Hao L.,No. 324 Hospital of Peoples Liberation Army |
Guo X.,Chongqing Medical University |
Zou C.,No. 324 Hospital of Peoples Liberation Army |
Zhou H.,No. 324 Hospital of Peoples Liberation Army |
And 4 more authors.
Croatian Medical Journal | Year: 2016
Aim To explore the effects of hyperbaric oxygen preconditioning (HBOP) on the permeability of blood-brain barrier (BBB) and expression of tight junction proteins under hypoxic conditions in vitro. Methods A BBB in vitro model was constructed using the hCMEC/D3 cell line and used when its trans-endothelial electrical resistance (TEER) reached 80-120 Ω· cm2 (tested by Millicell-Electrical Resistance System). The cells were randomly divided into the control group cultured under normal conditions, the group cultured under hypoxic conditions (2%O2) for 24 h (hypoxia group), and the group first subjected to HBOP for 2 h and then to hypoxia (HBOP group). Occludin and ZO-1 expression were analyzed by immunofluorescence assay. Results Normal hCMEC/D3 was spindle-shaped and tightly integrated. TEER was significantly reduced in the hypoxia (P = 0.001) and HBOP group (P = 0.014) compared to control group, with a greater decrease in the hypoxia group. Occludin membranous expression was significantly decreased in the hypoxia group (P = 0.001) compared to the control group, but there was no change in the HBOP group. ZO-1 membranous expression was significantly decreased (P = 0.002) and cytoplasmic expression was significantly increased (P = 0.001) in the hypoxia group compared to the control group, although overall expression levels did not change. In the HBOP group, there was no significant change in ZO-1 expression compared to the control group. Conclusion Hyperbaric oxygen preconditioning protected the integrity of BBB in an in vitro model through modulation of occludin and ZO-1 expression under hypoxic conditions.
Liu Z.,No. 324 Hospital of Peoples Liberation Army |
Wang Z.,Chongqing Medical University |
Lu B.,Chongqing Medical University |
Hu C.,Chongqing Medical University |
And 4 more authors.
Chinese Journal of Cancer Biotherapy | Year: 2013
Objective:To explore the inhibitory effect of miRNA-29a(mi-29a) on the proliferation of human gastric cancer cell lines SGC-7901 and AGS through over-expression of miR-29a mediated by the recombinant replication-deficient human adenovirus type 5 vector. Methods: The recombinant adenovirus Ad-miR-29a containing pre-miR-29a or control adenovirus Ad-LacZ containing LacZ gene was constructed and infected into human gastric cancer SGC-7901 and AGS cells, respectively. The expressions of miR-29a in SGC-7901 and AGS cells were detected by real-time PCR. CCK-8 assay was employed to examine the inhibitory effect of miR-29a on the proliferation of human gastric cancer cell lines. The flow cytometry assay was used to analyze cell cycle of SGC-7901 and AGS cells. The migration ablilities of SGC-7901 and AGS cells were assessed by Transwell assay. Results: Compared with the Ad-LacZ group, the Ad-miR29a group expressed higher level of miR-29a in both SGC-7901 and AGS cells ([17.35 ± 0. 71] vs [1.12 ± 0.09], [26. 50 ± 1.09] vs [0. 95 ± 0. 04], P<0. 01). The proliferation of S-7901 and AGS was significantly inhibited in the Ad-miR29a group as compared with that in the Ad-LacZ group. Six days after Ad-miR29a infection, the D value was significantly decreased ([0.54 ± 0.03] vs [0.77 ± 0.04], [0.70 ± 0.03] vs [0.88 ± 0.04], P < 0. 01). The proliferation of cells in the Ad-LacZ group showed no significant changes as compared with that in the uninfected group (P > 0.05). Meanwhile, The percentage of SGC-7901 or AGS cells arrested in Go/Gj period in the Ad-miR29a group was significantly higher than that in the Ad-LacZ group ([63.10 ± 4.91]% vs [47.60 ± 5. 31]%,[69.80 ± 3.15]% vs [54.60 ±4.22 J%, P < 0.05 J. However, no significant changes were found in the migration ability of gastric cancer SGC-7901 and AGS cells. Conclusion: miR-29a can effectively suppress the proliferation of human gastric cancer cells, which makes a promising new therapeutic target for gastric cancer.