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PP-44

Loganin reduces cellular senescence and mitochondrial dysfunction induced

by paclitaxel in skeletal muscle cells

#,1
1,2
1,2
Y u -Fan Chuang (莊雨凡), Cai-Rong Wu (吳彩榕), Wan-Hsuan Chang (張婉萱),
1,2
Ying-Jung Su (蘇盈蓉), Yi-Ching Lo (羅怡卿)* ,1,2,3

1 Department of Pharmacology, School of Medicine, College of Medicine, Kaohsiung
Medical University, Kaohsiung 80708, Taiwan
2 Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University,
Kaohsiung 80708, Taiwan
3 Department of Traditional Medicine, School of Medicine, College of Medicine, Kaohsiung
Medical University, Kaohsiung 80708, Taiwan
* E-mail: yichlo@kmu.edu.tw

Abstract
Cellular senescence, marked by permanent cell cycle arrest and senescence-associated
secretory phenotype (SASP)-driven inflammation, contributes to skeletal muscle dysfunction.
Paclitaxel, a common chemotherapeutic drug, induces skeletal muscle toxicity through
premature cellular senescence and mitochondrial dysfunction. In this study, we examined
whether loganin, a natural iridoid glycoside, could prevent these effects in C2C12 cells.
Loganin pretreatment significantly suppressed senescence markers, including p21 expression,
NFκB activation, Cdkn1a/Il6 upregulation, and SA-β-gal positivity. Moreover, it preserved
mitochondrial DNA content, membrane potential, and ATP levels, while reducing
mitochondrial ROS accumulation, highlighting its role in maintaining mitochondrial integrity.
Furthermore, loganin activated the SIRT1-AMPK axis and upregulated PGC-1α, TFAM, and
NRF1 to promote mitochondrial biogenesis, linking pathway activation to functional outcomes.
Together, these results indicate that loganin possesses novel protection against paclitaxel-
induced cellular senescence and mitochondrial dysfunction, suggesting loganin as a promising
candidate for improving muscle health during chemotherapy and warranting further in vivo
investigation.

Keywords: Cellular senescence; Loganin; Mitochondrial biogenesis; Paclitaxel; Skeletal
muscle