Combinatorial chemistry & high throughput screening · 2026
Exploring the Therapeutic Efficacy and Molecular Mechanisms of Fu-zheng-yi-qi Recipe in Ameliorating Cancer Cachexia-associated Muscle Atrophy.
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Hu Guangran, Li Xuan, Wu Yinqiu, Zhang Shengzhe, Jin Guilan, Ding Ning, Zhang Jun, Dai Hua
Аннотация
INTRODUCTION: 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.
METHODS: 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.
RESULTS: 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.
DISCUSSION: 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.
CONCLUSION: FZYQR exerts protective effects against CC-induced muscle atrophy, potentially through the modulation of the JNK/c-Jun signaling pathway.
METHODS: 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.
RESULTS: 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.
DISCUSSION: 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.
CONCLUSION: FZYQR exerts protective effects against CC-induced muscle atrophy, potentially through the modulation of the JNK/c-Jun signaling pathway.