaAsO2at a dose of 6.3 mg/kg body weight for 8 weeks) caused a significant accumulation of arsenic in testicular tissues as well as a decrease in the levels of testicular superoxide dismutase (SOD), catalase (CAT), reduced glutathione, and zinc. Moreover, it significantly decreased plasma testosterone, luteinizing hormone (LH), triiodothyronine (T3), and thyroxine (T4) levels and reduced sperm motility and sperm count. Arsenic (AS) led to a significant increase in testicular malondialdehyde (MDA), tumour necrosis factor alpha (TNF-α), nitric oxide (NO), and sperm abnormalities.S. platensisat a dose of 300 mg/kg was found to attenuate As-induced oxidative stress, testicular damage, and sperm abnormalities by its potent antioxidant activity.S. platensismay represent a potential therapeutic option to protect the testicular tissue from arsenic intoxication.

Class B Scavenger Receptors BI and BII Protect Against LPS-induced Acute Lung Injury in Mice by Mediating LPS Clearance

2021 ◽  
Author(s):  
Irina N. Baranova ◽  
Alexander V. Bocharov ◽  
Tatyana G. Vishnyakova ◽  
Zhigang Chen ◽  
Anna A. Birukova ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Transgenic Mice ◽  
Neutrophil Infiltration ◽  
Lavage Fluid ◽  
Protective Role ◽  
Lung Damage ◽  
Wild Type ◽  
Class B ◽  
Anti Inflammatory

Recent studies suggest an anti-inflammatory protective role for class B scavenger receptor BI (SR-BI) in endotoxin-induced inflammation and sepsis. Other data, including ours, provide evidence for an alternative role of SR-BI, facilitating bacterial and endotoxin uptake, and contributing to inflammation and bacterial infection. Enhanced endotoxin susceptibility of SR-BI deficient mice due to their anti-inflammatory glucocorticoid deficiency complicates understanding SR-BI’s role in endotoxemia/sepsis, calling for use of alternative models. In this study, using hSR-BI and hSR-BII transgenic mice, we found that SR-BI and to a lesser extent its splicing variant SR-BII, protects against LPS-induced lung damage. At 20 hours after intratracheal LPS instillation the extent of pulmonary inflammation and vascular leakage was significantly lower in hSR-BI and hSR-BII transgenic mice compared to wild type mice. Higher bronchoalveolar lavage fluid (BALF) inflammatory cell count and protein content as well as lung tissue neutrophil infiltration found in wild type mice was associated with markedly (2-3 times) increased pro-inflammatory cytokine production as compared to transgenic mice following LPS administration. Markedly lower endotoxin levels detected in BALF of transgenic vs. wild type mice along with the significantly increased BODIPY-LPS uptake observed in lungs of hSR-BI and hSR-BII mice 20 hours after the IT LPS injection suggest that hSR-BI and hSR-BII-mediated enhanced LPS clearance in the airways could represent the mechanism of their protective role against LPS-induced acute lung injury.

scholarly journals The Effect of Induced Diabetes Mellitus on the Cerebellar Cortex of Adult Male Rat and the Possible Protective Role of Oxymatrine: A Histological, Immunohistochemical and Biochemical Study

2021 ◽  
Author(s):  
Amany Mohamed Shalaby ◽  
Adel Mohamed Aboregela ◽  
Mohamed Ali Alabiad ◽  
Mona Tayssir Sadek
Keyword(s):  
Diabetes Mellitus ◽  
Purkinje Cells ◽  
Cerebellar Cortex ◽  
Adult Male ◽  
Protective Role ◽  
Diabetic Rats ◽  
Male Rats ◽  
Group I ◽  
Group Ii

Abstract Diabetes mellitus (DM) represents a widespread metabolic disease with a well-known neurotoxicity in both central and peripheral nervous systems. Oxymatrine is a traditional Chinese herbal medicine that has various pharmacological activities including; anti-oxidant, anti-apoptotic and anti-inflammatory potentials. The present work aimed to study the impact of diabetes mellitus on the cerebellar cortex of adult male albino rat and to evaluate the potential protective role of oxymatrine using different histological methods. Fifty-five adult male rats were randomly divided into three groups: group I served as control, group II was given oxymatrine (80 mg/kg/day) orally for 8 weeks and group III was given a single dose of streptozotocin (50mg/kg) intaperitoneally to induce diabetes. Then diabetic rats were subdivided into two subgroups: subgroup IIIa that received no additional treatment and subgroup IIIb that received oxymatrine similar to group II. The diabetic group revealed numerous changes in the Purkinje cell layer in the form of multilayer arrangement of Purkinje cells, shrunken cells with deeply stained nuclei as well as focal loss of the Purkinje cells. A significant increment in GFAP and synaptophysin expression was reported. Transmission electron microscopy showed irregularity and splitting of myelin sheaths in the molecular layer, dark shrunken Purkinje cells with ill-defined nuclei, dilated Golgi saccules and dense granule cells with irregular nuclear outlines in the granular layer. In contrast, these changes were less evident in diabetic rats that received oxymatrine. In conclusion, Oxymatrine could protect the cerebellar cortex against changes induced by DM.

