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Effects of mitochondria-targeted antioxidant SS-31 on cigarette smoke-induced airway inflammation and oxidative stress in a mouse model

ABSTRACT: Effects of mitochondria-targeted antioxidant SS-31 on cigarette smoke-induced airway inflammation and oxidative stress in a mouse model

PROVIDER: PRJNA687734 | ENA |

REPOSITORIES: ENA

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Effects of mitochondria-targeted antioxidant SS-31 on cigarette smoke-induced airway inflammation and oxidative stress in a mouse model

Project description:This study investigated whether mitochondria-targeted peptide SS-31 played a protective role in cigarette smoke (CS)-induced airway inflammation and oxidative stress in mice. Mice were exposed to CS for 4 weeks to establish a CS-induced airway inflammation model, then treated with SS-31. Pathological changes and oxidative stress in lung tissue, inflammatory cell counts and pro-inflammatory cytokines in bronchoalveolar lavage fluid (BALF) were examined. RNA sequencing from lung tissue and western blotting were conducted to investigate mechanisms. SS-31 attenuated CS-induced inflammatory injury of the airway. Numbers of total cells, neutrophils, and macrophages and levels of tumor necrosis factor α, interleukin 6, and matrix metallopeptidase 9 in BALF were markedly reduced by SS-31. SS-31 attenuated CS-induced oxidative stress by decresing malondialdehyde and myeloperoxidase levels, and increasing superoxide dismutase activity. It also reversed the expression of mitochondrial fission protein and optic atrophy 1 protein, and reduced cytochrome c release into the cytosol. RNA sequencing revealed that SS-31 changed CS-induced expression profiles and enriched MAPK pathway, western blotting confirmed that SS-31 inhibited the CS-activated MAPK pathway. SS-31 alleviates CS-induced airway inflammation and oxidative stress, possibly via the regulation of mitochondrial function and MAKP pathway, SS-31 may be a novel drug for CS-induced airway disorders.

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Transcriptional response of Mycobacterium tuberculosis to cigarette smoke condensate

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mouse lung resistance or sensitivity to cigarette smoke

Project description:We have investigated the effects of cigarette smoke exposure in three different strains of mice. DBA/2 and C57Bl/6J are susceptible to smoke and develop different lung changes in response to chronic exposure, while ICR mice are resistant to smoke and do not develop emphysema. The present study was carried out to determine early changes in the gene expression profile of mice exposed to cigarette smoke with either a susceptible or resistant phenotype.

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Diet-Induced Obesity Exacerbates Inflammatory and Oxidative Stress Responses in Mice Exposed to Cigarette Smoke

Project description:To identify biosignatures that describe these lifestyle susceptibility factors, we performed parallel exposures of regular weight (RW) C57BL/6 and diet-induced obese (DIO) C57BL/6 mice to cigarette smoke, either mainstream (MS) or sidestream (SS), mimicking both the smoker and environmental exposure through second-hand smoke, respectively. Transcriptional responses were measured by global microarray analysis of lung tissue. Groups (N=8 biological replicates) of RW and DIO C57BL/6 mice (15-weeks old at start of exposures) were exposed to either filtered air (sham controls, SC), mainstream (MS) or sidestream (SS) cigarette smoke by nose-only inhalation exposure for 5 hr/day for a total of eight exposures over two weeks as follows: 5 consecutive days of exposure, followed by 2 days with no exposure, then three days of exposure, with necropsies occurring the day following the last exposure.

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Time course of NHBE cells exposed to whole cigarette smoke

Project description:Gene expression patterns were assessed in normal human bronchial epithelial (NHBE) cells exposed to cigarette smoke from a reference cigarette (2R4F, University of Kentucky) and a typical American brand of "light" cigarettes ("Lights") in order to develop a better understanding of the genomic impact of tobacco exposure, which can ultimately define biomarkers that discriminate tobacco-related effects and outcomes in a clinical setting. NHBE cells were treated with whole cigarette smoke for 15 minutes and alterations to the transcriptome assessed at 2, 4, 8 and 24 hours post-exposure using high-density oligonucleotide microarrays. Keywords: time course, cigarette smoke exposure

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