Haem oxygenase-1: a target for dietary antioxidants

2004 ◽  
Vol 32 (6) ◽  
pp. 1003-1005 ◽  
Author(s):  
R.M. Ogborne ◽  
S.A. Rushworth ◽  
C.A. Charalambos ◽  
M.A. O'Connell
Keyword(s):  
Stress Response ◽  
Animal Models ◽  
Vascular Disease ◽  
Cell Types ◽  
Protective Role ◽  
Dietary Therapy ◽  
Protective Effects ◽  
Dietary Antioxidants ◽  
Naturally Occurring ◽  
Haem Oxygenase

HO-1 (haem oxygenase-1) is a stress-response enzyme involved in the catabolism of haem. In animal models, it plays a key protective role in vascular disease. HO-1 has anti-inflammatory effects in macrophages and is induced by a range of stimuli, including antioxidants, in various cell types. As dietary antioxidants are considered to be beneficial in vascular disease, their protective effects may occur through induction of HO-1. Emerging evidence suggests that a range of dietary and other naturally occurring antioxidants stimulate HO-1 expression in various cell types, although regulation by these compounds has not been investigated in detail. These studies suggest that HO-1 may be a target for dietary therapy in vascular disease.

scholarly journals Amniotic fluid stem cells ameliorate cisplatin-induced acute renal failure through induction of autophagy and inhibition of apoptosis

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Ekta Minocha ◽  
Rohit Anthony Sinha ◽  
Manali Jain ◽  
Chandra Prakash Chaturvedi ◽  
Soniya Nityanand
Keyword(s):  
Stem Cells ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Amniotic Fluid ◽  
Cell Types ◽  
Treated Group ◽  
Protective Role ◽  
Protective Effects ◽  
Amniotic Fluid Stem Cells

Abstract Background We have recently demonstrated that amniotic fluid stem cells (AFSC) express renal progenitor markers and can be differentiated in vitro into renal lineage cell types, viz, juxtaglomerular and renal proximal tubular epithelial-like cells. Here, we have evaluated the therapeutic efficacy of AFSC in a cisplatin-induced rat model of acute renal failure (ARF) and investigated the underlying mechanisms responsible for their renoprotective effects. Methods ARF was induced in Wistar rats by intra-peritoneal injection of cisplatin (7 mg/kg). Five days after cisplatin injection, rats were randomized into two groups and injected with either AFSC or normal saline intravenously. On days 8 and 12 after cisplatin injection, the blood biochemical parameters, histopathological changes, apoptosis and expression of pro-apoptotic, anti-apoptotic, and autophagy-related proteins in renal tissues were studied in both groups of rats. To further confirm whether the protective effects of AFSC on cisplatin-induced apoptosis were dependent on autophagy, chloroquine, an autophagy inhibitor, was administered by the intra-peritoneal route. Results Administration of AFSC in ARF rats resulted in improvement of renal function and attenuation of renal damage as reflected by significant decrease in blood urea nitrogen, serum creatinine levels, tubular cell apoptosis as assessed by Bax/Bcl2 ratio, and expression of the pro-apoptotic proteins, viz, PUMA, Bax, cleaved caspase-3, and cleaved caspase-9, as compared to the saline-treated group. Furthermore, in the AFSC-treated group as compared to the saline-treated group, there was a significant increase in the activation of autophagy as evident by increased expression of LC3-II, ATG5, ATG7, Beclin1, and phospho-AMPK levels with a concomitant decrease in phospho-p70S6K and p62 expression levels. Chloroquine administration led to significant reduction in the anti-apoptotic effects of the AFSC therapy and further deterioration in the renal structure and function caused by cisplatin. Conclusion AFSC led to amelioration of cisplatin-induced ARF which was mediated by inhibition of apoptosis and activation of autophagy. The protective effects of AFSC were blunted by chloroquine, an inhibitor of autophagy, highlighting that activation of autophagy is an important mechanism of action for the protective role of AFSC in cisplatin-induced renal injury.

