Activation of Nrf2 signalling pathway by tectoridin protects against ferroptosis in particulate matter‐induced lung injury

Dong, Tingting; Fan, Xinli; Zheng, Nan; Yan, Kun; Hou, Tianhua; Peng, Liping; Ci, Xinxin

doi:10.1111/bph.16085

Cited by 16 publications

(4 citation statements)

References 41 publications

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“…A recent study also showed that Nrf2 protects PM2.5 (20mg/kg)-induced lung injury through its regulation of iron-dependent cellular death or ferroptosis. This is supported by the observation that ferroptosis and lung injury in response to PM2.5 are more severe in Nrf2-deficient lung tissue and cellular model [68]. Similarly, Tectoridin (50-100 mg/kg), a bioactive molecule, also ameliorates PM2.5 (20mg/kg for 7 days)-induced lung injury as revealed by decreased morphological damage, necrosis, edema and inflammation with decreased IL-6 and TNF-through stimulation of antioxidant gene regulator Nrf2 and antioxidant genes like GSH and GPX4.…”

Section: Lessons From Studies Using Animal Models and Natural Compoundsmentioning

confidence: 59%

“…Similarly, Tectoridin (50-100 mg/kg), a bioactive molecule, also ameliorates PM2.5 (20mg/kg for 7 days)-induced lung injury as revealed by decreased morphological damage, necrosis, edema and inflammation with decreased IL-6 and TNF-through stimulation of antioxidant gene regulator Nrf2 and antioxidant genes like GSH and GPX4. Similarly, pretreatment of BEAS-2B cells with Tectoridin (25, 50 and 100 uM for 1 h) reduces PM2.5 (400µg/ml for 24h)-induced ROS generation through activation of Nrf2, GSH and inhibition of PM2.5-induced inflammatory MDA [68]. These results suggest that Tectoridin has potential to controlling PM2.5-induced oxidative stress, ferroptosis, and lung pathologies.…”

Section: Lessons From Studies Using Animal Models and Natural Compoundsmentioning

confidence: 67%

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Air-pollutant Particulate Matter 2.5 (PM2.5)-induced Inflammation and Oxidative Stress in Diseases: Possible Therapeutic Approaches

Ghosh

2023

Preprint

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Today, air pollution is the greatest threat to organismal healthspan. The environment of our planet earth, the habitat of over eight billion humans and estimated twenty billion billions other animals, is contaminated with a wide variety of pollutants. Unfortunately, humans, out of billions and billions of living organisms on earth, are solely responsible for polluting the environment through emitting pollutants like particulate matter from industry, fuel engine vehicles, biomass combustion, toxic fumes from blasting, and wildfire. In the modern world, human-caused air pollutants induce massive oxidative stress and inflammation, the major contributors in initiation and progression of many diseases including pulmonary, cardiovascular, renal, hepatic, reproductive, neurological, mental, and accelerated biological aging. The provocative question is the following: how can we solve this human-created problem? As it is not realistic to clean the environment at once from human-caused pollution, initiatives have been undertaken to develop novel therapeutic approaches to control air-pollutant-induced oxidative stress and inflammation to protect humans from pollution-induced devastating diseases. In this article, I discuss the key findings of numerous recent preclinical studies documenting first, the role of air pollutant PM2.5 in augmentation of inflammation, oxidative stress, and associated diseases; and second, the efficacies of different natural and synthetic compounds in amelioration of PM2.5-induced oxidative stress, inflammation, pyroptosis, and associated pathologies.

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Section: Lessons From Studies Using Animal Models and Natural Compoundsmentioning

confidence: 59%

Section: Lessons From Studies Using Animal Models and Natural Compoundsmentioning

confidence: 67%

Air-pollutant Particulate Matter 2.5 (PM2.5)-induced Inflammation and Oxidative Stress in Diseases: Possible Therapeutic Approaches

Ghosh

2023

Preprint

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“…This effect is achieved through the scavenging of hydroxyl and superoxide anion radicals [ 35 ]. Furthermore, tectoridin reverses lipid peroxidation induced by PM2.5 by activating the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway [ 36 ]. The antioxidant activity of esculin, a coumarin glucoside found in Cortex Fraxini, has been widely studied.…”

Section: Discussionmentioning

confidence: 99%

Induction of Autophagy by Extract from Corydalis heterocarpa for Skin Anti-Aging

Yang,

Nam,

Lee

et al. 2024

Marine Drugs

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The extracts of Corydalis heterocarpa, a salt-tolerant plant, exhibit diverse physiological properties, including anti-inflammatory, anticancer, and antiadipogenic effects. However, the anti-aging effects of C. heterocarpa extract (CHE) on human skin cells have not yet been investigated. In the present study, we determined that CHE inhibited senescence-associated β-galactosidase (SA-β-gal)-stained senescent human dermal fibroblasts (HDFs). Furthermore, CHE markedly suppressed the expression of major regulatory proteins involved in senescence, including p53, p21, and caveolin-1. Interestingly, CHE promoted autophagic flux, as confirmed by the formation of microtubule-associated protein 1 light chain 3B (LC3B) puncta and lysosomal activity. Notably, using RNA sequencing (RNA-seq), we showed that CHE selectively regulated the gene expression of leucine-rich repeat and sterile alpha motif-containing 1 (LRSAM1), an important regulator of autophagy. The adenosine-monophosphate activated protein kinase/mammalian target of rapamycin (AMPK/mTOR) pathway, which is essential for autophagy regulation, was also modulated by CHE. LRSAM1 depletion not only inhibited LC3B expression but also decreased the autophagy flux induced by CHE. Moreover, the knockdown of LRSAM1 suppressed the reversal of CHE-induced senescence in old HDFs. Collectively, our study has revealed the rejuvenating effects and molecular mechanisms of CHE, suggesting that CHE may be a promising anti-aging agent.

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“…Besides, Nrf2 signaling pathway is of utmost importance in the regulation of ferroptosis ( Dodson et al, 2019 ). Study has found that both SCL7A11 and GPX4 can be upregulated by activating Nrf2 signaling pathway, which can directly decompose lipid peroxidation products ( Dong et al, 2023 ). Many proteins participate in iron storage and transport, such as FTH1, FTL1, TFR1 and FPN1, are also regulated by Nrf2 ( Wang et al, 2022c ).…”

Section: Introductionmentioning

confidence: 99%

Molybdenum and cadmium co-induce apoptosis and ferroptosis through inhibiting Nrf2 signaling pathway in duck (Anas platyrhyncha) testes

Zhu,

Dai,

Wang

et al. 2024

Poultry Science

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Activation of Nrf2 signalling pathway by tectoridin protects against ferroptosis in particulate matter‐induced lung injury

Cited by 16 publications

References 41 publications

Air-pollutant Particulate Matter 2.5 (PM2.5)-induced Inflammation and Oxidative Stress in Diseases: Possible Therapeutic Approaches

Air-pollutant Particulate Matter 2.5 (PM2.5)-induced Inflammation and Oxidative Stress in Diseases: Possible Therapeutic Approaches

Induction of Autophagy by Extract from Corydalis heterocarpa for Skin Anti-Aging

Molybdenum and cadmium co-induce apoptosis and ferroptosis through inhibiting Nrf2 signaling pathway in duck (Anas platyrhyncha) testes

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