A Free Radical Scavenger (Lazaroid U75412E) Attenuates Tumor Necrosis Factor-Alpha Generation in a Rabbit Model of Smoke-Induced Lung Injury

Respiration ◽  
1997 ◽  
Vol 64 (5) ◽  
pp. 358-363 ◽  
Author(s):  
Shengjun Wang ◽  
Clark Lantz ◽  
Evelyn D. Rider ◽  
Guan Jie Chen ◽  
Veronica Breceda ◽  
...  
Keyword(s):  
Free Radical ◽  
Tumor Necrosis Factor ◽  
Lung Injury ◽  
Tumor Necrosis ◽  
Rabbit Model ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

Tumor Necrosis Factor: Alpha and Beta Subtypes Appear in Circulation during Onset of Sepsis-induced Lung Injury

1991 ◽  
Vol 143 (5_pt_1) ◽  
pp. 1076-1082 ◽  
Author(s):  
Sandra K. Leeper-Woodford ◽  
P. Declan Carey ◽  
Karl Byrne ◽  
John K. Jenkins ◽  
Bernard J. Fisher ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Lung Injury ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

scholarly journals Transcriptional Profiling of Lipopolysaccharide-Induced Acute Lung Injury

2004 ◽  
Vol 72 (12) ◽  
pp. 7247-7256 ◽  
Author(s):  
Samithamby Jeyaseelan ◽  
Hong Wei Chu ◽  
Scott K. Young ◽  
G. Scott Worthen
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Transcriptional Profiling ◽  
Lung Damage ◽  
Neutrophil Accumulation ◽  
Transcriptional Responses ◽  
Necrosis Factor Alpha ◽  
Neutrophil Influx ◽  
Inflammatory Genes ◽  
Proinflammatory Mediators

ABSTRACT Mortality associated with acute lung injury (ALI) induced by lipopolysaccharide (LPS) remains high in humans, warranting improved treatment and prevention strategies. ALI is characterized by the expression of proinflammatory mediators and extensive neutrophil influx into the lung, followed by severe lung damage. Understanding the pathogenesis of LPS-induced ALI is a prerequisite for designing better therapeutic strategies. In the present study, we used microarrays to gain a global view of the transcriptional responses of the lung to LPS in a mouse model of ALI that mimics ALI in humans. A total of 71 inflammation-associated genes were up-regulated in LPS-treated lungs, including a chemokine, LPS-induced CXC chemokine (LIX), whose role in the induction of ALI is unknown. Most of the inflammatory genes peaked at 2 h post-LPS treatment. Real-time reverse transcription-PCR confirmed the LPS-induced up-regulation of selected genes identified by microarray analysis, including LIX. The up-regulation of LIX, tumor necrosis factor alpha, and macrophage inflammatory protein 2 was confirmed at the protein level by enzyme-linked immunosorbent assays. To determine the role of LIX in the induction of ALI, we used both exogenous LIX and a LIX blocking antibody. Exogenous LIX alone elicited a neutrophil influx in the lungs, and the anti-LIX antibody attenuated the LPS-induced neutrophil accumulation in the lungs. Taken together, the results of our study demonstrate for the first time the temporal expression of inflammatory genes during LPS-induced ALI and suggest that early therapeutic intervention is crucial to attenuate lung damage. Moreover, we identified a role for LIX in the induction of ALI, and therefore LIX may serve as a novel therapeutic target for the minimization of ALI.

scholarly journals Oat Attenuation of Hyperglycemia-Induced Retinal Oxidative Stress and NF-B Activation in Streptozotocin-Induced Diabetic Rats

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Abdulrahman L. Al-Malki
Keyword(s):  
Oxidative Stress ◽  
Diabetic Retinopathy ◽  
Protective Role ◽  
Endothelial Damage ◽  
Diabetic Rats ◽  
Albino Rats ◽  
Mobility Shift ◽  
Microvascular Damage ◽  
Necrosis Factor Alpha ◽  
Diabetic Retina

The overproduction of reactive oxygen species (ROS) plays a central role in the pathogenesis of endothelial damage in diabetes. To assess the effect of oat on experimental diabetic retinopathy, five groups of Albino rats were studied: nondiabetic control, untreated diabetic, and diabetic rats treated with 5%, 10%, and 20% (W/W) oat of the diet for 12 weeks. Novel data were obtained in this study indicating a protective role of oat against oxidative stress and diabetic retinopathy. The effects of oat on parameters of oxidative stress, AGE, and nuclear factor kappa B (NF-B) were assessed by ELISA and NF-B activation by electrophoretic mobility shift assay. Tumor necrosis factor alpha (TNF) and vascular endothelial growth factor (VEGF) were also determined. After 12 weeks of diabetes, oat treatment reduced blood glucose levels, HbA1c, all oxidative stress markers, CML, normalized NF-B activation and TNF expression. Furthermore it reduced VEGF in the diabetic retina by 43% (). In conclusion, oat modulates microvascular damage through normalized pathways downstream of ROS overproduction and reduction of NF-B and its controlled genes activation, which may provide additional endothelial protection.

Sign in / Sign up

Export Citation Format

Share Document