ArticleJournal of natural medicines2024
Allicin ameliorates sepsis-induced acute kidney injury through Nrf2/HO-1 signaling pathway.
Article in Journal of natural medicines, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The trial behind it
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Targeting integrated cell death networks in sepsis‑associated acute kidney injury: Shared regulatory nodes and diet‑related small molecule modulation (Review).International journal of molecular medicine · 2026Review
- Heparin-binding protein aggravates sepsis-induced acute lung injury by inhibiting the PERK-Nrf2-HO-1 signaling pathway.Journal of molecular histology · 2026Article
- Therapeutic Potential of Allicin in Multi-System Inflammatory Diseases.Current issues in molecular biology · 2026Review
- Plant-based bioactives and oxidative stress in reproduction: anti-inflammatory and metabolic protection mechanisms.Frontiers in nutrition · 2025Review
- Mini-review: The health benefits and applications of allicin.Frontiers in pharmacology · 2025Review
- Mini-encyclopedia of mitochondria-relevant nutraceuticals protecting health in primary and secondary care-clinically relevant 3PM innovation.The EPMA journal · 2024Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury (AKI) is a complication that can be induced by different factors. Allicin is a class of organic sulfur compounds with anticancer and antibacterial effects, and has not been reported in sepsis-induced AKI (S-AKI). S-AKI was induced in c57BL/6 mice by cecal ligation puncture. In response to the treatment of allicin, the survival rate of mice with S-AKI was increased. Reduced levels of serum creatinine, blood urea nitrogen, UALB, KIM-1 and NGAL indicated an improvement in renal function of S-AKI mice. Allicin inhibited the inflammation and cell apoptosis, which evidenced by decreased levels of inflammatory cytokines and apoptosis-related proteins. Oxidative stress was evaluated by the levels of oxidative stress biomarkers, and suppressed by allicin. In addition, allicin-alleviated mitochondrial dysfunction was characterized by decreased JC-1 green monomer. These effects of allicin were also evidenced in HK2 cells primed with lipopolysaccharide (LPS). Both in vivo and in vitro experiments showed that the nuclear translocation of Nrf2 and the expression of HO-1 increased after allicin treatment, which was confirmed by ML385 and CDDO-Me. In summary, this study revealed the alleviating effect of allicin on S-AKI and demonstrated the promotive effect of allicin on nuclear translocation of Nrf2 for the first time. It was inferred that allicin inhibited the progression of S-AKI through Nrf2/HO-1 signaling pathway. This study makes contributions to the understanding of the roles of allicin in S-AKI.
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Registered trials
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