ArticleSAGE open medicine2019
Attenuation of lipopolysaccharide-induced lung inflammation by ascorbic acid in rats: Histopathological and ultrastructural study.
Article in SAGE open medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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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
7 citing papers in PubMed, 11 citations in OpenAlex.
- Current advancements in the mechanisms and animal models of acute exacerbation of pulmonary fibrosis: a systematic review.Frontiers in pharmacology · 2025Review
- Bone marrow-derived mesenchymal stem cells reduce CClRenal failure · 2024Article
- Vitamin C: Rationale for Its Use in Sepsis-Induced Acute Respiratory Distress Syndrome (ARDS).Antioxidants (Basel, Switzerland) · 2024Review
- Acute exacerbation of idiopathic pulmonary fibrosis model in the rats using bleomycin and lipopolysaccharides.Journal of advanced veterinary and animal research · 2023Article
- The effects of vitamin C on respiratory, allergic and immunological diseases: an experimental and clinical-based review.Inflammopharmacology · 2023Review
- Article
- Insights into the Role of Bioactive Food Ingredients and the Microbiome in Idiopathic Pulmonary Fibrosis.International journal of molecular sciences · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionLipopolysaccharide is a bacterial endotoxin that induces acute lung injury in experimental animals, which is similar to acute respiratory distress syndrome in humans. The induced tissue trauma ends in fibrosis. Understanding the pathogenesis is important in the prevention and treatment of the complications. This study was assigned to investigate the long-term lipopolysaccharide-induced lung injury and the postulated protective effect of ascorbic acid on these changes. MATERIALS AND
methodsTwenty-four adult male albino rats were divided into three groups. Group I was the controls, group II received lipopolysaccharide and group III received lipopolysaccharide and ascorbic acid. After 30 days of starting treatment, lung tissue samples were obtained.
resultsGroup II lung tissues showed marked thickening of the alveolar septa with collapsed alveolar sacs, detached bronchial epithelium, inflammatory cell infiltration and excessive deposition of collagen. Group III showed mild thickening of the alveolar walls, scanty inflammatory cell infiltration, mild parabronchial fibrosis and less marked collagen deposition. α-Smooth muscle actin staining of group II showed marked expression of the actin-positive cells. Less potential expression of the dye was found in group III. Ultrastructural examination of group II showed evident structural changes in pneumocytes with capillary basement membrane irregularity and interruption compared to uniform basement membrane in group III with less prominent intracellular changes in pneumocytes.
conclusionAscorbic acid attenuated the inflammatory response and fibrosis in the lungs of rats treated with lipopolysaccharide as evidenced by the histological, immunohistochemical and ultrastructural studies.
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Registered trials
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