ArticleCombinatorial chemistry & high throughput screening2026
Qishen Huoxue Granule Ameliorates LPS-induced Cardiomyocyte Injury by Suppressing Excessive Autophagy
Article in Combinatorial chemistry & high throughput screening, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
introductionQishen Huoxue Granule (QHG), a classical Traditional Chinese Medicine prescription, can reduce septic cardiomyopathy in clinic. However, the mechanism of QHG remains unclear. This study aims to investigate the mechanism and effect of QHG-contained serum (QHG-CS) on sepsis-induced cardiomyopathy (SICM).
methodsQHG was administered to Wistar rats via gavage to obtain QHG-CS. The chemical constituents of QHG-CS were identified via UPLC-Q-TOF-MS. In vitro, rat cardiomyocytes H9c2 cells isolated from embryonic BD1X rat heart tissue, and septic myocardial injury model was established by inducing H9c2 cells with lipopolysaccharide (LPS). Cell viability was assessed through CCK-8. Protein expression was determined using western blot, and gene expression was measured using real-time quantitative PCR. Cell autophagy was investigated by detecting LC3 expression using flow cytometry and immunofluorescence. In addition, three inhibitors, A779 (MasR), wortmannin (PI3K) and rapamycin (mTOR) were used to localize the potential therapeutic targets.
resultsQHG-CS significantly improved the survival of septic cardiomyocytes (p<0.0001). The expression of autophagy-related markers Beclin1, ATG5, and LC3II/I was increased in LPS-induced cardiomyocytes, which could be inhibited by QHG-CS. QHG-CS upregulated the mRNA expression of MasR, PI3K, and AKT, as well as the phosphorylation of PI3K, AKT, and mTOR. Moreover, A779 markedly lowered mRNA levels of MasR, PI3K, and mTOR, while wortmannin decreased mRNA levels of PI3K and mTOR, whereas rapamycin only suppressed mTOR phosphorylation. DISCUSSION: By inhibiting excessive autophagy through upregulation of the MasR/PI3K-AKT-mTOR pathway, QHG can alleviate sepsis-induced cardiomyocyte damage. This study provides novel perspectives for the management of sepsis-induced cardiac damage.
Indexed as
Identifiers
40277111What OpenQuestion 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 OpenQuestion graph.