Role of oxidative stress in chemical allergens induced skin cells activation

Corsini, Emanuela; Galbiati, Valentina; Nikitovic, Dragana; Tsatsakis, Aristidis

doi:10.1016/j.fct.2013.02.038

Cited by 104 publications

(54 citation statements)

References 95 publications

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“…Preconditioning with TDZD-8 attenuated the renal tissue damage in RI/RI rats. Previous studies have reported that RI/RI increased the production of ROS and dependent signaling cascades, reduced SOD activity, and increased the level of MDA [29-31]. NF-κB plays a critical role in the pathophysiology of RI/RI in DM with inflammation and oxidative stress [32, 33].…”

Section: Discussionmentioning

confidence: 99%

Activation of Nrf2/HO-1 Pathway by Glycogen Synthase Kinase-3β Inhibition Attenuates Renal Ischemia/Reperfusion Injury in Diabetic Rats

Shen

et al. 2017

Kidney Blood Press Res

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Background/Aims: Diabetes mellitus can exacerbate renal ischemia-reperfusion (I/R) injury (RI/RI). The aim of the present study was to evaluate the protective effect of GSK-3β inhibition (TDZD-8) on I/R-induced renal injury through the Nrf2/HO-1 pathway in a streptozocin (STZ)-induced diabetic rat model. Methods: STZ-induced diabetic rats preconditioned with TDZD-8 and ZnPP were subjected to renal I/R. The extent of renal morphologic lesions. Renal function was assessed from blood urea nitrogen (BUN) and serum creatinine (Scr), as determined utlizing commercial kits. Oxidative stress and inflammatory activity in the kidney tissue was estimated from levels of malondialdehyde (MDA), interleukin-10 (IL-10), tumor necrosis factor-α (TNF-α), and nitric oxide (NO), as well as the activities of superoxide dismutase (SOD) and glutathione (GSH) using qRT-PCR and ELISA. The expressions of Nrf2, HO-1, Bcl-2 and NF-κB in the renal tissue were measured by qRT-PCR and western blotting. Results: I/R-induced renal inflammation was reduced significantly by TDZD-8 pretreatment. Preconditioning with TDZD-8 suppressed NF-κB expression and enhanced Bcl-2 expression in the renal tissue. The upregulated level of malondialdehyde (MDA), and reduced activities of superoxide dismutase (SOD) and glutathione (GSH) in I/R-shocked rats were markedly restored by TDZD-8 pretreatment. Furthermore, pretreatment with TDZD-8 enhanced activation of the Nrf2/HO-1 pathway in the renal tissue of diabetic RI/RI rats. Conclusion: These findings suggest that preconditioning with TDZD-8 may protect the kidney from I/R-induced damage via the activation of the Nrf2/HO-1 pathway in STZ-induced diabetic rats. Further detailed studies are needed to further clarify the underlying mechanisms.

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Section: Discussionmentioning

confidence: 99%

Activation of Nrf2/HO-1 Pathway by Glycogen Synthase Kinase-3β Inhibition Attenuates Renal Ischemia/Reperfusion Injury in Diabetic Rats

Shen

et al. 2017

Kidney Blood Press Res

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“…contact allergens like trinitrochlorobenzene, bleomycine, or asbestos, induce ROS formation in keratinocytes as well as in Langerhans cells [30]. The process of allergic inflammatory response includes the degradation of hyaluronic acid.…”

Section: Origin Of Rmsmentioning

confidence: 99%

Reactive Molecule Species and Antioxidative Mechanisms in Normal Skin and Skin Aging

Wölfle¹,

Seelinger²,

Bauer

et al. 2014

Skin Pharmacol Physiol

111

123

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Reactive oxygen and nitrogen species (ROS/RNS) which may exist as radicals or nonradicals, as well as reactive sulfur species and reactive carbon species, play a major role in aging processes and in carcinogenesis. These reactive molecule species (RMS), often referred to as ‘free radicals' or oxidants, are partly by-products of the physiological metabolism. When RMS concentrations exceed a certain threshold, cell compartments and cells are injured and destroyed. Endogenous physiological mechanisms are able to neutralize RMS to some extent, thereby limiting damage. In the skin, however, pollutants and particularly UV irradiation are able to produce additional oxidants which overload the endogenous protection system and cause early aging, debilitation of immune functions, and skin cancer. The application of antioxidants from various sources in skin care products and food supplements is therefore widespread, with increasingly effective formulations being introduced. The harmful effects of RMS (aside from impaired structure and function of DNA, proteins, and lipids) are: interference with specific regulatory mechanisms and signaling pathways in cell metabolism, resulting in chronic inflammation, weakening of immune functions, and degradation of tissue. Important control mechanisms are: MAP-kinases, the aryl-hydrocarbon receptor (AhR), the antagonistic transcription factors nuclear factor-κB and Nrf2 (nuclear factor erythroid 2-related factor 2), and, especially important, the induction of matrix metalloproteinases which degrade dermal connective tissue. Recent research, however, has revealed that RMS and in particular ROS/RNS are apparently also produced by specific enzyme reactions in an evolutionarily adapted manner. They may fulfill important physiologic functions such as the activation of specific signaling chains in the cell metabolism, defense against infectious pathogens, and regulation of the immune system. Normal physiological conditions are characterized by equilibrium of oxidative and antioxidative mechanisms. The application of antioxidants in the form of 'cosmeceuticals' or systemic 'nutraceuticals' should aim to support a physiologically balanced oxidation status in the skin.

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“…These findings suggest that CSE induced TSLP production in vivo via oxidative stress and TNF-a receptor 1 activation. Oxidative stress leads to the activation of NF-kB (29), which is involved in the expression of TSLP. Oxidative stress also induced the production of oxidized lipids, which triggered TSLP production via stimulating TLR4 (30).…”

Section: Cigarette Smoke Extract (Cse)mentioning

confidence: 99%

Exacerbation of Allergic Diseases by Chemicals: Role of TSLP

Segawa

Hirasawa

2014

J Pharmacol Sci

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Abstract. Environmental chemicals, such as cigarette smoke and diesel exhaust, have been reported as risk factors that exacerbate allergic diseases. However, the exacerbation mechanisms induced by these chemicals are not yet fully understood. Thymic stromal lymphopoietin (TSLP) is produced mainly by epithelial cells and plays an important role as a master switch of allergic inflammation because it promotes Th2-type immune responses by inducing the activation of dendritic cells. Chemical compounds, such as formalin, have been shown to bind to proteins and form a new antigen that induces allergic responses. A second group of chemicals that enhance allergic responses to exogenous proteins have also been reported. We recently demonstrated that some of these chemicals induced TSLP production and may potentially augment Th2-type allergic responses. We proposed that TSLP-producing chemical compounds should be recognized as chemical allegro-accelerators.

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Role of oxidative stress in chemical allergens induced skin cells activation

Cited by 104 publications

References 95 publications

Activation of Nrf2/HO-1 Pathway by Glycogen Synthase Kinase-3β Inhibition Attenuates Renal Ischemia/Reperfusion Injury in Diabetic Rats

Activation of Nrf2/HO-1 Pathway by Glycogen Synthase Kinase-3β Inhibition Attenuates Renal Ischemia/Reperfusion Injury in Diabetic Rats

Reactive Molecule Species and Antioxidative Mechanisms in Normal Skin and Skin Aging

Exacerbation of Allergic Diseases by Chemicals: Role of TSLP

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