scholarly journals NARINGIN REVEALS AMELIORATIVE PROPERTY OVER ELEVATED OXIDATIVE STRESS LEVELS IN ANIMAL MODELS

2018 ◽  
Vol 11 (12) ◽  
pp. 46
Author(s):  
Zorawar Singh ◽  
Adeshwinder Kaur ◽  
Shivam Sharma
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Animal Models ◽  
Grapefruit Juice ◽  
Cardiac Fibrosis ◽  
Review Paper ◽  
Short Review ◽  
Protective Role ◽  
Naturally Occurring ◽  
Cell Components

Oxidative stress (OxiS) has been implicated in the pathogenesis of many diseases. Free radicals interact with different cell components including DNA, proteins, and lipids to become stable. In this process, these free radicals damage the integrity of these biological moieties and result in various health implications. Naringin (NG), a naturally occurring phytochemical commonly found in grapefruit juice has been explored for its protective role against OxiS. In this short review paper, an attempt has been made to compile the study reports revealing the antioxidative nature of NG in different animal models. Studies have reported NG as a potential antioxidant in various health ailments including diabetes, cardiac fibrosis, cognitive dysfunction, and neurodegeneration.

scholarly journals The novel inosine analogue, INO-2002, protects against diabetes development in multiple low-dose streptozotocin and non-obese diabetic mouse models of type I diabetes

2008 ◽  
Vol 198 (3) ◽  
pp. 581-589 ◽  
Author(s):  
Jon G Mabley ◽  
Pal Pacher ◽  
Kanneganti G K Murthy ◽  
William Williams ◽  
Garry J Southan ◽  
...  
Keyword(s):  
Animal Models ◽  
Type I Diabetes ◽  
Spontaneous Diabetes ◽  
Nod Mice ◽  
Diabetes Incidence ◽  
Type I ◽  
Protective Effects ◽  
Naturally Occurring ◽  
Anti Inflammatory

Endogenous purines including inosine have been shown to exert immunomodulatory and anti-inflammatory effects in a variety of disease models. The dosage of inosine required for protection is very high because of the rapid metabolism of inosine in vivo. The aim of this study was to determine whether a metabolic-resistant purine analogue, INO-2002, exerts anti-inflammatory effects in two animal models of type I diabetes. Type I diabetes was induced chemically with streptozotocin or genetically using the non-obese diabetic (NOD) female mouse model. Mice were treated with INO-2002 or inosine as required at 30, 100, or 200 mg/kg per day, while blood glucose and diabetes incidence were monitored. The effect of INO-2002 on the pancreatic cytokine profile was also determined. INO-2002 reduced both the hyperglycaemia and incidence of diabetes in both streptozotocin-induced and spontaneous diabetes in NOD mice. INO-2002 proved to be more effective in protecting against diabetes than the naturally occurring purine, inosine, when administered at the same dose. INO-2002 treatment decreased pancreatic levels of interleukin (IL)-12 and tumour necrosis factor-α, while increasing levels of IL-4 and IL-10. INO-2002 also reduced pancreatic levels of the chemokine MIP-1α. The inosine analogue, INO-2002, was protected more effectively than the naturally occurring purine, inosine, against development of diabetes in two separate animal models. INO-2002 exerts protective effects by changing the pancreatic cytokine expression from a destructive Th1 to a protective Th2 profile. The use of analogues of inosine such as INO-2002 should be considered as a potential preventative therapy in individuals susceptible to developing type I diabetes.

Haem oxygenase-1 overexpression alters intracellular iron distribution

2012 ◽  
Vol 449 (1) ◽  
pp. 189-194 ◽  
Author(s):  
Lilibeth Lanceta ◽  
Chi Li ◽  
Augustine M. Choi ◽  
John W. Eaton
Keyword(s):  
A549 Cells ◽  
Cell Types ◽  
Receptor Expression ◽  
Protective Effects ◽  
Intracellular Iron ◽  
Ferritin Synthesis ◽  
Redox Active ◽  
Consequent Reduction ◽  
Elevated Expression ◽  
Haem Oxygenase

