Age-Related Changes in Nuclear Factor Erythroid 2-Related Factor 2 and Reactive Oxygen Species and Mitochondrial Structure in the Tongues of Fischer 344 Rats

Baek, Min-Kwan; Lee, Hyon; Kim, Kyung-Ok; Kwon, Hyun-Jin; Chung, Myung‐Hee; Park, Hyoung-Min; Woo, Joo Hyun; Kim, Dong‐Young

doi:10.21053/ceo.2016.01095

Cited by 9 publications

(3 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…HO-1 is an important player in the cellular defense against oxidative stress and is highly induced by inflammatory cytokines [33]. Given that HO-1 is induced by a protective mechanism in response to harmful stimuli, the induction of HO-1 could be considered as a therapeutic approach for protection against oxidative stress [34].…”

Section: Discussionmentioning

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

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

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

View full text Add to dashboard Cite

show abstract

“…In the current study, the expression of Nrf2 and HO-1, as antioxidant molecules, was remarkably declined, while the expression of gp91phox was elevated in aged mice compared with young mice, which is similar to the previous results [ 16 ]. The levels of Nrf2 protein in aged rats were lower than in the young rats [ 48 ]. Thus, aging is sufficient to diminish cardiac Nrf2-ARE binding activity, and aged Nrf2 knockout mice exhibited decreased expression of antioxidant target genes [ 49 ].…”

Section: Discussionmentioning

confidence: 99%

The Synergy of Aging and LPS Exposure in a Mouse Model of Parkinson’s Disease

et al. 2018

View full text Add to dashboard Cite

Aging is an inevitable physiological challenge occurring in organisms over time, and is also the most important risk factor of neurodegenerative diseases. In this study, we observed cellular and molecular changes of different age mice and LPS-induced Parkinson disease (PD) model. The results showed that behavioral performance and dopaminergic (DA) neurons were declined, accompanied by increased expression of pro-inflammatory factors (TLR2, p-NF-kB-p65, IL-1β and TNF-α), as well as pro-oxidative stress factor gp91phox in aged mice compared with young mice. Aging exaggerated inflammatory M1 microglia, and destroyed the balance between oxidation and anti-oxidation. The intranasal LPS instillation induced PD model in both young and aged mice. The poor behavioral performance and the loss of DA neurons as well as TLR2, p-NF-kB-p65, IL-1β, TNF-α, iNOS and gp91phox were further aggravated in LPS-aged mice. Interestingly, the expression of Nrf2 and HO-1 was up-regulated by LPS only in young LPS-PD mice, but not in aged mice. The results indicate that the synergy of aging process and LPS exposure may prominently aggravate the DA neurons loss caused by more serious neuroinflammation and oxidative stress in the brain.

show abstract

“…Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) plays a key role in regulating antioxidant molecules in cells [18]. Enhancing NRF2 activity could prevent many diseases in which oxidative and inflammatory stress are crucial for pathogenesis [19, 20]. It is well known that activation of the Nrf2 signaling protects cells against radiation-induced oxidative damage [21, 22].…”

Section: Introductionmentioning

confidence: 99%

Ferroptosis inhibitor alleviates Radiation-induced lung fibrosis (RILF) via down-regulation of TGF-β1

et al. 2019

View full text Add to dashboard Cite

Background Radiation-induced lung fibrosis (RILF) is a severe and life-threatening complication of thoracic radiotherapy. Cell death is the key issue in RILF. Ferroptosis is a form programmed cell death implicated in the pathologies of inflammation. This study aimed to investigate the role of ferroptosis in RILF, and the effectiveness and the potential underlying mechanism of ferroptosis inhibitor on RILF. Methods Immunofluorescence, western blot and RT-PCR assays were performed to examine the ferroptosis maker glutathione peroxidase 4 (GPX4) in a mice RILF model. The lung tissue sections were stained with hematoxylin and eosin (H&E), Masson trichrome staining and Sirius-Red staining to evaluate the histopathological changes in RILF mice. Reactive oxygen species (ROS) and hydroxyproline (HYP) in lungs were measured by the relevant kits. The serum levels of inflammatory cytokines (TNF-α, IL-6, IL-10, and TGF-β1) were measured with Elisa. The protein and mRNA levels of GPX4, nuclear factor (erythroid-derived 2)-like 2 (Nrf2), hemeoxygenase-1 (HO1) and quinone oxidoreductase 1 (NQO1) in lungs were examined by western blot and RT-PCR. Results GPX4 levels of the irradiated lungs were significantly down-regulated than the groups with no irradiation, and the ferroptosis inhibitor, liproxstatin-1, increased GPX4 levels significantly in RILF mice. Treatment with liproxstatin-1 lowered the Szapiel and Ashcroft scores significantly, down-regulated the levels of ROS and HYP in lungs and reduced the serum inflammatory cytokines levels in RILF mice. The protein and the mRNA levels of Nrf2, HO1 and NQO1 were up-regulated by liproxsratin-1 in RILF. Conclusions Our data suggested that ferroptosis played a critical role in RILF, ferroptosis inhibitor liproxstatin-1 alleviated RILF via down-regulation of TGF-β1 by the activation of Nrf2 pathway. The effectiveness of ferroptosis inhibition on RILF provides a novel therapeutic target for RILF.

show abstract

Age-Related Changes in Nuclear Factor Erythroid 2-Related Factor 2 and Reactive Oxygen Species and Mitochondrial Structure in the Tongues of Fischer 344 Rats

Cited by 9 publications

References 28 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

The Synergy of Aging and LPS Exposure in a Mouse Model of Parkinson’s Disease

Ferroptosis inhibitor alleviates Radiation-induced lung fibrosis (RILF) via down-regulation of TGF-β1

Contact Info

Product

Resources

About