ArticleAnalytical cellular pathology (Amsterdam)2026
Xinlikang Capsule Alleviates Chemotherapy-Induced Fatigue by Inhibiting the PI3K/AKT-mTOR-FoxO Pathway.
Article in Analytical cellular pathology (Amsterdam), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Xinlikang Capsule Alleviates Chemotherapy-Induced Fatigue by Inhibiting the PI3K/AKT-mTOR-FoxO Pathway.Analytical cellular pathology (Amsterdam) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
objectiveChemotherapy-induced fatigue (CIF) remains a clinically challenging condition with limited therapeutic options. This study aimed to elucidate the therapeutic potential and underlying mechanisms of the multiherbal Xinlikang (XLK) capsule against CIF using an integrated strategy that combined network pharmacology prediction with experimental validation.
methodsA murine CIF model was established using 5-fluorouracil (5-FU). XLK was administered at various doses to evaluate its efficacy through comprehensive assessments, including behavioral tests (weight-bearing swimming, tail suspension, and grip strength), histopathology (hematoxylin-eosin [H&E] and periodic acid-Schiff [PAS] staining), and metabolic indices (lactate and ATP levels). To investigate the mechanisms, an integrated network pharmacology approach was employed to identify bioactive components of XLK, predict their potential targets, and construct a "component-target-pathway" network. Core signaling pathways implicated in CIF were prioritized via protein-protein interaction (PPI) and KEGG enrichment analyses. Key predictions were subsequently verified by Western blot analysis.
resultsXLK treatment significantly ameliorated fatigue-like behaviors, improved muscle glycogen storage, and restored lactate and ATP homeostasis in CIF mice (all p < 0.05). Network pharmacology predicted that the anti-CIF effect of XLK was closely associated with the regulation of energy metabolism-related pathways, particularly the PI3K/AKT-mTOR-FoxO signaling axis. Experimental validation confirmed that XLK significantly modulated the expression and phosphorylation levels of key proteins (e.g., p-PI3K, p-AKT, and p-mTOR) within this pathway in the skeletal muscle or relevant tissues of CIF model mice (all p < 0.05).
conclusionXLK enhances cellular energy homeostasis by regulating the PI3K/AKT-mTOR-FoxO signaling axis, thereby alleviating CIF. These findings provide a mechanistic rationale for the clinical application of XLK against CIF.
Indexed as
Identifiers
What Socratic holds
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.