scholarly journals Peroxisomes in disease.

1979 ◽  
Vol 27 (10) ◽  
pp. 1371-1373 ◽  
Author(s):  
S Goldfischer
Keyword(s):  
Mitochondrial Respiration ◽  
Metabolic Disorders ◽  
Morphological Changes ◽  
Oxygen Toxicity ◽  
Experimental Models ◽  
Alcoholic Cardiomyopathy ◽  
Widespread Distribution ◽  
Models Of Disease

Cytochemical, biochemical and morphological changes in peroxisomes have been described in human metabolic disorders, in experimental models of disease and in response to drugs and toxins. These include the cerebrohepatorenal syndromes, in which peroxisomes can not be detected and mitochondrial respiration is inhibited, atherosclerosis, alcoholic cardiomyopathy, and tolerance to oxygen toxicity. Although information on the role of peroxisomes in disease is limited, increased awareness of their widespread distribution and the availability of an improved cytochemical procedure for staining peroxisomes in human specimens should provide new insights into their function.

scholarly journals Herbal Medicines for the Treatment of Nonalcoholic Steatohepatitis: Current Scenario and Future Prospects

2014 ◽  
Vol 2014 ◽  
pp. 1-18 ◽  
Author(s):  
Ravirajsinh Jadeja ◽  
Ranjitsinh V. Devkar ◽  
Srinivas Nammi
Keyword(s):  
Nonalcoholic Steatohepatitis ◽  
Metabolic Disorders ◽  
Therapeutic Potential ◽  
Current Knowledge ◽  
Herbal Medicines ◽  
Experimental Models ◽  
Treatment Schedule ◽  
Herbal Extracts ◽  
Current Scenario

Nonalcoholic steatohepatitis (NASH) is a multifactorial disease and has close correlations with other metabolic disorders. This makes its treatment difficult using a single pharmacological drug. Use of plant extract/decoction or polyherbal formulation to treat various liver diseases is very well mentioned in various traditional systems of medicine (Ayurveda, Japanese or traditional Chinese Medicine, and Kampo medicine). Medicinal herbs are known for their multifaceted implications and thus can form an effective treatment schedule against NASH. Till date, several plant extracts, polyherbal formulations, and phytochemicals have been evaluated for their possible therapeutic potential in preventing onset and progression of NASH in experimental models, but clinical studies using the same are sparse. Herbal extracts with antioxidants, antidiabetic, and antihyperlipidemic properties have been shown to ameliorate symptoms of NASH. This review article is a meticulous compilation of our current knowledge on the role of natural products in alleviating NASH and possible lacunae in research that needs to be addressed.

Abstract 391: Endogenous Drp1 Modulates Cardiac Respiration Through mPTP and Independent of Fission

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Huiliang Zhang ◽  
Sara Bisetto ◽  
Shey-Shing Sheu ◽  
Wang Wang
Keyword(s):  
Mitochondrial Respiration ◽  
Morphological Changes ◽  
Regulation Of Respiration ◽  
Dominant Negative Mutant ◽  
Mitochondrial Morphology ◽  
Mouse Heart ◽  
Rat Cardiomyocytes ◽  
Adult Cardiomyocytes ◽  
Mitochondrial Ros

Background: The cardiac mitochondria exhibit a stable morphology with a rather low level of dynamic changes. However, fission and fusion proteins, such as dynamin-related protein 1 (DRP1) are abundant in the heart. Whether these proteins bear other functions in the heart than mitochondrial dynamics regulation are largely unknown. We hypothesize that endogenous DRP1 in the heart regulates mitochondrial respiration independent of fission. Methods: Mitochondrial respiration was determined by measuring the OCR with Seahorse assay or Clark type electrode in adult rat cardiomyocytes or mitochondria isolated from adult mouse heart. Confocal imaging was used to quantify mitochondrial morphology in adult cardiomyocytes and H9C2 myoblasts. To evaluate the role of mitochondrial permeability transition pore (mPTP), we monitored superoxide flashes (SOF) and laser-induced mPTP openings, and used cyclophilin D knockout mice (CypD KO). Mitochondrial ROS and Ca2+ were also monitored. Results: Inhibiting the DRP1 GTPase activity by Mdivi-1 or overexpression of the dominant-negative mutant (DRP1-K38A) induced mild mitochondrial morphological changes in adult cardiomyocytes, and inhibited mitochondrial respiration. Modulation of fission/fusion by overexpressing DRP1 or treating cells with S3, a compound facilitates fusion, exhibited significant morphological changes, but failed to influence respiration. Therefore, endogenous DRP1 activity may regulate respiration in the heart and this effect is dissociated with morphological changes. Further, inhibiting DRP1 activity attenuated the frequency of SOF, indicating decreased transient mPTP openings, delayed laser-induced permanent mPTP opening, and increased mitochondrial Ca2+. Inhibiting DRP1 activity decreased mitochondrial ROS levels. The role of DRP1 inhibition on respiration absents in CypD KO myocytes, suggesting the involvement of mPTP in the modulation of respiration by endogenous DRP1. Conclusion: These results suggest that endogenous DRP1 positively regulates respiration in the heart. This effect is likely independent of its role in mitochondrial fission. DRP1 regulation of respiration may involve transient opening of mPTP and contribute to mitochondrial Ca2+ and ROS signaling.

