Among many antioxidants that are used for the repairing of oxidative stress induced skin damages, we identified the enriched astaxanthin extract (EAE) from Haematococcus pluvialis as a viable ingredient. EAE was extracted from the red microalgae through supercritical fluid carbon dioxide extraction. To compare the effectiveness, EAE wastreated on human dermal fibroblasts with other components, phorbol 12-myristate 13-acetate (PMA), and doxycycline. With sirius red staining and quantitative real-time polymerase chain reaction (qRT-PCR), we found that PMA decreased the collagen concentration and production while overall the addition of doxycycline and EAE increased the collagen concentration in a trial experiments. EAE increased collagen contents through inhibited MMP1 and MMP3 mRNA expression and induced TIMP1, the antagonists of MMPs protein, gene expression. As for when tested for various proteins through western blotting, it was seen that the addition of EAE increased the expression of certain proteins that promote cell proliferation. Testing those previous solutions using growth factor assay, it was noticeable that EAE had a positive impact on cell proliferation and vascular endothelial growth factor (VEGF) than doxycycline, indicating that it was a better alternative treatment for collagen production. To sum up, the data confirmed the possible applications as medical cosmetology agentsand food supplements.

Traumatic wounds inflict small- and large-fiber sensory nerve damage, causing neuropathic pain in scar tissue, thus impairing patients' quality of life and leading to the development of psychological disorders. Autologous fat grafting has been clinically shown to improve scar quality, but few studies have explored the effects of this technique on pain. The purpose of this study was to assess the effect of fat grafting on treating neuropathic scar pain. From February 2008 to January 2013, 13 patients who were identified using the Douleur Neuropathique 4 Questions (scores>4/10) were enrolled in this study. The Visual Analog Scale (VAS) and Neuropathic Pain Symptom Inventory (NPSI) were used to evaluate pain preoperatively and 1 week, 4 weeks, and 24 weeks postoperatively. The mechanism of trauma, scar location and size, duration of allodynia, fat graft volume, pharmacologic therapy duration, and total follow-up time were recorded. Thirteen patients experiencing neuropathic pain were enrolled in this study. The mean±SD age was 33.08±16.35 years. The mean duration of pain was 4.29±2.85 months. The mean VAS score before treatment was 7.54±1.05. The mean VAS scores decreased by 4.38±1.66 after 1 week of treatment (P=0.009), 5.38±2.06 after 4 weeks of treatment, and 5.62±2.18 after 24 weeks of treatment. The mean NPSI scores were 49.38±13.25 before treatment, 25±14.4 after 1 week of treatment (P=0.004), 21±17.78 after 4 weeks of treatment, and 14.62±16.88 after 24 weeks of treatment. The 13 patients followed a mean of 24 weeks; 10 (77%) of the patients had improvement of 5 or greater on the VAS score. The mean follow-up period was 19.3±12.26 months (range, 6-38 months). No surgical complications were noted in this series. In our study, both VAS and NPSI scores decreased significantly, revealing that the autologous fat grafting can alleviate neuropathic scar pain 1 week after operation and in the long term.

We have demonstrated that high glucose treatment results in progressive suppression of keratinocyte locomotion and elucidated the molecular mechanisms involved. These results provide a reasonable explanation for the poor wound healing seen in patients with DM.

Burn-induced neuropathic pain is complex, and fat grafting has reportedly improved neuropathic pain. However, the mechanism of fat grafting in improving neuropathic pain is unclear. Previous investigations have found that neuroinflammation causes neuropathic pain, and anti-inflammatory targeting may provide potential therapeutic opportunities in neuropathic pain. We hypothesized that fat grafting in burn scars improves the neuropathic pain through anti-inflammation. Burn-induced scar pain was confirmed using a mechanical response test 4 weeks after burn injuries, and autologous fat grafting in the scar area was performed simultaneously. After 4 weeks, the animals were sacrificed, and specimens were collected for the inflammation test, including COX-2, iNOS, and nNOS in the injured skin and spinal cord dorsal horns through immunohistochemistry and Western assays. Furthermore, pro-inflammatory cytokines (IL-1 β and TNF-α) in the spinal cord were collected. Double immunofluorescent staining images for measuring p-IκB, p-NFκB, p-JNK, and TUNEL as well as Western blots of AKT, Bax/Bcl-2 for the inflammatory process, and apoptosis were analyzed. Fat grafting significantly reduced COX2, nNOS, and iNOS in the skin and spinal cord dorsal horns, as well as IL-1β and TNF-α, compared with the burn group. Moreover, regarding the anti-inflammatory effect, the apoptosis cells in the spinal cord significantly decreased after the fat grafting in the burn injury group. Fat grafting was effective in treating burn-induced neuropathic pain through the alleviation of neuroinflammation and ameliorated spinal neuronal apoptosis.