Induction or ectopic overexpression of HO-1 (haem oxygenase 1) protects against a wide variety of disorders. These protective effects have been variably ascribed to generation of carbon monoxide (released during cleavage of the alpha-methene bridge of haem) and/or to production of the antioxidant bilirubin. We investigated HO-1-overexpressing A549 cells and find that, as expected, HO-1-overexpressing cells are resistant to killing by hydrogen peroxide. Surprisingly, these cells have approximately twice the normal amount of intracellular iron which usually tends to amplify oxidant killing. However, HO-1-overexpressing cells contain only ~25% as much ‘loose’ (probably redox active) iron. Indeed, inhibition of ferritin synthesis [via siRNA (small interfering RNA) directed at the ferritin heavy chain] sensitizes the HO-1-overexpressing cells to peroxide killing. It appears that HO-1 overexpression leads to enhanced destruction of haem, consequent 2–3-fold induction of ferritin, and compensatory increases in transferrin receptor expression and haem synthesis. However, there is no functional haem deficiency because cellular oxygen consumption and catalase activity are similar in both cell types. We conclude that, at least in many cases, the cytoprotective effects of HO-1 induction or forced overexpression may derive from elevated expression of ferritin and consequent reduction of redox active ‘loose’ iron.

Monosodium Glutamate Toxicity and the Possible Protective Role of L–Carnitine

2018 ◽  
Vol 6 (1) ◽  
pp. 45-56
Author(s):  
Lalrinzuali Sailo ◽  
◽  
Meesala Krishna Murthy ◽  
Khandayataray Pratima ◽  
Vikas Kumar Roy ◽  
...  
Keyword(s):  
Human Subjects ◽  
Monosodium Glutamate ◽  
Essential Amino Acids ◽  
Protective Role ◽  
Glutamate Toxicity ◽  
Common Salt ◽  
Genotoxic Effects ◽  
Naturally Occurring ◽  
Flavour Enhancer

Monosodium glutamate is naturally available non-essential amino acids, which found in naturally occurring foods and used as flavour enhancer worldwide. Monosodium glutamate is believed to be linked with diverse health problems. The aim of the study was toxic effects of monosodium glutamate (MSG) and the protective role of L-carnitine, light on the available literature from last 25 years about diverse toxicity studies which had been carried out on animal and human models. Google scholar, NCBI, PUBMED, EMBASE, Wangfang databases, and Web of Science databases were used to retrieve the available studies. MSG was linked with deleterious effects particularly in animals including induction of obesity, diabetes, hepatotoxic, neurotoxic and genotoxic effects showed in Literature. Few reports revealed increased hunger, food intake, and obesity in human subjects due to MSG consumption. Hepatotoxic, neurotoxic, and genotoxic effects of monosodium glutamate on humans carried out very limitedly. High consumption of monosodium glutamate may be linked with harmful health effects showed in available literatures. So, it is recommended to use common salt instead of MSG. Furthermore, intensive research is required to explore monosodium glutamate–related molecular and metabolic mechanisms. L-carnitine can protect from Hepatotoxic, neurotoxic, renal impairment and genotoxic effects functionally, biochemically and histopathologically with a corresponding reduction of oxidative stress.

Compounds from Ilex paraguariensis extracts have antioxidant effects in the brains of rats subjected to chronic immobilization stress

2017 ◽  
Vol 42 (11) ◽  
pp. 1172-1178 ◽  
Author(s):  
Ana C. Colpo ◽  
Maria Eduarda de Lima ◽  
Marisol Maya-López ◽  
Hemerson Rosa ◽  
Cristina Márquez-Curiel ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Immobilization Stress ◽  
Brain Regions ◽  
Protective Role ◽  
Ilex Paraguariensis ◽  
Protective Effects ◽  
Species Formation ◽  
Lipid And Protein Oxidation ◽  
Response To Stress ◽  
Chronic Immobilization Stress

