Induction of heme oxygenase-1 expression by root canal sealers in human gingival fibroblasts is augmented by oxidative stress

2007 ◽  
Vol 80B (2) ◽  
pp. 499-504 ◽  
Author(s):  
Fu-Mei Huang ◽  
Yu-Chao Chang
Keyword(s):  
Oxidative Stress ◽  
Heme Oxygenase ◽  
Root Canal ◽  
Human Gingival Fibroblasts ◽  
Heme Oxygenase 1 ◽  
Gingival Fibroblasts ◽  
Root Canal Sealers

scholarly journals In Vitro Comparison of Cytotoxicity of Four Root Canal Sealers on Human Gingival Fibroblasts

2015 ◽  
Vol 69 (1) ◽  
pp. 24 ◽  
Author(s):  
Alma KonjhodzicPrcic ◽  
Omer Gorduysus ◽  
Selen Kucukkaya ◽  
Burcu Atila ◽  
Sevda Muftuoglu ◽  
...  
Keyword(s):  
Root Canal ◽  
Human Gingival Fibroblasts ◽  
Gingival Fibroblasts ◽  
Root Canal Sealers ◽  
In Vitro Comparison

scholarly journals Investigating the cytotoxicity of four types of freshly prepared root canal sealers using human gingival fibroblasts

2021 ◽  
Vol 15 (6) ◽  
pp. 1824-1828
Author(s):  
Ehsan Mostajeran ◽  
Shirin Asgarani ◽  
Hamid Razavian
Keyword(s):  
Multivariate Analysis ◽  
Root Canal ◽  
Culture Medium ◽  
Colorimetric Method ◽  
Human Gingival Fibroblasts ◽  
Fibroblast Cells ◽  
Gingival Fibroblasts ◽  
Experimental Laboratory ◽  
Root Canal Sealers ◽  
Over Time

Introduction: One of the most important characteristics of endodontic treatment seals is their biocompatibility. The aim of present study was to investigate the cytotoxicity of four types of freshly prepared root canal sealers using human gingival fibroblasts. Materials and Methods: In this experimental laboratory study, freshly prepared sealers were investigated. To investigate the cytotoxicity, each sample was extracted separately in RPMI-1640 (Sigma Aldrich-USA). Then, the resulting extracts were exposed to C165 fibroblast cells in culture medium for 1, 3 and 7 days. Then, the level of cytotoxicity was assessed by MTT colorimetric method based on the level of light absorption. In the present study, multivariate analysis of variance was used to analyze the data. Results: The results showed that the cytotoxicity of AH 26 and tgsealer sealers decreased and MTA Fillapex sealer increased over time. Also, Adseal sealer did not follow a logical trend but, in general, its cytotoxicity increased over time. In addition, based on mean of all data obtained from each sealer, MTA Fillapex had the lowest cytotoxicity and Adseal had the highest cytotoxicity, and AH 26 cytotoxicity was higher than that of tgsealer. Conclusion: According to the results of the present study, the MTA-based sealer of MTA Fillapex has the lowest cytotoxicity. Keywords: Root canal sealers, fibroblasts, freshly prepared roots

The up-regulation of heme oxygenase-1 expression in human gingival fibroblasts stimulated with nicotine

2005 ◽  
Vol 40 (3) ◽  
pp. 252-257 ◽  
Author(s):  
Yu-Chao Chang ◽  
Chung-Chih Lai ◽  
Li-Fen Lin ◽  
Wei-Fen Ni ◽  
Chung-Hung Tsai
Keyword(s):  
Heme Oxygenase ◽  
Human Gingival Fibroblasts ◽  
Heme Oxygenase 1 ◽  
Gingival Fibroblasts

scholarly journals Regulation and Role of Heme Oxygenase‐1 (HO‐1) During Inflammation in Human Gingival Fibroblasts (HGF)

2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
Sheedeh Madani ◽  
Michel Evans ◽  
Mariah Chambers ◽  
Grzegorz Gorski ◽  
Mansoor Madani ◽  
...  
Keyword(s):  
Heme Oxygenase ◽  
Human Gingival Fibroblasts ◽  
Heme Oxygenase 1 ◽  
Gingival Fibroblasts

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 Heme Oxygenase-1 Induction by Cobalt Protoporphyrin Ameliorates Cholestatic Liver Disease in a Xenobiotic-Induced Murine Model

2021 ◽  
Vol 22 (15) ◽  
pp. 8253
Author(s):  
Jung-Yeon Kim ◽  
Yongmin Choi ◽  
Jaechan Leem ◽  
Jeong Eun Song
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Heme Oxygenase ◽  
Murine Model ◽  
Liver Diseases ◽  
Transforming Growth Factor ◽  
Heme Oxygenase 1 ◽  
Cholestatic Liver Disease ◽  
Hepatocyte Apoptosis ◽  
Cobalt Protoporphyrin

Cholestatic liver diseases can progress to end-stage liver disease and reduce patients’ quality of life. Although their underlying mechanisms are still incompletely elucidated, oxidative stress is considered to be a key contributor to these diseases. Heme oxygenase-1 (HO-1) is a cytoprotective enzyme that displays antioxidant action. It has been found that this enzyme plays a protective role against various inflammatory diseases. However, the role of HO-1 in cholestatic liver diseases has not yet been investigated. Here, we examined whether pharmacological induction of HO-1 by cobalt protoporphyrin (CoPP) ameliorates cholestatic liver injury. To this end, a murine model of 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) diet feeding was used. Administration of CoPP ameliorated liver damage and cholestasis with HO-1 upregulation in DDC diet-fed mice. Induction of HO-1 by CoPP suppressed the DDC diet-induced oxidative stress and hepatocyte apoptosis. In addition, CoPP attenuated cytokine production and inflammatory cell infiltration. Furthermore, deposition of the extracellular matrix and expression of fibrosis-related genes after DDC feeding were also decreased by CoPP. HO-1 induction decreased the number of myofibroblasts and inhibited the transforming growth factor-β pathway. Altogether, these data suggest that the pharmacological induction of HO-1 ameliorates cholestatic liver disease by suppressing oxidative stress, hepatocyte apoptosis, and inflammation.

