Arsenic modulates heme oxygenase-1, interleukin-6, and vascular endothelial growth factor expression in endothelial cells: roles of ROS, NF-κB, and MAPK pathways

Wang, Lisu; Kou, Mei Chun; Weng, Ching Yi; Hu, Ling; Wang, Ying Jan; Wu, Ming-Jiuan

doi:10.1007/s00204-012-0845-z

Cited by 91 publications

(54 citation statements)

References 78 publications

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“…Cellular reactions to NLC system were investigated with some modification of the technique determined for cytotoxicity measurement of ALA-NLC aqueous dispersion using [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazonium bromide); MTT] assay (Lai & Hsieh, 2012;Liu et al, 2012;Wang et al, 2012b). HaCaT cells with a density of 5 Â 10 3 cells/well were seeded into 96-well plates and incubated for 24 h to endow cell attachment.…”

Section: Determination Of Cell Viabilitymentioning

confidence: 99%

Alpha-lipoic acid-loaded nanostructured lipid carrier: sustained release and biocompatibility to HaCaT cellsin vitro

Wang

Xia²

2013

Drug Delivery

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ALA-loaded nanostructured lipid carrier (ALA-NLC) was designed to improve physicochemical stability and water solubility, and promote sustained release of ALA as well as determine the biocompatibility of ALA-NLC. The ALA-NLC manufactured using hot high-pressure homogenization technique was investigated in terms of size, zeta potential, FTIR analysis and release behavior. In vitro cytotoxicity and biocompatibility were determined by incubating with HaCaT cells using the MTT assay, HE staining and Hoechst 33342 staining. Cell behavior and cellular division of HaCaT cells untreated and treated by ALA-NLC were investigated in real-time images gathered using time-lapse imaging system. The release investigation illustrated that only 6.9% of ALA released in 30 min from ALA-NLC formation, whereas it was 30.3% in free ALA system. ALA-NLC possessed a satisfactory release behavior of sustained release up to 72 h. It showed that ALA-NLC did not exert hazardous effect on HaCaT cells up to 81.9 mg/L without morphological alterations, revealing a satisfactory biocompatibility. Evidence was provided from time-lapse imaging system that cell behavior and cellular division of ALA-NLC treated HaCaT cells were in accordance with the control. These results of this investigation demonstrated that NLC encapsulated ALA formation (ALA-NLC) can improve stability, solubility and release of ALA; ALA-NLC was biocompatible to HaCaT cells.

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Section: Determination Of Cell Viabilitymentioning

confidence: 99%

Alpha-lipoic acid-loaded nanostructured lipid carrier: sustained release and biocompatibility to HaCaT cellsin vitro

Wang

Xia²

2013

Drug Delivery

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“…Also, arsenic may inhibit many enzymes and damage protein structures. The cytokines secreted after cellular damage increases the migration of inflammation to cells and tissues, so the inflammatory period is triggered (27,28).…”

Section: Discussionmentioning

confidence: 99%

“…It also triggers an inflammatory period where applied alpha lipoic acid decreases proinflammatory molecule levels (43). In another study, arsenic reportedly stimulated production of proinflammatory cytokines, IL-1B, IL-6, MCP-1, and C reactive protein through inducible nitric oxide synthase (iNOS) in the vascular system (27). There are no data in the literature on the effects of melatonin on MCP-1 levels during arsenic toxicity.…”

