No abstract

No abstract

Nucleus pulposus (NP) degeneration is the major cause of degenerative disc disease (DDD). This condition cannot be treated or attenuated by traditional open or minimally invasive surgical options. However, a combination of stem cells, growth factors (GFs) and biomaterials present a viable option for regeneration. Injectable biomaterials act as carriers for controlled release of GFs and deliver stem cells to target tissues through a minimally invasive approach. In this study, injectable gelatin methacryloyl microspheres (GMs) with controllable, uniform particle sizes were rapidly biosynthesized through a low-cost electrospraying method. The GMs were used as delivery vehicles for cells and GFs, and they exhibited good mechanical properties and biocompatibility and enhanced the in vitro differentiation of laden cells into NP-like phenotypes. Furthermore, this integrated system attenuated the in vivo degeneration of rat intervertebral discs, maintained NP tissue integrity and accelerated the synthesis of extracellular matrix. Therefore, this novel therapeutic system is a promising option for the treatment of DDD.

The integration of mesenchymal stem cell sheet and bFGF-loaded fibrin gel in knitted PLGA scaffolds synergistically promoted rat At regeneration

Inflammation and neuronal apoptosis aggravate the secondary damage after spinal cord injury (SCI). Rehmannioside A (Rea) is a bioactive herbal extract isolated from Rehmanniae radix with low toxicity and neuroprotection effects. Rea treatment inhibited the release of pro‐inflammatory mediators from microglial cells, and promoted M2 polarization in vitro, which in turn protected the co‐cultured neurons from apoptosis via suppression of the NF‐κB and MAPK signalling pathways. Furthermore, daily intraperitoneal injections of 80 mg/kg Rea into a rat model of SCI significantly improved the behavioural and histological indices, promoted M2 microglial polarization, alleviated neuronal apoptosis, and increased motor function recovery. Therefore, Rea is a promising therapeutic option for SCI and should be clinically explored.

Over‐activated osteoclastogenesis, which is initiated by inflammation, has been implicated in osteoporosis. Corilagin, a natural compound extracted from various medicinal herbaceous plants, such as Cinnamomum cassia, has antioxidant and anti‐inflammatory activities. We found that Corilagin suppressed osteoclast differentiation in a dose‐dependent manner, significantly decreased osteoclast‐related gene expression and impaired bone resorption by osteoclasts. Moreover, phosphorylation of members of the nuclear factor‐kappaB (NF‐κB) and PI3K/AKT signalling pathways was reduced by Corilagin. In a murine model of osteoporosis, Corilagin inhibited osteoclast functions in vivo and restored oestrogen deficiency‐induced bone loss. In conclusion, our findings suggested that Corilagin inhibited osteoclastogenesis by down‐regulating the NF‐κB and PI3K/AKT signalling pathways, thus showing its potential possibility for the treatment of osteoporosis.

Background A growing body of research shows that drug monomers from traditional Chinese herbal medicines have antineuroinflammatory and neuroprotective effects that can significantly improve the recovery of motor function after spinal cord injury (SCI). Here, we explore the role and molecular mechanisms of Alpinetin on activating microglia‐mediated neuroinflammation and neuronal apoptosis after SCI. Methods Stimulation of microglia with lipopolysaccharide (LPS) to simulate neuroinflammation models in vitro, the effect of Alpinetin on the release of pro‐inflammatory mediators in LPS‐induced microglia and its mechanism were detected. In addition, a co‐culture system of microglia and neuronal cells was constructed to assess the effect of Alpinetin on activating microglia‐mediated neuronal apoptosis. Finally, rat spinal cord injury models were used to study the effects on inflammation, neuronal apoptosis, axonal regeneration, and motor function recovery in Alpinetin. Results Alpinetin inhibits microglia‐mediated neuroinflammation and activity of the JAK2/STAT3 pathway. Alpinetin can also reverse activated microglia‐mediated reactive oxygen species (ROS) production and decrease of mitochondrial membrane potential (MMP) in PC12 neuronal cells. In addition, in vivo Alpinetin significantly inhibits the inflammatory response and neuronal apoptosis, improves axonal regeneration, and recovery of motor function. Conclusion Alpinetin can be used to treat neurodegenerative diseases and is a novel drug candidate for the treatment of microglia‐mediated neuroinflammation.

No abstract