Cepharanthine Inhibits Doxorubicin-Induced Cellular Senescence by Activating Autophagy via the MTOR Signaling Pathway

January 2023 in “ Discovery medicine ”

Jun Chen, Chun-hong Xia, Rui Dong, Xianguo Liu, Jing Xia

Cepharanthine Doxorubicin cellular senescence autophagy mTOR signaling pathway NIH3T3 cell lines cardiotoxicity myelosuppression aging-related proteins aging-related genes Cep Dox

TLDR Cepharanthine helps reduce cell aging caused by the cancer drug Doxorubicin by boosting cell cleanup processes.

The study investigates the effects of Cepharanthine (Cep) on Doxorubicin (Dox)-induced cellular senescence in NIH3T3 cell lines. Dox, a common anticancer drug, causes cardiotoxicity and myelosuppression, linked to cellular senescence. Cep, known for treating various conditions including hair loss, was tested for its potential to alleviate Dox-induced senescence. Results showed that Cep reduced the proportion of senescent cells and the expression of aging-related proteins and genes. Mechanistically, Cep restored autophagy dysfunction and suppressed the mTOR signaling pathway, enhancing cell viability. This research suggests Cep as a potential antiaging therapy by modulating autophagy and mTOR signaling.

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