Protective effects of α‐lipoic acid on cultured human nasal fibroblasts exposed to urban particulate matter

Lee, Dong Chang; Choi, Hyunsu; Oh, Joo Suk; Lee, Do Hee; Kim, Sung Won; Kim, Soo Whan; Kim, Byung Guk; Cho, Jin Hee; Lee, Joohyung

doi:10.1002/alr.22296

Cited by 9 publications

(7 citation statements)

References 44 publications

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“…Fibroblasts also play a key role in chronic inflammation of the nasal cavity by releasing various inflammatory cytokines [13,14]. We confirmed in previous studies that urban PM (UPM) induces the expression of proinflammatory cytokines in human nasal fibroblasts [15,16]. These results indicated that upper respiratory diseases such as allergy and chronic rhinitis might be caused by UPM-exposed fibroblasts.…”

Section: Introductionsupporting

confidence: 85%

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Activation of the Nrf2/HO-1 pathway by curcumin inhibits oxidative stress in human nasal fibroblasts exposed to urban particulate matter

Kim

Choi

et al. 2020

BMC Complement Med Ther

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Background: Particulate matter (PM) can cause various negative acute and chronic diseases of the respiratory system, including the upper airways. Curcumin has been reported to have anti-inflammatory and anti-oxidative effects; therefore, we investigated the effects of curcumin on nasal fibroblasts exposed to urban PM (UPM). Methods: Samples of inferior turbinate tissue were obtained from six patients. Flow cytometry was used to assess the levels of reactive oxygen species (ROS) following the treatment of nasal fibroblasts with UPM and/or curcumin. We evaluated the effects of UPM and/or curcumin on the expression of phosphorylated ERK, Nrf2, HO-1, and SOD2 in fibroblasts by Western blotting. Results: When UPM was applied to nasal fibroblasts, ROS production was significantly increased in a dosedependent manner. UPM-exposed fibroblasts caused the activation of ERK to increase HO-1 expression and decrease SOD2 expression. Treatment with curcumin reduced the UPM-mediated increase in ROS; this decrease in ROS occurred in a dose-dependent manner. The UPM-induced activation of ERK was inhibited by curcumin. Nrf2 production was also promoted to increase the expression of HO-1 and SOD2 by curcumin. Conclusion: Curcumin reduced ROS production caused by UPM in human nasal fibroblasts in a dose-dependent manner, suggesting that curcumin has anti-oxidative effects and may be useful in the treatment of nasal diseases caused by UPM, such as allergic and chronic rhinitis.

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Section: Introductionsupporting

confidence: 85%

“…Western blotting was performed as described previously [16]. Nasal fibroblasts were first cultured in 100 mm dishes (5 × 10 5 cells) for 24 h, and then washed twice with PB, and treated with various concentrations of UPM (0-200 μg/mL) and curcumin (0-5 μM) simultaneously.…”

Section: Western Blottingmentioning

confidence: 99%

Activation of the Nrf2/HO-1 pathway by curcumin inhibits oxidative stress in human nasal fibroblasts exposed to urban particulate matter

Kim

Choi

et al. 2020

BMC Complement Med Ther

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“…In addition, α-LA treatment decreased cell death and ROS production in urban particulate matter (UPM)-exposed fibroblasts via the Nrf2, HO-1, and NQO-1 pathways. Also, α-LA treatment abrogated increases in IL-6 and IL-8 levels induced by UPM in nasal fibroblasts [32]. Moreover, it has been reported that α-LA ameliorated hepatic steatosis in rats of diabetes fed with high fat by increasing antioxidant defense systems through Nrf2 and consequently decreasing oxidative stress and hepatic TNF-α [33].…”

Section: Discussionmentioning

confidence: 99%

α-Lipoic Acid Inhibits IL-8 Expression by Activating Nrf2 Signaling in Helicobacter pylori-infected Gastric Epithelial Cells

