[Study on the damage of the tight junctions of nasal mucosal epithelial cells by artemisia annua pollen].

Objective: To investigate the damage and mechanism of artemisia annua pollen on tight junction of human nasal mucosa epithelial cells (HNEpC). Methods: HNEpC were cultured in vitro. Different concentrations of artemisia annua pollen (0, 20, 40, 80, 100, 160, 200 µg/ml) were used to intervene the cells for 24 h, and the cell proliferation activity was detected by the CCK-8 method. The expression and phosphorylation of p38MAPK signaling pathway were detected by Western Blot before and after the intervention of SB203580, a p38MAPK inhibitor in HNEpC. Immunofluorescence chemical staining, Western Blot and quantitative real-time PCR (qPCR) were used to observe the expression and distribution of tight junctions Occludin and Claudin-1. SPSS 21.1 software was used for statistical analysis. Results: CCK-8 results showed that, compared with the control group, the proliferation activity of HNEpC increased after 6 h intervention with different concentrations of artemisia annua pollen (all P<0.05). After 12 h of intervention, the proliferation activity of HNEpC in the 20, 40, 80, 100 and 160 µg/ml groups was not significantly changed (all P>0.05), while that in the 200 µg/ml group was decreased (P<0.05). After the intervention for 24 h, the proliferation activity of cells in the 20 and 40 µg/ml groups was not significantly changed (all P>0.05), while that in the 80, 100, 160 and 200 µg/ml groups was decreased (all P<0.05). Immunofluorescence staining showed that the Occludin and Claudin-1 proteins in the normal control group were localized on the cell membrane and expressed more and formed a ring structure around the cell membrane. However, under the intervention of high concentration artemisia annua pollen, its expression level decreased, appeared broken, fuzzy, and nonuniform distribution. Western Blot and qPCR results showed that after 24 h of intervention, the expression levels of HNEpC Claudin-1 protein and its mRNA in the pollen groups (40, 80, 100, 160, 200 µg/ml) of artemisia annua decreased compared with those of those of the control group (mRNA expression levels were 0.567±0.214, 0.443±0.109, 0.462±0.160, 0.497±0.134, 0.388±0.076 compared with 1.001±0.067, respectively, all P<0.05). However, the mRNA of Occludin protein and its mRNA only decreased in the 200 µg/ml treatment group (mRNA expression level was 0.631±0.109 compared with 1.016±0.026, P<0.05), while all the other treatment groups increased (mRNA expression levels were 1.258±0.134, 1.827±0.103, 2.429±0.077, 1.707±0.085, 1.477±0.066 compared with 1.016±0.026, respectively, all P<0.05). Western Blot showed that p-p38MAPK expression increased after intervention with 100, 160, 200 µg/ml artemisia annua pollen for 24 h. SB203580 could inhibit the decreasing expression of Occludin caused by artemisinin pollen (mRNA expression was 1.255±0.179 compared with 0.631±0.109, P<0.05), but had no effect on Claudin-1 protein expression. Conclusion: Pollen from artemisia annua may activate p38MAPK signaling pathway and destroy the close connection of HNEpC.

Analysis of correlation between the number of lenticulostriate arteries and hypertension based on high-resolution MR angiography findings.

BACKGROUND AND PURPOSE: Hypertension, one of the most important risk factors for strokes, is associated with altered arterial anatomy and function. In this study, we compared the visualization of the LSAs by 3T 3D-TOF-MRA and DSA and quantitatively examined the LSAs in patients with hypertension by using 3D-TOF-MRA. MATERIALS AND METHODS: We first examined 126 patients with 3D-TOF-MRA and DSA and determined the number of LSAs. In addition, we examined 60 patients with hypertension and 60 nonhypertensive volunteers with 3D-TOF-MRA and determined the quantitative differences between the LSAs of these 2 groups. RESULTS: The mean number of LSA stems visualized by DSA and 3D-TOF-MRA on 1 side was 4.1 ± 0.74 and 3.9 ± 0.94, respectively (P = .0617). The average number of LSA stems on both sides was 4.7 ± 0.8 in patients with hypertension and 6.3 ± 1.9 in nonhypertensive volunteers (P < .0001). The mean number of LSAs in the young hypertensive group (<50 years of age) and its age-matched nonhypertensive group was 4.8 ± 1.1 and 7.6 ± 1.2, respectively (P < .0001) and that in the old hypertensive group (≥50 years of age) and its age-matched nonhypertensive group was 4.6 ± 0.9 and 5.0 ± 1.0, respectively (P = .1088). CONCLUSIONS: LSA detection showed good correlation between 3T 3D-TOF-MRA and DSA. As determined by 3D-TOF-MRA, there was a significant decrease in the number of LSA stems in patients with hypertension compared with that in nonhypertensive volunteers; moreover, the difference in young subjects was more than that in the elderly.

Establishment of an experimental intracranial internal carotid artery model and the application in covered-stent navigability testing.

BACKGROUND AND PURPOSE: The carotid siphon is a natural barrier to intracranial interventions. Our aim was to make a model of the human intracranial internal carotid artery (ICA) and to test the navigability of covered stents for intracranial applications. MATERIALS AND METHODS: A digital tube was made on the basis of raw MR images of the human ICA. It was transferred into 10 physical models and then coated with silicone by using a 3D rapid prototyping (RP) machine. Ten dogs then underwent surgery. Their common carotid arteries (CCAs) were exposed, cut, and passed through 1 of the tubes. Finally, the vascular models were made by reanastomosis of their CCAs. Eight expended polytetrafluoroethylene (e-PTFE) covered stents (two 3.5 x 16 mm, two 3.5 x 13 mm, two 3.5 x 10 mm, and two 3.5 x 7 mm) were implanted 1 week later. Two dogs remained as controls. The performance of the device was evaluated by angiography and histopathologic examination. RESULTS: Ten animal models were successfully constructed. There was no vascular spasm or thrombosis when assessed by angiography. Destruction of the tunica intima and media was found in the 3.5 x 16 mm stent group. Destruction of the endothelium was found in the 3.5 x 13 mm stent group, and only flattening of the endothelium was found in the 3.5 x 10 mm and 3.5 x 7 mm stent groups. CONCLUSIONS: The experimental model was thought to simulate adequately the geometry of the human ICA and, thus, would be an effective tool for the research and testing of neurovascular devices. The length of the stent is 1 factor influencing the navigability in tortuous vessels.