DOI: 10.1177/22313354261485431 ISSN: 2231-3354

Anti-aging Effects of Angelica keiskei Leaf Extract on Skeletal Muscle: Associations with NF-κB p65 and PGC-1α in a D-galactose Model

Maria Dara Novi Handayani, Sultanto Rajasah, Rita Dewi, Ian Pranandi, Andrea Aprilia, Ferbian Milas Siswanto

Aging-associated skeletal muscle dysfunction is highly interlinked to chronic inflammation and mitochondrial dysregulation, with the suppression of PGC-1α representing a key molecular event. The use of natural phytochemicals to prevent aging-related pathological conditions has received increasing attention, including Angelica keiskei . This study examined the effects of A. keiskei leaf extract on skeletal muscle in a D-galactose (D-gal)-induced aging rat model, focusing on NF-κB p65 protein levels and PGC-1α-associated mitochondrial regulatory markers. Male rats were administered D-gal to induce accelerated aging and subsequently treated with A. keiskei extract. NF-κB p65 levels were assessed by ELISA, while the mRNA expression of Ppargc1a and its target gene Tfam , and mitochondrial antioxidants ( Sod2 , Txn1 , and Prdx1 ) in skeletal muscle tissue was quantified using real-time quantitative PCR. Administration of D-gal markedly increased NF-κB p65 protein levels, reduced the Ppargc1a and Tfam expression, and inhibited the mRNA expression of Sod2 , Txn1 , and Prdx1 , suggesting that inflammation impairs mitochondrial biogenesis and antioxidant defenses. Treatment with A. keiskei extract reduced NF-κB p65 protein levels, restored Ppargc1a mRNA expression, and partially restored antioxidant-related gene expression. These data indicate that A. keiskei extract attenuates the molecular characteristics of skeletal muscle aging through the suppression of inflammaging and the preservation of the PGC-1α-dependent mitochondrial regulatory pathways. This study collectively provides preliminary preclinical evidence that A. keiskei leaf extract may attenuate selected molecular and functional features of D-gal-induced skeletal muscle aging through changes consistent with reduced inflammatory signaling and preservation of PGC-1α-associated mitochondrial regulation.

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