Troxerutin Stimulates Osteoblast Differentiation of Mesenchymal Stem Cell and Facilitates Bone Fracture Healing.

Troxerutin (TRX), a semi-synthetic derivative of the natural bioflavonoid rutin, is a bioactive flavonoid widely abundant in various fruits and vegetables. Known as vitamin P4, TRX has been demonstrated to have several activities including anti-inflammation, anti-oxidants, vasoprotection, and immune support in various studies. Although rutin, the precursor of troxerutin, was reported to have a protective role against bone loss, the function of TRX in skeletal system remains unknown. In the present study, we found that TRX promoted osteogenic differentiation of human mesenchymal stem cells (MSCs) in a concentration-dependent manner by stimulating the alkaline phosphatase (ALP) activity, calcium nodule formation and osteogenic marker genes expression in vitro. The further investigation demonstrated that TRX stimulated the expression of the critical transcription factor ß-catenin and several downstream target genes of Wnt signaling, thus activated Wnt/ß-catenin signaling. Using a femur fracture rats model, TRX was found to stimulate new bone formation and accelerate the fracture healing in vivo. Collectively, our data demonstrated that TRX could promote osteogenesis in vitro and facilitate the fracture healing in vivo, indicating that TRX may be a promising therapeutic candidate for bone fracture repair.

[Changes of Substance P in the substantia gelatinosa of the dorsal horn field after liquid nitrogen freezing of severed nerve for prevention of terminal neuroma].

OBJECTIVE: To determine the changes of Substance P in the substantia gelatinosa of the dorsal horn field after transient liquid nitrogen freezing of severed rat sciatic nerve for prevention of terminal neuroma. METHODS: The bilateral sciatic nerves of 20 SD rats were severed, and the left sciatic nerves was subjected to transient liquid nitrogen freezing with the right sciatic nerve as control. After 20 and 28 weeks, the nerve ends were resected and prepared for microscopic examination, and Substance P in the substantia gelatinosa of the dorsal horn field was determined by immunohistochemistry. RESULTS: Typical neuromas occurred in the severed ends of the right sciatic nerves but not in the left sciatic nerves. The distribution and optical density of Substance P in the substantia gelatinosa of the dorsal horn field was significantly smaller in the left than in the right nerves (P<0.05). CONCLUSION: Liquid nitrogen freezing of the severed sciatic nerve results in decreased release of Substance P in the substantia gelatinosa of the dorsal horn field, suggesting that noxious stimulation may increase Substance P release in the substantia gelatinosa of the dorsal horn field.

[Acidic fibroblast growth factor for preventing motor endplate degeneration and muscular atrophy after motor nerve injury: a morphological and electrophysiological study].

OBJECTIVE: To explore measures to prevent motor endplate degeneration and muscular atrophy after motor nerve injury. METHODS: Thirty Sprague-Dawley rats were randomized into 3 equal groups. In two of the groups, the right common peroneal nerves of the rats were transected and immediately sutured with implantation of collagen gel carrier of acidic fibroblast growth factor (aFGF) or the empty carrier into the denervated tibialis anterior muscles. In the control group, the transected nerves were sutured without implantation. Six weeks after the operation, morphological and electrophysiological examinations were performed. RESULTS: In the control rats and those with empty collagen gel carrier implantation, obvious motor endplate degeneration and muscular atrophy occurred, which were not obvious in rats receiving aFGF carrier implantation. The decrement of repetitive nerve stimulation was significantly greater in the former two groups than in the latter. CONCLUSION: Implantation of collagen gel carrier of aFGF may prevent motor endplate degeneration and facilitate functional recovery of the neuromuscular junction after motor nerve injury.