Go-sha-jinki-Gan (GJG) ameliorates allodynia in chronic constriction injury-model mice via suppression of TNF-α expression in the spinal cord.

BACKGROUND: Alternative medicine is noted for its clinical effect and minimal invasiveness in the treatment of neuropathic pain. Go-sha-jinki-Gan, a traditional Japanese herbal medicine, has been used for meralgia and numbness in elderly patients. However, the exact mechanism of GJG is unclear. This study aimed to investigate the molecular mechanism of the analgesic effect of GJG in a chronic constriction injury model. RESULTS: GJG significantly reduced allodynia and hyperalgesia from the early phase (von Frey test, p<0.0001; cold-plate test, p<0.0001; hot-plate test p»0.011; two-way repeated measures ANOVA). Immunohistochemistry and Western blot analysis revealed that GJG decreased the expression of Iba1 and tumor necrosis factor-a in the spinal cord. Double staining immunohistochemistry showed that most of the tumor necrosis factor-a was co-expressed in Iba1-positive cells at day 3 post-operation. GJG decreased the phosphorylation of p38 in the ipsilateral dorsal horn. Moreover, intrathecal injection of tumor necrosis factor-a opposed the anti-allodynic effect of GJG in the cold-plate test. CONCLUSIONS: Our data suggest that GJG ameliorates allodynia in chronic constriction injury model mice via suppression of tumor necrosis factor-a expression derived from activated microglia. GJG is a promising drug for the treatment of neuropathic pain induced by neuro-inflammation.

Go-sha-jinki-Gan (GJG), a traditional Japanese herbal medicine, protects against sarcopenia in senescence-accelerated mice.

Sarcopenia is characterized by age-associated skeletal muscle atrophy and reduced muscle strength; currently, no pharmaceutical treatment is available. Go-sha-jinki-Gan (GJG) is a traditional Japanese herbal medicine that is used to alleviate various age-related symptoms, especially motor disorders. Here, we investigated the effect of GJG on aging-associated skeletal muscle atrophy by using senescence-accelerated mice (SAMP8). Immunohistochemical and western blotting analyses clearly showed that GJG significantly reduced the loss of skeletal muscle mass and ameliorated the increase in slow skeletal muscle fibers in SAMP8 mice compared to control mice. The expression levels of Akt and GSK-3ß, the phosphorylation of FoxO4, and the phosphorylations of AMPK and mitochondrial-related transcription factors such as PGC-1α were suppressed, while the expression of MuRF1 increased in SAMP8 mice, but approximated that in senescence-accelerated aging-resistant (SAMR1) mice after GJG treatment. We demonstrate for the first time that GJG has a therapeutic effect against sarcopenia.