scholarly journals Experimental models of stress

2006 ◽  
Vol 8 (4) ◽  
pp. 417-432 ◽  
Keyword(s):  
Stress Response ◽  
Experimental Models ◽  
Comprehensive Analysis ◽  
Laboratory Animals ◽  
Stress Induction ◽  
Key Features ◽  
Models Of Disease

Illustrating the complexity of the stress response and its multifaceted manifestations is the leading idea of this overview of experimental paradigms used for stress induction in laboratory animals. The description of key features of models based on naturalistic stressors, pharmacological challenges, and genomic manipulations is complemented by comprehensive analysis of physiological, behavioral, neurochemical, and endocrine changes and their appropriateness as outcome readouts. Particular attention has been paid to the role of sex and age as determinants of the dynamics of the stress response. Possible translational applications of stress-inducing paradigms as models of disease are briefly sketched.

scholarly journals Neuronal morphology alterations in autism and possible role of oxytocin

2019 ◽  
Vol 53 (1) ◽  
pp. 46-54 ◽  
Author(s):  
Hisham El Falougy ◽  
Barbora Filova ◽  
Daniela Ostatnikova ◽  
Zuzana Bacova ◽  
Jan Bakos
Keyword(s):  
Morphological Changes ◽  
Autism Spectrum ◽  
Experimental Models ◽  
Cellular Level ◽  
Neuronal Morphology ◽  
Imaging Data ◽  
Brain Areas ◽  
Microstructural Alterations ◽  
Associated Proteins

AbstractCurrent understanding of the neuroanatomical abnormalities in autism includes gross anatomical changes in several brain areas and microstructural alterations in neuronal cells as well. There are many controversies in the interpretation of the imaging data, evaluation of volume and size of particular brain areas, and their functional translation into a broad autism phenotype. Critical questions of neuronal pathology in autism include the concept of the reversible plasticity of morphological changes, volume alterations of brain areas, and both short- and long-term consequences of adverse events present during the brain development. At the cellular level, remodeling of the actin cytoskeleton is considered as one of the critical factors associated with the autism spectrum disorders. Alterations in the composition of the neuronal cytoskeleton, in particular abnormalities in the polymerization of actin filaments and their associated proteins underlie the functional consequences in behavior resulting in symptoms and clinical correlates of autism spectrum disorder. In the present review, a special attention is devoted to the role of oxytocin in experimental models of neurodevelopmental disorders manifesting alterations in neuronal morphology.

Clinical, morphological and biochemical signs of polymycotoxicosis in highly productive cows

2020 ◽  
pp. 14-17
Author(s):  
Irina A. Shkuratova ◽  
◽  
Lyudmila I. Drozdova ◽  
Aleksander I. Belousov ◽  
Keyword(s):  
Metabolic Disorders ◽  
Hepatorenal Syndrome ◽  
Morphological Changes ◽  
Clinical Manifestations ◽  
The Body ◽  
Feed Mixture ◽  
Milk Productivity ◽  
Structural Disorders ◽  
Increased Sensitivity ◽  
Penicillium Spp

Mycotoxicological monitoring of forages shows that the problem of mycotoxicosis has been relevant for several decades. Minimal doses of mycotoxins in feed lead to a decrease in milk productivity, increased sensitivity to infectious and non-infectious diseases. When several mycotoxins enter the body simultaneously, a synergistic effect develops, causing a significant increase in toxicity. Feed contaminated with several types of fungi and their toxins is dangerous for dairy cattle. It was found that the feed mixture contained the types of associations of Aspergillus spp. fungi + Fusarium; Aspergillus spp. + Penicillium spp. + Mucor spp; Fusarium + Penicillium; Mucor spp. + Fusarium + Ustilaginales. Pathogenetic features of metabolic and morphological changes in highly productive cows with polymycotoxicosis were studied. Feeding food contaminated with various metabolites of mold fungi leads to the development of signs of chronic toxemia in animals. Clinical manifestations are the development of diarrhea and dehydration, with a decrease in milk productivity. Metabolic disorders feature the development of an inflammatory process, metabolic acidosis, hyperfermentonemia, with an increase in the amount of creatinine and urea in the blood serum. Metabolic signs indicate the development of hepatorenal syndrome due to structural disorders of the liver and kidneys. Histological signs of polymicotoxicosis are intracapillary and hemorrhagic glomerulonephritis, hepatocyte micronecrosis, and proliferation of connective tissue stroma cells, which leads to the development of atrophic cirrhosis in the interstitial and circular phases.

scholarly journals Adipose Tissue Immunomodulation and Treg/Th17 Imbalance in the Impaired Glucose Metabolism of Children with Obesity

