Journal of ethnopharmacology · 2026
Jintiange ameliorates age-related sarcopenia by inhibiting the cGAS-STING signaling pathway via maintaining mitochondrial homeostasis.
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Xu Yuan, Li Xiao-Li, Guo Yi-Xun, Wu Ruo-Bing, He Ming-Chao, Zhang Yan
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Jintiange (JTG), a substitute for natural tiger bone, has been approved in China for the treatment of osteoporosis, osteoarthritis and rheumatoid arthritis. Clinical observations indicate that JTG can improve skeletal muscle atrophy and enhance skeletal muscle strength. However, the role and mechanism of action of JTG in sarcopenia remain unclear.
AIM OF THE STUDY: This study aimed to investigate the therapeutic effects and the underlying mechanisms of JTG on age-related sarcopenia.
MATERIALS AND METHODS: The 12-month-old male mice were orally treated with three doses of JTG for 3 months. The grip strength, weight-loaded swimming time, muscle mass (quadriceps femoris, gastrocnemius, tibialis anterior and soleus muscles), and the cross-sectional area (CSA) of myofibers were measured. The transcriptomic sequencing, RT-PCR, Western blot, immunofluorescence, and immunohistochemistry were employed. Additionally, the other mice, after oral administration with JTG for 3 months, experienced a 3-month withdrawal period to observe the long-term effects of JTG on skeletal muscle.
RESULTS: The treatment with JTG significantly enhanced grip strength and muscle mass, extended weight-loaded swimming time, elevated CSA, and up-regulated the expressions of muscular regulatory factors, as well as down-regulated the expressions of MuRF-1 and Atrogin-1 in the ubiquitin-proteasome system. The administration of 12-month-old mice with JTG for 3 months profoundly reduced the expression levels of senescence-associated secretory phenotypes and of age-related markers (β-gal, P53 & P16). JTG improved mitochondrial quality by promoting mitochondrial biogenesis through increased expression of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) and mitochondrial transcription factor A (TFAM), restoring mitochondrial dynamics via regulation of mitofusin-1 (MFN-1) and fission 1 (FIS-1), and activating PINK1/Parkin-mediated mitochondrial autophagy. The benefit of JTG on maintaining mitochondrial homeostasis led to the reduction in the leakage of mitochondrial DNA (mtDNA) into cytoplasm, thereby attenuating the activation of cGAS-STING signaling pathway and lowering NF-κB-evoked chronic low-grade inflammation in skeletal muscle, ultimately ameliorating age-related sarcopenia. After drug withdrawal for 3 months, the mice in JTG-treated groups still displayed better muscular performance than those vehicle-treated mice with the same age (18-month-old).
CONCLUSIONS: JTG benefits for alleviating aging conditions of skeletal muscle by maintaining mitochondrial homeostasis, thus, effectively ameliorates age-related sarcopenia by blocking the cGAS-STING signaling pathway.
AIM OF THE STUDY: This study aimed to investigate the therapeutic effects and the underlying mechanisms of JTG on age-related sarcopenia.
MATERIALS AND METHODS: The 12-month-old male mice were orally treated with three doses of JTG for 3 months. The grip strength, weight-loaded swimming time, muscle mass (quadriceps femoris, gastrocnemius, tibialis anterior and soleus muscles), and the cross-sectional area (CSA) of myofibers were measured. The transcriptomic sequencing, RT-PCR, Western blot, immunofluorescence, and immunohistochemistry were employed. Additionally, the other mice, after oral administration with JTG for 3 months, experienced a 3-month withdrawal period to observe the long-term effects of JTG on skeletal muscle.
RESULTS: The treatment with JTG significantly enhanced grip strength and muscle mass, extended weight-loaded swimming time, elevated CSA, and up-regulated the expressions of muscular regulatory factors, as well as down-regulated the expressions of MuRF-1 and Atrogin-1 in the ubiquitin-proteasome system. The administration of 12-month-old mice with JTG for 3 months profoundly reduced the expression levels of senescence-associated secretory phenotypes and of age-related markers (β-gal, P53 & P16). JTG improved mitochondrial quality by promoting mitochondrial biogenesis through increased expression of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) and mitochondrial transcription factor A (TFAM), restoring mitochondrial dynamics via regulation of mitofusin-1 (MFN-1) and fission 1 (FIS-1), and activating PINK1/Parkin-mediated mitochondrial autophagy. The benefit of JTG on maintaining mitochondrial homeostasis led to the reduction in the leakage of mitochondrial DNA (mtDNA) into cytoplasm, thereby attenuating the activation of cGAS-STING signaling pathway and lowering NF-κB-evoked chronic low-grade inflammation in skeletal muscle, ultimately ameliorating age-related sarcopenia. After drug withdrawal for 3 months, the mice in JTG-treated groups still displayed better muscular performance than those vehicle-treated mice with the same age (18-month-old).
CONCLUSIONS: JTG benefits for alleviating aging conditions of skeletal muscle by maintaining mitochondrial homeostasis, thus, effectively ameliorates age-related sarcopenia by blocking the cGAS-STING signaling pathway.