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Nerve regeneration includes regrowth of injured axons as well as myelination, restoration of synaptic connections and recovery of physiological functions. Platelet-rich plasma (PRP) is prepared from the patient's own blood and contains growth factors that influence wound healing and used in various surgical fields including oral and maxillofacial surgery. When platelets are activated either ex vivo or in vivo, growth factors and proteins were released from platelets' alpha granules. Recent studies proved that PRP could promote regeneration of injured peripheral nerve. This review focuses on current trials using PRP to promote nerve regeneration and repairment, and proposes potential clinical application of PRP for nerve injury in the future.

Stachydrine is a major constituent of Chinese herb leonurus heterophyllus sweet, which is used in clinics to promote blood circulation and dispel blood stasis. Our study aimed to investigate the role of stachydrine in human umbilical vein endothelial cells (HUVECs) injury induced by anoxia-reoxygenation. Cultured HUVECs were divided randomly into control group, anoxia-reoxygenation (A/R) group and 4 A/R+stachydrine groups. HUVECs in the control group were exposed to normoxia for 5 hours, while in all A/R groups, HUVECs underwent 3 hours anoxia followed by 2 hours reoxygenation, and HUVECs in the 4 A/R+stachydrine groups were treated with 10(-8) M, 10(-7) M, 10(-6) M and 10(-5) M (final concentration) of stachydrine respectively. After anoxia-reoxygenation, tissue factor (TF) was over-expressed, cell viability and the concentrations of SOD, GSH-PX and NO were declined, while LDH, MDA and ET-1 were over-produced (p < 0.05 to 0.001 vs. the control group). However, in stachydrine treated groups, TF expression was inhibited at both mRNA and protein levels, while the declined cell viability and SOD, GSH-PX, NO as well as the enhanced LDH, MDA and ET-1 levels occurred during anoxia-reoxygenation were ameliorated and reversed effectively (p < 0.05 to 0.01 versus A/R group). Consequently, our findings indicate that TF plays an important role in the development of anoxia-reoxygenation injury of HUVECs, stachydrine ameliorates HUVECs injury induced by anoxia-reoxygenation and its putative mechanisms are related to inhibition of TF expression.

Intravenous injection of human or mouse serum or platelet material secreted from appropriately stimulated platelets ("releasate") together with antigen alleviates the immunosuppression in SJL/J mice induced by injection of irradiated lymphoma cells or in (CB6)F1 mice induced by injection of concanavalin A. We now report that injection of releasate from 10(6) human platelets restores plaque-forming cells to the unsuppressed number; greater amounts increase responses further. Immunoregulatory activity is released from platelets exposed to thrombin in parallel with other alpha-granule components. Heparin-agarose absorbs activity. Purified platelet factor 4 (PF4) has activity; beta-thromboglobulin and platelet-derived growth factor have little or none. Activity in serum is neutralized by goat anti-human PF4. An enzymatic step is necessary for production of immunoregulatory activity. Releasates boiled immediately after platelet aggregation with 250 nM A23187 or those produced by adding A23187 in the presence of 100 microM serine protease inhibitor (p-amidinophenyl)methanesulfonyl fluoride (APMSF) are ineffective, whereas releasates boiled or mixed with APMSF after incubation for 60 min are active. Activity is generated by incubating a mixture of heparin-absorbed releasate (as enzyme source) and heparin-agarose eluate of releasate made in the presence of APMSF (as substrate source). The enzymatic step does not alter the heparin-neutralizing activity of PF4. Apparently a secreted platelet protease converts PF4 to a form with immunoregulatory activity.

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