Immobilization induces oxidative damage to the brain. Ilex paraguariensis extracts (Mate) and their major natural compound, chlorogenic acid (CGA), exert protective effects against reactive oxygen species formation. Here, the effects of Mate and CGA on oxidative damage induced by chronic immobilization stress (CIS) in the cortex, hippocampus, and striatum were investigated. For CIS, animals were immobilized for 6 h every day for 21 consecutive days. Rats received Mate or CGA by intragastric gavage 30 min before every restraint session. Endpoints of oxidative stress (levels of lipid peroxidation, protein carbonylation, and reduced (GSH) and oxidized (GSSG) forms of glutathione) were evaluated following CIS. While CIS increased oxidized lipid and carbonyl levels in all brain regions, CGA (and Mate to a lesser extent) attenuated lipid and protein oxidation as compared with control groups. GSH/GSSG balance showed a tendency to increase in all regions in response to stress and antioxidants. Taken together, our results support a protective role of dietary antioxidants against the neuronal consequences of stress.

scholarly journals Heme Oxygenase-1 Deficiency and Oxidative Stress: A Review of 9 Independent Human Cases and Animal Models

2021 ◽  
Vol 22 (4) ◽  
pp. 1514 ◽  
Author(s):  
Akihiro Yachie
Keyword(s):  
Oxidative Stress ◽  
Animal Models ◽  
Heme Oxygenase ◽  
Inflammatory Diseases ◽  
Cell Types ◽  
Pharmacological Intervention ◽  
Heme Oxygenase 1 ◽  
Inflammatory Reactions

Since Yachie et al. reported the first description of human heme oxygenase (HO)-1 deficiency more than 20 years ago, few additional human cases have been reported in the literature. A detailed analysis of the first human case of HO-1 deficiency revealed that HO-1 is involved in the protection of multiple tissues and organs from oxidative stress and excessive inflammatory reactions, through the release of multiple molecules with anti-oxidative stress and anti-inflammatory functions. HO-1 production is induced in vivo within selected cell types, including renal tubular epithelium, hepatic Kupffer cells, vascular endothelium, and monocytes/macrophages, suggesting that HO-1 plays critical roles in these cells. In vivo and in vitro studies have indicated that impaired HO-1 production results in progressive monocyte dysfunction, unregulated macrophage activation and endothelial cell dysfunction, leading to catastrophic systemic inflammatory response syndrome. Data from reported human cases of HO-1 deficiency and numerous studies using animal models suggest that HO-1 plays critical roles in various clinical settings involving excessive oxidative stress and inflammation. In this regard, therapy to induce HO-1 production by pharmacological intervention represents a promising novel strategy to control inflammatory diseases.

scholarly journals Emerging Roles for Browning of White Adipose Tissue in Prostate Cancer Malignant Behaviour

2021 ◽  
Vol 22 (11) ◽  
pp. 5560
Author(s):  
Alejandro Álvarez-Artime ◽  
Belén García-Soler ◽  
Rosa María Sainz ◽  
Juan Carlos Mayo
Keyword(s):  
Prostate Cancer ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Tumor Development ◽  
Cell Types ◽  
Protective Role ◽  
Bioactive Molecules ◽  
Brown Adipose ◽  
Endocrine Organs

In addition to its well-known role as an energy repository, adipose tissue is one of the largest endocrine organs in the organism due to its ability to synthesize and release different bioactive molecules. Two main types of adipose tissue have been described, namely white adipose tissue (WAT) with a classical energy storage function, and brown adipose tissue (BAT) with thermogenic activity. The prostate, an exocrine gland present in the reproductive system of most mammals, is surrounded by periprostatic adipose tissue (PPAT) that contributes to maintaining glandular homeostasis in conjunction with other cell types of the microenvironment. In pathological conditions such as the development and progression of prostate cancer, adipose tissue plays a key role through paracrine and endocrine signaling. In this context, the role of WAT has been thoroughly studied. However, the influence of BAT on prostate tumor development and progression is unclear and has received much less attention. This review tries to bring an update on the role of different factors released by WAT which may participate in the initiation, progression and metastasis, as well as to compile the available information on BAT to discuss and open a new field of knowledge about the possible protective role of BAT in prostate cancer.

scholarly journals Protective Effects of 6,7,4′-Trihydroxyflavanone on Hypoxia-Induced Neurotoxicity by Enhancement of HO-1 through Nrf2 Signaling Pathway

