Objective To explore the effects of hyperbaric oxygen preconditioning (HBOP) on close connection of endothelial cells in in-vitro blood-brain barrier and possible mechanism involved.Methods The blood-brain barrier model was developed by using hCMEC/D3 cell line.Then, the cultured cells were randomly divided into 3 groups: the blank control group (Group A), the hypoxia group (Group B) and the HBOP group (Group C).Millicel1-ERS was used to test TEER, while immunofluorescence was performed to detect changes in the expressions of occludin and ZO-1.Results The normal cultured hCMEC/D3 displayed a spindle shape,with the cells closely connected and the value of TEER as high as 80-120 Ω · cm2 , indicating that the in vitro blood-brain barrier model was successfully established.Relative to the TEER value of group A [107.17 ±l0.41)Ω·cm2], theTEER values of group B and group C [(50.02±6.87)Ω · cm2, (83.81 ±8.22) Ω · cm2] all decreased quite considerably, with the TEER value of group B decreasing more significantly.Immunofluorenscence detection results indicated that as compared with group A, the expression level of occludin in group B decreased significantly, while no significant expression level of occludin was noticed in group C.As compared with group A, ZO-1 expression level in the cell membrane of group B decreased significantly, while the expression level of cytoplasm increased, and there were no significant changes in ZO-1 expression level in group C.Conclusions HBO preconditioning could decrease changes in the expression levels of occludin and ZO-1 induced by hypoxia.

Objective To explore the effects of hyperbaric oxygen preconditioning (HBOP) on close connection of endothelial cells in in-vitro blood-brain barrier and possible mechanism involved.Methods The blood-brain barrier model was developed by using hCMEC/D3 cell line.Then, the cultured cells were randomly divided into 3 groups: the blank control group (Group A), the hypoxia group (Group B) and the HBOP group (Group C).Millicel1-ERS was used to test TEER, while immunofluorescence was performed to detect changes in the expressions of occludin and ZO-1.Results The normal cultured hCMEC/D3 displayed a spindle shape,with the cells closely connected and the value of TEER as high as 80-120 Ω · cm2 , indicating that the in vitro blood-brain barrier model was successfully established.Relative to the TEER value of group A [107.17 ±l0.41)Ω·cm2], theTEER values of group B and group C [(50.02±6.87)Ω · cm2, (83.81 ±8.22) Ω · cm2] all decreased quite considerably, with the TEER value of group B decreasing more significantly.Immunofluorenscence detection results indicated that as compared with group A, the expression level of occludin in group B decreased significantly, while no significant expression level of occludin was noticed in group C.As compared with group A, ZO-1 expression level in the cell membrane of group B decreased significantly, while the expression level of cytoplasm increased, and there were no significant changes in ZO-1 expression level in group C.Conclusions HBO preconditioning could decrease changes in the expression levels of occludin and ZO-1 induced by hypoxia.

Objective To investigate the relationship between the residual forward blood flow and the therapeutic outcome in patients with acute cerebral infarction after arterial thrombolysis treatment. Methods During the period from January 2009 to December 2013 at authors’ hospital, a total of 40 patients with acute anterior circle cerebral infarction were treated with arterial thrombolysis. The clinical data were retrospectively analyzed. The patients were divided into group A (n=23) when residual forward blood flow and/or collateral circulation were presented, and group B (n=17) if no residual forward blood flow and/or collateral circulation were detected. The NIHSS scores and hemorrhagic transformation state were determined 14 days after the thrombolysis treatment, and the results were compared between the two groups. Results In group A, 21 cases (91.3%) showed complete or partial re- canalization of the infracted vessels, and asymptomatic hemorrhagic transformation was seen in one case. The pre-treatment NIHSS score was 12.69 ± 3.88 and the post-treatment NIHSS score was 6.05 ± 3.25. In group B, complete or partial re-canalization of the infracted vessels was seen in 15 cases (88.2%), asymptomatic hemorrhagic transformation was found in one case and symptomatic hemorrhagic transformation occurred in one case, who died of massive cerebral hemorrhage seven hours after the thrombolysis treatment. The pre-treatment NIHSS score was 13.51 ± 4.19 and the post-treatment NIHSS score was 8.68 ± 5.16. The differences between the two groups were statistically significant (P < 0.05). The obvious effect rate in group A and group B was 68.1% and 43.8% respectively, and the effective rate in group A and group B was 86.3% and 56.3% respectively, indicating that the clinical outcome of group A was much better than that of group B. Conclusion The therapeutic effect of arterial thrombolysis for acute cerebral infarction patients is not only closely related to the time window but also to the residual forward blood flow. The more the residual forward blood flow there is, the better the therapeutic result with less risk of hemorrhagic transformation will be.

Human stomach cancer cell line BGC-823 was treated by Tween 80 in combination with hyperthermia 39℃ to 43℃ for 20 to 100 minutes, respectively. The cell ultrastructure and succinate dehydrogenase (SDH) activity were studied at 0 hr, 48hr and 96hr after treatment respectively. Normal human fibroblast was used as control. The main changes of BGC-823 cells induced by hyperthermia were: dilation of endoplasmic reticulum, swelling of mitochondria, increase of fat droplets and decrease in SDH activity. After treatment at 43℃, the mitochondria showed vesicles or myelin figures and the polyribosomes tended to disaggregate. In nuclei, heterochromatin increased and the nucleolus become a dense homogeneous spot or annular ring. A few cells got necrosis. Effects of Tween 80 on BGC-823 cells were similar to that of hyperthermia. When Tween 80 combined with heating, marked synergic action was observed and the damage of membrane structure appeared earlier and more seriously. The effects of 41℃ combined with Tween 80 for 100 minutes were similar to that of 43℃ for 100 minutes alone. The critical temperature of hyperthermia for BGC-823 cells decreased to 41℃. The responses of the human fetal lung fibroblasts were slight and reversible. The results mentioned above suggested that the Tveen 80 enhanced the damage effect of hyperthermia on the tumor cells by decreasing the phase transition temperature of the tumor cells.