Sipeimine attenuates PM2.5-induced lung toxicity via suppression of NLRP3 inflammasome-mediated pyroptosis through activation of the PI3K/AKT pathway

Huang, Demei; Shen, Zherui; Zhao, Sijing; Pei, Caixia; Jia, Nan; Wang, Yilan; Wu, Yongcan; Wang, Xiaomin; Shi, Shihua; He, Yacong; Wang, Zhenxing; Wang, Fei

doi:10.1016/j.cbi.2023.110448

Cited by 10 publications

(8 citation statements)

References 64 publications

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“…Pretreatment of rats with Rosavidin (50-100 mg/kg/day for 3 days) diminishes PM2.5 (7.5mg/kg twice in 36h at 0h and 24h)-induced inflammation and ameliorates lung pathologies in rats through inhibition of inflammatory and apoptotic regulators including IL-1, Nlrp3 inflammasome, and caspase. This study further demonstrated that Nlrp3 specific activator nigericin blunts Rosavidin-mediated amelioration of PM2.5-induced lung pathologies [63]. Therefore, Rosavidin has potential to be a remedy to controlling PM2.5-induced inflammation and pyroptosis-driven lung pathologies.…”

Section: Lessons From Studies Using Animal Models and Natural Compoundssupporting

confidence: 57%

“…activator nigericin [55]. Thus, Sipeimine effectively ameliorates PM2.5-induced inflammation, oxidative stress, pyroptosis and lung injury in both rodent models.…”

Section: Lessons From Studies Using Animal Models and Natural Compoundsmentioning

confidence: 83%

“…These results indicate that Bergapten is a potential natural therapeutic agent to treat CARAS and PM2.5-induced worst lung pathologies. Similarly, the efficacy of Rosavidin, a phenylpropanoid compound having multiple biological activities extracted from the Rhodiola crenulata plant, in amelioration of PM2.5induced lung pathology has been examined in a rat model [63]. Pretreatment of rats with Rosavidin (50-100 mg/kg/day for 3 days) diminishes PM2.5 (7.5mg/kg twice in 36h at 0h and 24h)-induced inflammation and ameliorates lung pathologies in rats through inhibition of inflammatory and apoptotic regulators including IL-1, Nlrp3 inflammasome, and caspase.…”

Section: Lessons From Studies Using Animal Models and Natural Compoundsmentioning

confidence: 99%

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Air-pollutant particulate matter 2.5 (PM2.5)-induced inflammation and oxidative stress in diseases: Possible therapeutic approaches

Asish K Ghosh

2024

Int. J. Sci. Res. Arch.

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Today, air pollution is one of the greatest threats to organismal healthspan. The environmental air of earth is contaminated with a wide variety of artificially generated pollutants like fine particulate matter (PM2.5) emitting from industry, fuel engine vehicles, biomass combustion, fumes from blasting, crop residue burning, and wildfire. The air pollutant PM2.5 induces massive oxidative stress and inflammation, the major contributors in initiation and progression of numerous diseases including pulmonary, cardiovascular, renal, hepatic, reproductive, neurological, mental, and accelerated biological aging. The provocative question is the following: how can we solve this air pollution associated problem? As it is not realistic to clean the environment at once from artificially generated toxic pollution, initiatives have been undertaken to develop novel therapeutic approaches to control air-pollutant-induced oxidative stress and inflammation and associated devastating diseases. The primary goal of this review article is to discuss systematically 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. Further investigation on the safety of these compounds will be helpful to select effective and non-toxic compound(s) for clinical trial and drug development.

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Section: Lessons From Studies Using Animal Models and Natural Compoundssupporting

confidence: 57%

“…activator nigericin [55]. Thus, Sipeimine effectively ameliorates PM2.5-induced inflammation, oxidative stress, pyroptosis and lung injury in both rodent models.…”

Section: Lessons From Studies Using Animal Models and Natural Compoundsmentioning

confidence: 83%

Section: Lessons From Studies Using Animal Models and Natural Compoundsmentioning

confidence: 99%

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Air-pollutant particulate matter 2.5 (PM2.5)-induced inflammation and oxidative stress in diseases: Possible therapeutic approaches

Asish K Ghosh

2024

Int. J. Sci. Res. Arch.

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“…In the same year, Zhang et al (32) demonstrated that the exosomes derived from bone marrow mesenchymal stem cells could activate the yes-associated protein/β-catenin axis to suppress NLRP3-mediated lung pyroptosis and further alleviate acute lung injury induced by cardiopulmonary bypass. In 2023, Huang et al (33) demonstrated that sipeimine could activate the PI3K/AKT pathway to inhibit lung pyroptosis and thus attenuate lung toxicity induced by fine particulate matter (PM2.5). In the setting of regional lung IR injury, some studies have also confirmed the occurrence of cell pryoptosis in the damaged lung tissues, which could become a therapeutic target for alleviating lung pathological damage (34,35).…”