mentioning

confidence: 99%

The effects of melatonin on liver functions in arsenic-induced liver damage

Bali

Bilir

Emir

et al. 2016

UCD

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The effects of melatonin on liver functions in arsenic-induced liver damage INTRODUCTION Arsenic, one of the most prevalent element on earth, belongs to the group of heavy metals (1, 2). Inorganic arsenic, which is the most prevalent type, dominates sea water, surface waters, and underground water. Conversely, organic forms of arsenic are found within natural gas and petroleum (3). Arsenic can easily change oxidation steps and chemical forms in nature. Arsenic valence and type are affected by redox potential, pH of the water, microbiologic activity, and the presence of ions like sulfur, iron, and calcium (3). In recent years, arsenic exposure has increased because of pollution and industrial development (4). Particularly, the agriculture chemicals used in dyes, ceramics, cancer drugs, mining operations, and herbicides and insecticides are leading routes of exposition (5-7). Long periods of arsenic intake by mouth or through inhalation cause both metabolic and structural changes in the hepatocyte mitochondria (8). Arsenic causes hepatocyte degeneration, inflammation, and necrosis. It also causes increased apoptosis, oxidative damage, and damage at lipid peroxidation (9, 10).Melatonin is primarily secreted from a neuroendocrine organ called the pineal gland. It is also secreted from the skin, the retina, testicles, bone marrow, thrombocytes, lymphocytes, and the gastrointestinal system (11-17). Melatonin synthesis and release are both stimulated by darkness and repressed by light. Melatonin is a strong free radical sweeper agent, as demonstrated in both in vivo and in vitro studies (18)(19)(20). It is much more powerful than all known antioxidants due to its free radical catching effects. Studies have shown that it is a more potent antioxidant than vitamin E and glutathione (21,22). This is primarily because melatonin can dissolve in either water or fat, thus affecting all cell components (19-23). Melatonin also reportedly has regulatory effects on immunity and anti-inflammation (24-26). The aim of this study was to investigate the regulatory effects of melatonin on arsenic toxicity by monitoring hepatic enzymes and inflammatory markers in rats whose livers were intentionally damaged by arsenic for experimental purposes. MATERIAL AND METHODS Study GroupTwenty-four male Sprague-Dawley rats were used in the experiment. Rats were kept at 22°C under illumination control (14 hours light/10 hours dark cycle). They were monitored in standard cages in an Objective: Arsenic exposure is increasing in communities due to environmental pollution and industrial development. Arsenic is toxic to organ systems because it causes oxidative stress, enzymatic inhibition, and damage to protein structures. The liver, for example, is an organ that may be damaged by arsenic, and this damage may cause various clinical conditions like hepatic failure or cancer. Melatonin is a hormone that acts like an antioxidant, an anti-inflammatory agent, and a cytoprotective agent. In this study, we aimed to evaluate melatonin's protective effects on li...

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“…Complex regulatory regions indicate the possibility that several signal transduction pathways may be involved in HO-1 regulation, including mitogen-activated protein kinase, protein kinase C and tyrosine protein kinase (27,28). A recent study indicated that the PI3K/Akt pathway also has a role in HO-1 regulation.…”

Section: Discussionmentioning

confidence: 99%

Post-conditioning with sevoflurane induces heme oxygenase-1 expression via the PI3K/Akt pathway in lipopolysaccharide-induced acute lung injury

Zhao

Wu²,

Zhang

et al. 2014

Molecular Medicine Reports

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Abstract. The aim of the present study was to explore the regulatory mechanism of heme oxygenase-1 (HO-1) expression induced by sevoflurane (Sevo) in lipopolysaccharide (LPS)-induced acute lung injury (ALI). Sprague-Dawley rats were divided randomly into six groups: (A) Control, (B) 2.4% Sevo only, (C) LY294002 (PI3K inhibitor) only, (D) LPS + 2.4% Sevo, (E) LY294002 + LPS + 2.4% Sevo and (F) LPS only. The pathological changes in wet/dry weight ratio (W/D), the activities of superoxide dismutase, myeloperoxidase (MPO), malondialdehyde, and HO-1, as well as the expression of intercellular adhesion molecule (ICAM-1), HO-1, phospho-phosphatidylinositol 3-kinase (pPI3K) and phospho-Akt (pAkt) were recorded. Sevo post-conditioning was able to effectively protect from ALI with decreasing pathomorphological scores, MPO activity, W/D and the mRNA and protein expression levels of ICAM-1. Sevo promotes HO-1 expression via the PI3K/protein kinase B (PI3K/Akt) pathway with activation of pPI3K and pAkt. Inhibition of the PI3K/Akt pathway by LY294002 partly eliminates the protective effects of Sevo. It is concluded that Sevo post-conditioning has a vital role in inducing the upregulation of HO-1 expression via the PI3K/Akt pathway to alleviate ALI.

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Arsenic modulates heme oxygenase-1, interleukin-6, and vascular endothelial growth factor expression in endothelial cells: roles of ROS, NF-κB, and MAPK pathways

Cited by 91 publications

References 78 publications

Alpha-lipoic acid-loaded nanostructured lipid carrier: sustained release and biocompatibility to HaCaT cellsin vitro

Alpha-lipoic acid-loaded nanostructured lipid carrier: sustained release and biocompatibility to HaCaT cellsin vitro

The effects of melatonin on liver functions in arsenic-induced liver damage

Post-conditioning with sevoflurane induces heme oxygenase-1 expression via the PI3K/Akt pathway in lipopolysaccharide-induced acute lung injury

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