The Distribution of Transplanted Umbilical Cord Mesenchymal Stem Cells in Large Blood Vessel of Experimental Design With Traumatic Brain Injury.

The authors aim to track the distribution of human umbilical cord mesenchymal stem cells (MSCs) in large blood vessel of traumatic brain injury -rats through immunohistochemical method and small animal imaging system. After green fluorescent protein (GFP) gene was transfected into 293T cell, virus was packaged and MSCs were transfected. Mesenchymal stem cells containing GFP were transplanted into brain ventricle of rats when the infection rate reaches 95%. The immunohistochemical and small animal imaging system was used to detect the distribution of MSCs in large blood vessels of rats. Mesenchymal stem cells could be observed in large vessels with positive GFP expression 10 days after transplantation, while control groups (normal group and traumatic brain injury group) have negative GFP expression. The vascular endothelial growth factor in transplantation group was higher than that in control groups. The in vivo imaging showed obvious distribution of MSCs in the blood vessels of rats, while no MSCs could be seen in control groups. The intravascular migration and homing of MSCs could be seen in rats received MSCs transplantation, and new angiogenesis could be seen in MSCs-transplanted blood vessels.

[Protective effect of Xingnaojing injection on traumatic brain injury].

OBJECTIVE: To investigate the protective effect and mechanism of Xingnaojing(Traditional Chinese Medicine) injection on brain injury in rats. METHODS: Sixty-three healthy adult male SD rats were randomly divided into 3 groups (n = 21): sham operation group, model group, xingnaojing group. The model of traumatic brain injury model group and Xingnaojing group used the free fall impact injury method, the sham operation group underwent craniotomy, did not cause brain damage. Xingnaojing group in rats after 10 min by tail vein injection Xingnaojing injection 10 ml/(kg x d), model group and sham operation group were intravenously injected with 0.9% sodium chloride solution, three groups were administered continuously for 7 days. At administration of the seventh days compared the S-100B protein in the serum and neuro specific enolase (NSE) level, the water content of brain tissue, serum superoxide dismutase (SOD), malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) content, and neurological function of rats among groups. RESULTS: Compared with the sham operation group, the nerve defect, brain water content, MDA, S100B protein and NSE levels were obvigusly increased in Xingnaojing group and model group; SOD, GSH-Px content decreased significantly; In Xingnaojing group nerve impairment and brain moisture were significantly lower than those of model group, the serum MDA, S-100B protein and NSE levels were significantly lower than those in the model group, the SOD, GSH-Px activity was significantly higher than that in the model group. CONCLUSION: Xingnaojing injection has protective effects on rat brain injury, and its mechanism may be related to reduce brain edema after traumatic brain injury and inhibit the reaction of oxygen free radical, protect nerve cells.

Curcumin attenuates ischemia-like injury induced IL-1ß elevation in brain microvascular endothelial cells via inhibiting MAPK pathways and nuclear factor-κB activation.

Inflammatory reactions play a key role in the cerebral injury after stroke or other ischemic brain diseases. Curcumin, which is extracted from herb turmeric, has been reported to have anti-inflammatory effects. The present study was aimed to investigate the anti-inflammatory effects of curcumin on oxygen-glucose deprivation (OGD) injured brain microvascular endothelial cells (BMECs). Rat BMECs were used and the results showed that OGD induced a significant elevation of the leakage of lactate dehydrogenase and the secretion of the proinflammation cytokine, IL-1ß. Activation of p38, JNK MAPKs, and NF-κB in BMECs was also observed after OGD. The treatment of curcumin (20 µM) inhibited the increased production of IL-1ß both at the protein and mRNA levels. The increased phosphorylation of p38 and JNK induced by OGD was decreased under the treatment of curcumin, whereas the p38 inhibitor, SB203580, significantly inhibited OGD-induced IL-1ß production, but the JNK inhibitor, SP600125, failed to do so. These results suggest that the inhibition of IL-1ß by curcumin may dependent on the p38 signaling pathway. The OGD-induced IL-1ß production was also inhibited by the NF-κB inhibitor, and curcumin suppressed OGD-induced NF-κB activation. Furthermore, the NF-κB activation was attenuated by the SB203580, indicating that NF-κB activation was dependent on p38 signaling pathway. The present study suggests that curcumin displays an anti-inflammatory effect on OGD-injured BMECs via down-regulating of MAPK and NF-κB signaling pathways and might have therapeutic potential for the ischemic brain diseases.

Tropism mechanism of stem cells targeting injured brain tissues by stromal cell-derived factor-1.

OBJECTIVE: To explore the role and function of stromal cell-derived factor-1 (SDF-1) in stem cells migrating into injured brain area. METHODS: Rat-derived nerve stem cells (NSCs) were isolated and cultured routinely. Transwell system was used to observe the migration ability of NSCs into injured nerve cells. Immunocytochemistry was used to explore the expression of chemotactic factor receptor-4 (CXCR-4) in NSCs. In vivo, we applied immunofluorescence technique to observe the migration of NSCs into injured brain area. Immunofluorescence technique and Western blotting were used to test expression level of SDF-1. After AMD3100 (a special chemical blocker) blocking CXCR-4, the migration ability of NSCs was tested in vivo and in vitro, respectively. RESULTS: NSCs displayed specific tropism for injured nerve cells or traumatic brain area in vivo and in vitro. The expression level of SDF-1 in traumatic brain area increased remarkably and the expression level of CXCR-4 in the NSCs increased simultaneously. After AMD3100 blocking the expression of CXCR-4, the migration ability of NSCs decreased significantly both in vivo and in vitro. CONCLUSIONS: SDF-1 may play a key role in stem cells migrating into injured brain area through specially combining with CXCR-4.