Effects of photoelectric therapy on proliferation and apoptosis of scar cells by regulating the expression of microRNA-206 and its related mechanisms.

Human skin fibroblast (HSF) cells were irradiated with different energy lasers to detect cell proliferation, apoptosis, and expression of microRNA-206 and protein, and to further summarise the therapeutic effect of laser on scar cells. Human scar cell line HSF cells were cultured in three groups. The control group was not irradiated by laser, the low-energy group was irradiated by 10 J/cm2 laser, and the high-energy group was irradiated by 20 J/cm2 laser. After irradiation, HSF cells were cultured for 20 hours. Cell proliferation was detected by MTT assay. Cell cycle and apoptosis were detected by flow cytometry. Transwell migration assay was used to detect cell migratory ability. Reverse transcription polymerase chain reaction (RT-PCR) was used to detect miR-206 and mTOR gene levels. The levels of MMP-9, Bax, Bcl-2, cyclin D1, and mTOR signalling pathway proteins were detected by Western blotting assays. The results showed that after laser irradiation, the proliferation of cells decreased, and the difference between the control group and the experimental group was significant (P < .05). The higher the energy was, the greater the upregulation of apoptosis was. Apoptosis and cell migration increased (P < .05). The expressions of microRNA-206, MMP-9, and Bax were upregulated, while the expressions of mTOR, Bcl-2, and cyclin D1 were downregulated. To sum up, laser irradiation can significantly inhibit the proliferation of HSF cells, affect cell cycle, and increase cell apoptosis and migratory ability.

[Effects of Huoxue Zhitong decoration on transmembrane protein I and II induced apoptosis of signal transmission of the epidural scar tissue].

OBJECTIVES: To study the effect of Houxue Zhitong decoration on the expression of the mitochondria-initiated apoptosis pathway and transmembrane protein I an II of the epidural scar tissue. METHODS: A total of 60 New Zealand rabbits (weight: 2.5-3.0 kg) were randomly divided into four groups, sham operation group (D, n=15), control group (B, n=14), sodium hyaluronate group (C, n=15), Houxue Zhitong decoration group (D, n=15). Except for group A, 1.0 cm x 1.0 cm dura mater uncovered area laminectomy was performed at I (4) and I(5), covered with 0.5 ml sodium hyaluronate in group C, covered with same amount of saline in group B and D. First 2 weeks after operation, animals in group D were lavaged with 2.5 ml/kg Houxue Zhitong decoction by one a day for 14 days. Five rabbits of each group selected randomly were killed in the 2,4,8 weeks after laminectomy. The specimens were prepared for determination of the expression of Fas and FasL, at scar tissue by semiquantitative reserve transcription-polymerase chain reaction (RT-PCR). The degree of scar adhesion was evaluated according by Rydell method. RESULTS: The adhesion area in group B was larger than of group C and D in the 4th and 8th week. However, the number of fibroblasts and inflammantory cells in group D was the least among the three groups in the 8th week. At 2, 4, 8 weeks after operation, as compared with group B the expression of Fas, FasL of group C and D were decreased (P < 0.05). Especially, at 2 weeks, as compared with group B the expression of this two cytokines of group D was significant decreased (P < 0.05), too. In group C and D the duramater adhesion was decreased (P < 0.05). The proliferation of fibroblast and fibroblastic function were inhibited (P < 0.05). CONCLUSION: Huoxue Zhitong is able to down-regulated the expression of Fas, FasL, which inhibited the proliferation of fibroblast, the fibroblastic function and the synthesis of extracellular matrix in the epidural scar tissue. It is an effective way of reducing peridural scar formation and prevent the failed back surgery syndrome.

Traumatic brain injury results in disparate regions of chondroitin sulfate proteoglycan expression that are temporally limited.

Axonal injury is a major hallmark of traumatic brain injury (TBI), and it seems likely that therapies directed toward enhancing axon repair could potentially improve functional outcomes. One potential target is chondroitin sulfate proteoglycans (CSPGs), which are major axon growth inhibitory molecules that are generally, but not always, up-regulated after central nervous system injury. The current study was designed to determine temporal changes in cerebral cortical mRNA or protein expression levels of CSPGs and to determine their regional localization and cellular association by using immunohistochemistry in a controlled cortical impact model of TBI. The results showed significant increases in versican mRNA at 4 and 14 days after TBI but no change in neurocan, aggrecan, or phosphacan. Semiquantitative Western blot (WB) analysis of cortical CSPG protein expression revealed a significant ipsilateral decrease of all CSPGs at 1 day after TBI. Lower CSPG protein levels were sustained until at least 14 days, after which the levels began to normalize. Immunohistochemistry data confirm previous reports of regional increases in CSPG proteins after CNS injury, seen primarily within the developing glial scar after TBI, but also corroborate the WB data by revealing wide areas of pericontusional tissue that are deficient in both extracellular and perineuronal net-associated CSPGs. Given the evidence that CSPGs are largely inhibitory to axonal growth, we interpret these data to indicate a potential for regional spontaneous plasticity after TBI. If this were the case, the gradual normalization of CSPG proteins over time postinjury would suggest that this may be temporally as well as regionally limited.