scholarly journals Resveratrol Protects C6 Astrocyte Cell Line against Hydrogen Peroxide-Induced Oxidative Stress through Heme Oxygenase 1

PLoS ONE ◽  
2013 ◽  
Vol 8 (5) ◽  
pp. e64372 ◽  
Author(s):  
André Quincozes-Santos ◽  
Larissa Daniele Bobermin ◽  
Alexandra Latini ◽  
Moacir Wajner ◽  
Diogo Onofre Souza ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Cell Line ◽  
Heme Oxygenase ◽  
Heme Oxygenase 1

Dexrazoxane does not protect against doxorubicin-induced damage in young rats

2003 ◽  
Vol 285 (2) ◽  
pp. H499-H506 ◽  
Author(s):  
Stéphanie Héon ◽  
Martin Bernier ◽  
Nicolas Servant ◽  
Stevan Dostanic ◽  
Chunlei Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Weight Gain ◽  
Heme Oxygenase ◽  
Caspase 3 ◽  
Exercise Program ◽  
Female Rats ◽  
Male Rats ◽  
Heme Oxygenase 1 ◽  
Cardiac Damage

Doxorubicin (DOX), an anticancer drug, causes a dose-dependent cardiotoxicity. Some evidence suggests that female children have an increased risk for DOX-mediated cardiac damage. To determine whether the iron chelator dexrazoxane (DXR) could reduce DOX-induced cardiotoxicity in the young, we injected day 10 neonate female and male rat pups with a single dose of saline or DOX, DXR, or DXR + DOX (20:1). We followed body weight gain with growth, measured cardiac hypertrophy after a 2-wk swim exercise program, markers of apoptosis (Bcl-2, BAX, BNIP1, caspase 3 activation), oxidative stress (heme oxygenase 1, protein carbonyl levels), the chaperone protein clusterin, and the transcriptional activator early growth response gene-1 (Egr-1) in hearts of nonexercised and exercised rats on neonate day 38. All DOX-alone and DXR + DOX-treated rats showed decreased weight gain, with female rats affected earlier than male rats. DXR-alone, DOX-alone, and DXR + DOX-treated rats had an increased heart weight-to-body weight (heart wt/body wt) ratio after the exercise program with female rats showing the largest increase in heart wt/body wt. Drug-treated females also showed increased cardiac apoptosis, as measured by the increased expression of the proapoptotic proteins BAX and BNIP1 and the appearance of caspase 3 activation products, and oxidative stress, as measured by increased heme oxygenase 1 expression, and reduced Egr-1 and clusterin expression when compared with the similarly treated male rats. We conclude that DXR preinjection did not reduce DOX-induced noncardiac and cardiac damage and that young female rats were more susceptible to DXR and DOX toxicities than age-matched male rats.

Abstract TP102: Modulation of Neuroinflammation by Haptoglobin Reduces Oxidative Stress and Improves ICH Outcomes

Stroke ◽  
2016 ◽  
Vol 47 (suppl_1) ◽  
Author(s):  
Jenna Leclerc ◽  
Alex Dang ◽  
Juan Santiago-Moreno ◽  
Sylvain Dore
Keyword(s):  
Oxidative Stress ◽  
Heme Oxygenase ◽  
Functional Outcomes ◽  
Ferric Iron ◽  
Heme Oxygenase 1 ◽  
High Morbidity ◽  
Blood Components ◽  
Autologous Whole Blood ◽  
The Brain ◽  
Histological Staining

Intracerebral hemorrhage (ICH) is a stroke subtype associated with high morbidity and mortality. With breakdown of the blood-brain barrier and entry of toxic blood components and metabolites within the brain, a highly oxidative environment ensues and leads to a toxic neuroinflammatory cascade. A major cause of the debilitation following brain hemorrhage is due to the direct toxicity of blood components, notably hemoglobin (Hb), the most upstream precipitating factor in the cascade. The acute phase plasma protein haptoglobin (Hp) binds Hb and inhibits its cytotoxic, pro-oxidative, and pro-inflammatory properties. In this study, we investigated whether the local and specific overexpression of Hp would aid in the safe detoxification and clearance of free Hb, thereby protecting the neuropil from Hb-mediated oxidative stress and improving ICH outcomes. Hp was overexpressed locally within the brain using uniquely designed adeno-associated viral vectors and ICH was induced using the intrastriatal autologous whole blood injection model. Functional outcomes were assessed by a 24-point neurological deficit score. At 72h post-hemorrhage, mice were sacrificed and brains collected for histological staining. Hp-overexpressing mice demonstrated smaller lesion volumes (p<0.05) with less blood accumulation (p<0.05) and improve neurologic status after ICH (p<0.05) when compared to an identically treated control group (n=11-13/group). Histological staining for Iba-1, GFAP, heme oxygenase-1, 4-hydroxynonenal, ferric iron, and myeloperoxidase was performed and revealed: 1) significantly less heme oxygenase-1 expression and lipid peroxidation, 2) a trend towards reduced peripheral neutrophil infiltration, 3) significantly increased cortical microgliosis and cortical and striatal astrogliosis, and 4) no changes in ferric iron content or striatal microgliosis. In conclusion, Hp overexpression in the brain reduces ICH-induced brain injury and improves functional outcomes. Locally modulating brain Hp levels could represent an important clinically relevant strategy for the treatment of ICH.

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