ArticleMedical science monitor : international medical journal of experimental and clinical research2019
Allicin Improves Lung Injury Induced by Sepsis via Regulation of the Toll-Like Receptor 4 (TLR4)/Myeloid Differentiation Primary Response 88 (MYD88)/Nuclear Factor kappa B (NF-κB) Pathway.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 31 citations in OpenAlex.
- Therapeutic Potential of Allicin in Multi-System Inflammatory Diseases.Current issues in molecular biology · 2026Review
- Modulation of Toll-like Receptors with Natural Compounds: A Therapeutic Avenue Against Inflammaging?International journal of molecular sciences · 2025Review
- Bioactive Polysaccharides Prevent Lipopolysaccharide-Induced Intestinal Inflammation via Immunomodulation, Antioxidant Activity, and Microbiota Regulation.Foods (Basel, Switzerland) · 2025Article
- Article
- Unveiling the Potential of Sulfur-Containing Gas Signaling Molecules in Acute Lung Injury: A Promising Therapeutic Avenue.Current issues in molecular biology · 2024Review
- Allicin ameliorates sepsis-induced acute kidney injury through Nrf2/HO-1 signaling pathway.Journal of natural medicines · 2024Article
- Identification and Analysis of PANoptosis-Related Genes in Sepsis-Induced Lung Injury by Bioinformatics and Experimental Verification.Journal of inflammation research · 2024Article
- Allicin protects against LPS-induced cardiomyocyte injury by activating Nrf2-HO-1 and inhibiting NLRP3 pathways.BMC cardiovascular disorders · 2023Article
- Allicin Alleviated LPS-Induced Mastitis via the TLR4/NF-κB Signaling Pathway in Bovine Mammary Epithelial Cells.International journal of molecular sciences · 2023Article
- Editorial: "Small molecules targeting transmembrane receptors and ion channels in drug discovery".Frontiers in molecular biosciences · 2023Article
- Black Garlic and Thiosulfinate-Enriched Extracts as Adjuvants to Ceftriaxone Treatment in a Rat Peritonitis Model of Sepsis.Biomedicines · 2022Article
- Plants' bioactive secondary metabolites in the management of sepsis: Recent findings on their mechanism of action.Frontiers in pharmacology · 2022Review
- Allicin, an Antioxidant and Neuroprotective Agent, Ameliorates Cognitive Impairment.Antioxidants (Basel, Switzerland) · 2021Review
- Deletion of TLR4 attenuates lipopolysaccharide-induced acute liver injury by inhibiting inflammation and apoptosis.Acta pharmacologica Sinica · 2021Article
- Article
- Detecting Critical Functional Ingredients Group and Mechanism of Xuebijing Injection in Treating Sepsis.Frontiers in pharmacology · 2021Article
- Sufentanil attenuates inflammation and oxidative stress in sepsis-induced acute lung injury by downregulating KNG1 expression.Molecular medicine reports · 2020Article
- Modulation of neutrophil (dys)function by Ayurvedic herbs and its potential influence on SARS-CoV-2 infection.Journal of Ayurveda and integrative medicineReview
- Ischemic Postconditioning Mitigates Lipopolysaccharide-induced Acute Lung Injury in Rats.In vivo (Athens, Greece)Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND The aim of this study was to assess the effects and mechanisms of allicin in a sepsis-induced lung injury in vivo study. MATERIAL AND METHODS The rats (n=54) were divided into 6 groups: Normal, DMSO, LPS, LPS+LD, LPS+MD, and LPS+HD groups. After being treated by different methods, we collected the lung tissues of different groups and evaluated the pathology by HE staining and positive apoptosis cells by TUNEL. We assessed the W/D ratio, inflammatory cytokines (TNF-alpha, IL-6 and IL-1ß), and relative protein expressions (TLR4, MyD88, NF-kappaB, caspase-3, and caspase-9) by IHC assay. RESULTS Compared with LPS group, the lung injury and positive cell number of allicin treated groups were significantly improved with dose-dependent (P<0.05, respectively) and the W/D ratio and TNF-alpha, IL-6 and IL-1ß concentration were significantly down-regulation compared with those of LPS group with dose-dependent (P<0.05, respectively). By IHC, the TLR4, MyD88, NF-kappaB, caspase-3 and caspase-9 protein activities of allicin treated groups were significantly suppressed compared with those of LPS group (P<0.05, respectively) in lung tissues. CONCLUSIONS This in vivo study shows that allicin improved sepsis-induced lung injury by regulation of TLR4/MyD88/NF-kappaB.
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