ArticleCurrent molecular medicine2024
Albiflorin Alleviates Sepsis-induced Acute Liver Injury through mTOR/p70S6K Pathway.
Article in Current molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Albiflorin, a Monoterpene Glycoside, Protects Myoblasts against Hydrogen Peroxide-Induced Apoptosis by Activating the Nrf2/HO-1 Axis.Biomolecules & therapeutics · 2025Article
- Bioinformatics study of the TNFRSF1A mechanism involved in acute liver injury in sepsis through the mTOR signaling pathway.Histology and histopathology · 2025Article
- Liver injury in sepsis: manifestations, mechanisms and emerging therapeutic strategies.Frontiers in immunology · 2025Review
- Modulation of Gut Microbial Community and Metabolism byNutrients · 2024Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundSepsis often induces hepatic dysfunction and inflammation, accounting for a significant increase in the incidence and mortality rates. To this end, albiflorin (AF) has garnered enormous interest due to its potent anti-inflammatory activity. However, the substantial effect of AF on sepsis-mediated acute liver injury (ALI), along with its potential mechanism of action, remains to be explored.
methodsAn LPS-mediated primary hepatocyte injury cell model in vitro and a mouse model of CLP-mediated sepsis in vivo were initially built to explore the effect of AF on sepsis. Furthermore, the hepatocyte proliferation by CCK-8 assay in vitro and animal survival analyses in vivo for the survival time of mice were carried out to determine an appropriate concentration of AF. Then, flow cytometry, Western blot (WB), and TUNEL staining analyses were performed to investigate the effect of AF on the apoptosis of hepatocytes. Moreover, the expressions of various inflammatory factors by ELISA and RT-qPCR analyses and oxidative stress by ROS, MDA, and SOD assays were determined. Finally, the potential mechanism of AF alleviating the sepsis-mediated ALI via the mTOR/p70S6K pathway was explored through WB analysis.
resultsAF treatment showed a significant increase in the viability of LPS-inhibited mouse primary hepatocytes cells. Moreover, the animal survival analyses of the CLP model mice group indicated a shorter survival time than the CLP+AF group. AF-treated groups showed significantly decreased hepatocyte apoptosis, inflammatory factors, and oxidative stress. Finally, AF exerted an effect by suppressing the mTOR/p70S6K pathway.
conclusionIn summary, these findings demonstrated that AF could effectively alleviate sepsis-mediated ALI via the mTOR/p70S6K signaling pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.