Children ◽  
2021 ◽  
Vol 8 (7) ◽  
pp. 554
Author(s):  
Stefania Croce ◽  
Maria Antonietta Avanzini ◽  
Corrado Regalbuto ◽  
Erika Cordaro ◽  
Federica Vinci ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Glucose Metabolism ◽  
Th17 Cells ◽  
Metabolic Disorders ◽  
Potential Role ◽  
Immune Monitoring ◽  
Metabolic Dysfunction ◽  
Impaired Glucose Metabolism ◽  
T Cell Infiltration

In the last few decades, obesity has increased dramatically in pediatric patients. Obesity is a chronic disease correlated with systemic inflammation, characterized by the presence of CD4 and CD8 T cell infiltration and modified immune response, which contributes to the development of obesity related diseases and metabolic disorders, including impaired glucose metabolism. In particular, Treg and Th17 cells are dynamically balanced under healthy conditions, but imbalance occurs in inflammatory and pathological states, such as obesity. Some studies demonstrated that peripheral Treg and Th17 cells exhibit increased imbalance with worsening of glucose metabolic dysfunction, already in children with obesity. In this review, we considered the role of adipose tissue immunomodulation and the potential role played by Treg/T17 imbalance on the impaired glucose metabolism in pediatric obesity. In the patient care, immune monitoring could play an important role to define preventive strategies of pediatric metabolic disease treatments.

scholarly journals Role of endocannabinoid CB1 receptors in Streptozotocin-induced uninephrectomised Wistar rats in diabetic nephropathy

2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Jayarami Reddy Medapati ◽  
Deepthi Rapaka ◽  
Veera Raghavulu Bitra ◽  
Santhosh Kumar Ranajit ◽  
Girija Sankar Guntuku ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Morphological Changes ◽  
Serum Levels ◽  
Cb1 Receptors ◽  
Protective Effects ◽  
Renal Hypertrophy ◽  
Necrosis Factor Alpha

Abstract Background The endocannabinoid CB1 receptor is known to have protective effects in kidney disease. The aim of the present study is to evaluate the potential agonistic and antagonistic actions and to determine the renoprotective potential of CB1 receptors in diabetic nephropathy. The present work investigates the possible role of CB1 receptors in the pathogenesis of diabetes-induced nephropathy. Streptozotocin (STZ) (55 mg/kg, i.p., once) is administered to uninephrectomised rats for induction of experimental diabetes mellitus. The CB1 agonist (oleamide) and CB1 antagonist (AM6545) treatment were initiated in diabetic rats after 1 week of STZ administration and were given for 24 weeks. Results The progress in diabetic nephropathy is estimated biochemically by measuring serum creatinine (1.28±0.03) (p < 0.005), blood urea nitrogen (67.6± 2.10) (p < 0.001), urinary microprotein (74.62± 3.47) (p < 0.005) and urinary albuminuria (28.31±1.17) (p < 0.0001). Renal inflammation was assessed by estimating serum levels of tumor necrosis factor alpha (75.69±1.51) (p < 0.001) and transforming growth factor beta (8.73±0.31) (p < 0.001). Renal morphological changes were assessed by estimating renal hypertrophy (7.38± 0.26) (p < 0.005) and renal collagen content (10.42± 0.48) (p < 0.001). Conclusions From the above findings, it can be said that diabetes-induced nephropathy may be associated with overexpression of CB1 receptors and blockade of CB1 receptors might be beneficial in ameliorating the diabetes-induced nephropathy. Graphical abstract

scholarly journals Exploring the Potential Role of the Gut Microbiome in Chemotherapy-Induced Neurocognitive Disorders and Cardiovascular Toxicity

Cancers ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 782
Author(s):  
Sona Ciernikova ◽  
Michal Mego ◽  
Michal Chovanec
Keyword(s):  
Cardiovascular Diseases ◽  
Cancer Survivors ◽  
Cancer Patients ◽  
Gut Microbiome ◽  
Late Effects ◽  
Fecal Microbiota Transplantation ◽  
Experimental Models ◽  
Neurocognitive Disorders ◽  
Cardiovascular Toxicity

Chemotherapy, targeting not only malignant but also healthy cells, causes many undesirable side effects in cancer patients. Due to this fact, long-term cancer survivors often suffer from late effects, including cognitive impairment and cardiovascular toxicity. Chemotherapy damages the intestinal mucosa and heavily disrupts the gut ecosystem, leading to gastrointestinal toxicity. Animal models and clinical studies have revealed the associations between intestinal dysbiosis and depression, anxiety, pain, impaired cognitive functions, and cardiovascular diseases. Recently, a possible link between chemotherapy-induced gut microbiota disruption and late effects in cancer survivors has been proposed. In this review, we summarize the current understanding of preclinical and clinical findings regarding the emerging role of the microbiome and the microbiota–gut–brain axis in chemotherapy-related late effects affecting the central nervous system (CNS) and heart functions. Importantly, we provide an overview of clinical trials evaluating the relationship between the gut microbiome and cancer survivorship. Moreover, the beneficial effects of probiotics in experimental models and non-cancer patients with neurocognitive disorders and cardiovascular diseases as well as several studies on microbiota modulations via probiotics or fecal microbiota transplantation in cancer patients are discussed.

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