Exploring the Therapeutic Efficacy and Molecular Mechanisms of Fu-zheng-yi-qi Recipe in Ameliorating Cancer Cachexia-associated Muscle Atrophy.

Authors

Guangran Hu, Xuan Li, Yinqiu Wu, Shengzhe Zhang, Guilan Jin, Ning Ding, Jun Zhang, Hua Dai

Published in

Combinatorial chemistry & high throughput screening. Oct 02, 2026. Epub Oct 02, 2026.

Abstract

Cancer Cachexia (CC) is a systemic wasting syndrome characterized by persistent skeletal muscle depletion. This study aims to systematically evaluate the therapeutic effect of the Fu-zheng-yi-qi recipe (FZYQR) against CC and to explore the potential molecular mechanisms underlying its ameliorative effects on muscle atrophy.
The components of FZYQR were characterized using UPLC-Class Plus/VION IMS QTof. Pharmacological network analysis was performed to predict the therapeutic targets of FZYQR. An in vivo tumor cachexia model was established by subcutaneously implanting C26 tumor cells into male BALB/c mice. The therapeutic efficacy of FZYQR was evaluated by monitoring changes in body weight, grip strength, skeletal muscle mass, pathological progression, blood biochemical parameters, and inflammatory cytokine levels. The therapeutic mechanism underlying muscle atrophy was validated by qPCR and Western blot.
Among the major bioactive components of FZYQR, luteolin and quercetin play critical roles in treating CC. FZYQR significantly ameliorated muscle atrophy and associated symptoms in a well-established mouse model of CC. Mechanistically, upon FZYQR intervention, the expression level of JUN in skeletal muscle tissues of cachectic mice was markedly inhibited, accompanied by downregulation of the muscle atrophy biomarkers Atrogin-1 and MuRF1.
The specific mechanism underlying CC-induced muscle atrophy remains to be further elucidated. This study demonstrates the therapeutic potential of FZYQR for CC, and also provides a research strategy for the future development of natural products with anti-muscle atrophy effects.
FZYQR exerts protective effects against CC-induced muscle atrophy, potentially through the modulation of the JNK/c-Jun signaling pathway.

PMID:
42861806
Bibliographic data and abstract were imported from PubMed on 12 Oct 2026.

Read full publication at:
Please sign in to see all details.

Stats

1-terrible, 9-excellent. How would you rate this publication? Sign in in to submit your rating.

Post a comment

You need to be signed in to post comments. You can sign in here.

Comments

There are no comments yet.