Section: Discussionmentioning

confidence: 99%

Sulforaphane Alleviates Postresuscitation Lung Pyroptosis Possibly via Activating the Nrf2/Ho-1 Pathway

Li,

Yang,

Xie

et al. 2023

Shock

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Introduction Sulforaphane (SFN), known as the activator of the nuclear factor E2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) pathway, has been proven to protect the lung against various pathological stimuli. The present study aimed to investigate the effect of SFN on lung injury induced by systemic ischemia reperfusion following cardiac arrest and resuscitation. Methods After animal preparation, twenty-four pigs were randomly divided into Sham group (n = 6), cardiopulmonary resuscitation group (CPR, n = 9), or CPR + SFN group (n = 9). The experimental model was then established by 10 min of cardiac arrest followed by 6 min of CPR. Once spontaneous circulation was achieved, a dose of 2 mg/kg of SFN diluted in 20 ml of saline was intravenously infused with a duration of 5 min. During 4 h of observation after resuscitation, extravascular lung water index (ELWI), pulmonary vascular permeability index (PVPI), and oxygenation index (OI) were regularly evaluated. At 24 h after resuscitation, lung tissues were harvested to evaluate the score of lung histopathological injury, the activity of superoxide dismutase (SOD), the contents of malondialdehyde (MDA), interleukin-1β (IL-1β), and interleukin-18 (IL-18), and the expression levels of NOD-like receptor pyrin domain 3 (NLRP3), cleaved caspase 1, gasdermin D (GSDMD), GSDMD N-terminal (GSDMD-N), Nrf2, and HO-1. Results During CPR, spontaneous circulation was achieved in 6 and 7 pigs in the CPR and CPR + SFN groups, respectively. After resuscitation, the indicators of lung injury (ELWI, PVPI, and OI) were all better in the CPR + SFN group than in the CPR group, in which the differences in ELWI and PVPI at 2, and 4 h after resuscitation were significant between the two groups. In addition, SFN significantly reduced lung injury score, improved oxidative imbalance (SOD, MDA), decreased pyroptosis-related proinflammatory cytokines (IL-1β, IL-18), downregulated pyroptosis-related proteins (NLRP3, cleaved caspase 1, GSDMD, GSDMD-N), and activated the Nrf2/HO-1 pathway when compared to the CPR group. Conclusions SFN produced effective post-resuscitation lung protection through alleviating lung pyroptosis possibly via activating the Nrf2/HO-1 pathway in pigs.

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“…Notably, Michaudel et al [51] demonstrated that the administration of xanthurenic acid reduced body weight loss, disease activity index (DAI), colon length shortening, and histological score in a DSS-induced experimental colitis mouse model compared to the control group (1). Sipeimine (5) has been shown to protect against lung damage induced by fine particulate matter [52,53], while peimisine (6), peimine (7), and peiminine (8) have exhibited anti-inflammatory effects in LPS-induced RAW264.7 cells [54,55]. Additionally, peimisine (6) and peimine (7) have been reported to have antitussive effects [56,57].…”

Section: Discussionmentioning

confidence: 99%

Hydroethanolic Extract of Fritillariae thunbergii Bulbus Alleviates Dextran Sulfate Sodium-Induced Ulcerative Colitis by Enhancing Intestinal Barrier Integrity

et al. 2023

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The incidence of ulcerative colitis (UC), an inflammatory disorder of the gastrointestinal tract, has rapidly increased in Asian countries over several decades. To overcome the limitations of conventional drug therapies, including biologics for UC management, the development of herbal medicine-derived products has received continuous attention. In this study, we evaluated the beneficial effects of a hydroethanolic extract of Fritillariae thunbergii Bulbus (FTB) in a mouse model of DSS-induced UC. The DSS treatment successfully induced severe colonic inflammation and ulceration. However, the severity of colitis was reduced by the oral administration of FTB. Histopathological examination showed that FTB alleviated the infiltration of inflammatory cells (e.g., neutrophils and macrophages), damage to epithelial and goblet cells in the colonic mucosal layer, and fibrotic lesions. Additionally, FTB markedly reduced the gene expression of proinflammatory cytokines and extracellular matrix remodeling. Immunohistochemical analysis showed that FTB alleviated the decrease in occludin and zonula occludens-1 expression induced by DSS. In a Caco-2 monolayer system, FTB treatment improved intestinal barrier permeability in a dose-dependent manner and increased tight junction expression. Overall, FTB has potential as a therapeutic agent through the improvement of tissue damage and inflammation severity through the modulation of intestinal barrier integrity.

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Sipeimine attenuates PM2.5-induced lung toxicity via suppression of NLRP3 inflammasome-mediated pyroptosis through activation of the PI3K/AKT pathway

Cited by 10 publications

References 64 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

Sulforaphane Alleviates Postresuscitation Lung Pyroptosis Possibly via Activating the Nrf2/Ho-1 Pathway

Hydroethanolic Extract of Fritillariae thunbergii Bulbus Alleviates Dextran Sulfate Sodium-Induced Ulcerative Colitis by Enhancing Intestinal Barrier Integrity

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