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 341 ◽  
Author(s):  
Hyun-Su Lee ◽  
Gil-Saeng Jeong
Keyword(s):  
Signaling Pathway ◽  
Neurodegenerative Disorders ◽  
Nuclear Translocation ◽  
Protoporphyrin Ix ◽  
Protective Role ◽  
Osteoclast Formation ◽  
Protective Effects ◽  
Protein Levels ◽  
Nrf2 Signaling Pathway ◽  
Pre Treatment

Since hypoxia-induced neurotoxicity is one of the major causes of neurodegenerative disorders, including the Alzheimer’s disease, continuous efforts to find a novel antioxidant from natural products are required for public health. 6,7,4′-trihydroxyflavanone (THF), isolated from Dalbergia odorifera, has been shown to inhibit osteoclast formation and have an antibacterial activity. However, no evidence has reported whether THF has a protective role against hypoxia-induced neurotoxicity. In this study, we found that THF is not cytotoxic, but pre-treatment with THF has a cytoprotective effect on CoCl2-induced hypoxia by restoring the expression of anti-apoptotic proteins in SH-SY5y cells. In addition, pre-treatment with THF suppressed CoCl2-induced hypoxia-related genes including HIF1α, p53, VEGF, and GLUT1 at the mRNA and protein levels. Pre-treatment with THF also attenuated the oxidative stress occurred by CoCl2-induced hypoxia by preserving antioxidant proteins, including SOD and CAT. We revealed that treatment with THF promotes HO-1 expression through Nrf2 nuclear translocation. An inhibitor assay using tin protoporphyrin IX (SnPP) confirmed that the enhancement of HO-1 by pre-treatment with THF protects SH-SY5y cells from CoCl2-induced neurotoxicity under hypoxic conditions. Our results demonstrate the advantageous effects of THF against hypoxia-induced neurotoxicity through the HO-1/Nrf2 signaling pathway and provide a therapeutic insight for neurodegenerative disorders.

scholarly journals Protective Effects of Statins Administration in European and North American Patients Infected with COVID-19: A Meta-analysis

2021 ◽  
Author(s):  
Mairi Pucci ◽  
Diletta Onorato ◽  
Giovanni Carpene ◽  
Brandon Michael Henry ◽  
Fabian Sanchis-Gomar ◽  
...  
Keyword(s):  
Confidence Interval ◽  
Statin Therapy ◽  
Odds Ratio ◽  
Meta Analysis ◽  
Protective Role ◽  
Favorable Effect ◽  
Current Evidence ◽  
Severe Illness ◽  
Protective Effects ◽  
Time Data

AbstractSevere acute respiratory syndrome coronavirus 2 has spread rapidly throughout the world, becoming an overwhelming global health emergency. The array of injuries caused by this virus is broad and not limited to the respiratory system, but encompassing also extensive endothelial and systemic tissue damage. Since statins effectively improve endothelial function, these drugs may have beneficial effects in patients with coronavirus disease 2019 (COVID-19). Therefore, this investigation aimed to provide an updated overview on the interplay between statins and COVID-19, with particular focus on their potentially protective role against progression toward severe or critical illness and death. A systematic electronic search was performed in Scopus and PubMed up to present time. Data on statins use and COVID-19 outcomes especially in studies performed in Europe and North America were extracted and pooled. A total of seven studies met our inclusion criteria, totaling 2,398 patients (1,075 taking statins, i.e., 44.8%). Overall, statin usage in Western patients hospitalized with COVID-19 was associated with nearly 40% lower odds of progressing toward severe illness or death (odds ratio: 0.59; 95% confidence interval: 0.35–0.99). After excluding studies in which statin therapy was started during hospital admission, the beneficial effect of these drugs was magnified (odds ratio: 0.51; 95% confidence interval: 0.41–0.64). In conclusion, although randomized trials would be necessary to confirm these preliminary findings, current evidence would support a favorable effect of statins as adjuvant therapy in patients with COVID-19. Irrespective of these considerations, suspension of statin therapy seems highly unadvisable in COVID-19 patients.

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