ArticleJournal of thoracic disease2020
Schisandra A ameliorates cigarette smoke extract and lipopolysaccharide-induced oxidative stress in lung epithelial cells.
Article in Journal of thoracic disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 13 citations in OpenAlex.
- The Mechanism of Traditional Chinese Medicine and Natural Medicine in Treating Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2025Review
- Ginseng Saponin Rb1 Attenuates Cigarette Smoke Exposure-Induced Inflammation, Apoptosis and Oxidative Stress via Activating Nrf2 and Inhibiting NF-κB Signaling Pathways.International journal of chronic obstructive pulmonary disease · 2023Article
- Effects of Antioxidant on Oxidative Stress and Autophagy in Bronchial Epithelial Cells Exposed to Particulate Matter and Cigarette Smoke Extract.Tuberculosis and respiratory diseases · 2022Article
- The treatment of Qibai Pingfei Capsule on chronic obstructive pulmonary disease may be mediated by Th17/Treg balance and gut-lung axis microbiota.Journal of translational medicine · 2022Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe previous studies reported the antioxidant and anti-inflammatory properties of Schisandrin A (Sch A). This study aimed to investigate the ability of Sch A to protect against lung oxidative stress induced by the combination of cigarette smoke extract and lipopolysaccharide (LPS) in an
methodsThe cell viability was determined by using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Colorimetry was used to detect the changes in antioxidant markers. Quantitative real-time polymerase chain reaction (RT-PCR) was used to examine the mRNA levels of interleukin-8 (IL-8) and heme oxygenase-1 (HO-1). The levels of IL-8 and HO-1 in the supernatant were determined by enzyme-linked immunosorbent assay, and Western blot analysis was performed to measure the phosphorylation and protein expression levels of nuclear factor-κB.
resultsSch A inhibited the excessive proliferation of pulmonary epithelial cells, decreased malondialdehyde content, and increased the expression levels of superoxide dismutase and glutathione after the combined treatment of cigarette smoke extract and LPS. Also, Sch A downregulated the expression of IL-8 and upregulated the expression of HO-1 mRNA in lung epithelial cells and cell supernatants, and resulted in the downregulation of the protein expression level of phosphorylated nuclear factor-κB.
conclusionsSch A inhibited the oxidative stress of lung epithelial cells induced by the combination of cigarette smoke extract and LPS. Sch A may be a potential therapeutic medication for COPD.
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Registered trials
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