2019

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Helicobacter pylori (H. pylori) causes gastritis and gastric cancers. Oxidative stress is involved in the pathological mechanism of H. pylori-induced gastritis and gastric cancer induction. Therefore, reducing oxidative stress may be beneficial for preventing the development of H. pylori-associated gastric diseases. Nuclear factor erythroid-2-related factor 2 (Nrf2) is a crucial regulator for the expression of antioxidant enzyme heme oxygenase-1 (HO-1), which protects cells from oxidative injury. α-Lipoic acid (α-LA), a naturally occurring dithiol, shows antioxidant and anti-inflammatory effects in various cells. In the present study, we examined the mechanism by which α-LA activates the Nrf2/HO-1 pathway, suppresses the production of pro-inflammatory cytokine interleukine-8 (IL-8), and reduces reactive oxygen species (ROS) in H. pylori-infected AGS cells. α-LA increased the level of phosphorylated and nuclear-translocated Nrf2 by decreasing the amount of Nrf2 sequestered in the cytoplasm by complex formation with Kelch-like ECH1-associated protein 1 (KEAP 1). By using exogenous inhibitors targeting Nrf2 and HO-1, we showed that up-regulation of activated Nrf2 and of HO-1 results in the α-LA-induced suppression of interleukin 8 (IL-8) and ROS. Consumption of α-LA-rich foods may prevent the development of H. pylori-associated gastric diseases by decreasing ROS-mediated IL-8 expression in gastric epithelial cells.

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“…15,16 In other studies, UPM exposure resulted in increased reactive oxygen species production in nasal fibroblasts; furthermore, the expression of oxidative stressrelated genes (HSP1a, HSP8, and SOD) and tissue damage-related genes (MMP-15, MMP-19, and Slpi) was increased in a time-dependent manner. 17 In another study on a physiologically relevant olfactory cellular model, key mitochondrial functions were perturbed by UPM exposure via a mechanism involving NPTX1. 4 Nevertheless, there is a lack of research into the effects of UPM on the olfactory epithelium and corresponding functional disruption, as well as the underlying mechanisms, based on animal models.…”

Section: Discussionmentioning

confidence: 99%

“…We used an animal model where the nose was exposed to UPM directly, which is similar to the actual human environment; this might offer important data in this context. In several other studies, 14,15,17 cells exposed to UPM were analyzed; however, these studies do not reflect actual bioavailability. Second, our results are comprehensive and synthetic, including behavioral FFT results for olfactory function as well as cytological genetic and protein expression data.…”

Section: Discussionmentioning

confidence: 99%

Effects of Urban Particulate Matter on the Olfactory System in a Mouse Model

Kim

Park

Cho

et al. 2021

Am J Rhinol�Allergy

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Background Exposure to urban particulate matter (UPM) is linked to the aggravation of various health problems. Although the nasal cavity is the first barrier to encounter UPM, there is a lack of studies on the impact of UPM on the olfactory area. The purpose of this study was to investigate the cytotoxic effects of UPM on mouse olfactory epithelium, the underlying pathophysiology involved, and changes in cytokine levels. Methods Mice were divided into 4 groups: control, 400UPM (administered 400 µg UPM daily; standard reference material 1649b; average particle diameter 10.5 μm) 1week, 400UPM 2weeks, and recovery 1week after 400UPM 2weeks (n = 10, 6, 6, and 6, respectively). Olfactory function was evaluated by conducting a food-finding test once a week. The olfactory neuroepithelium was harvested for histologic examination, gene ontology, quantitative real-time polymerase chain reaction, and western blotting. Results Compared to those in the control group, olfactory marker protein, olfactory receptor 1507, adenylyl cyclase 3, and GNAL mRNA levels were lower and S-100, 2′,3′-cyclic nucleotide 30-phosphodiesterase, nerve growth factor receptor-associated protein, brain-derived neurotrophic factor, and tachykinin receptor mRNA levels were higher in the 400UPM group olfactory neuroepithelium. There were no significant differences in neuroepithelial inflammatory marker levels between the 400UPM and saline group. Conclusions UPM decreased olfactory function and might have cytotoxic effects on the olfactory epithelium. Olfactory ensheathing cells and trigeminal nerve might be related to the regeneration of the olfactory epithelium after olfactory destruction associated with UPM.

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Protective effects of α‐lipoic acid on cultured human nasal fibroblasts exposed to urban particulate matter

Cited by 9 publications

References 44 publications

Activation of the Nrf2/HO-1 pathway by curcumin inhibits oxidative stress in human nasal fibroblasts exposed to urban particulate matter

Activation of the Nrf2/HO-1 pathway by curcumin inhibits oxidative stress in human nasal fibroblasts exposed to urban particulate matter

α-Lipoic Acid Inhibits IL-8 Expression by Activating Nrf2 Signaling in Helicobacter pylori-infected Gastric Epithelial Cells

Effects of Urban Particulate Matter on the Olfactory System in a Mouse Model

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