Cytotoxicity of mesoporous silica modified by amino and carboxyl groups on vascular endothelial cells.

Mesoporous silica is widely used because of its unique and excellent properties, especially it can be used as a drug carrier and gene carrier in the biomedical field. After the mesoporous silica is put into clinical use, it is more likely to be exposed in human body. Therefore, the effect of mesoporous silica on human body cannot be ignored. The injury of vascular endothelial cells is a prerequisite for the occurrence of many cardiovascular diseases. As a drug and gene carrier, mesoporous silica increases its contact with vascular endothelial cells, so its toxic effect on cardiovascular system cannot be ignored. In this study, amino (NH2 ) and carboxyl (COOH) were modified on mesoporous silica SBA-15 by post-grafting. The results showed that it still maintained the one-dimensional hexagonal mesoporous structure of SBA-15 and had typical mesoporous structure. Then human umbilical vein endothelial cells (HUVECs) were infected with SBA-15, NH2 -SBA-15, and COOH-SBA-15. The results showed that the functionalized mesoporous silica SBA-15 had cytotoxicity to HUVECs and damaged the cell membrane, but compared with the unmodified mesoporous silica SBA-15 the cytotoxicity of functionalized mesoporous silica SBA-15 was lower and the toxicity of carboxyl modified group was the lowest. By comparing the cell inhibition rate and the expression level of lactate dehydrogenate and reactive oxygen species induced by the three materials, oxidative damage and cell membrane damage may be two mechanisms of cytotoxicity. Mesoporous silica SBA-15 has an effect on cardiovascular system by inducing the high expression of nitric oxide, intercellular adhesive molecule-1 and vascular cell adhesive molecule-1 in HUVECs. In summary, our results show that mesoporous silica is toxic to vascular endothelial cells.

Association of polymorphisms in stress-related TNFα and NPY genes with the metabolic syndrome in Han and Hui ethnic groups.

BACKGROUND: Metabolic syndrome (MS) is a cluster of complicated disorders caused by the interactive influencing factors of heredity and environment, which predisposes to many cnacers. RESULTS from epidemic research indicate that stress is tightly related to the pathogenesis of MS and neoplasia. This paper aims to investigate the association between psychological stress and MS with respect to the tumor necrosis factor alpha (TNFα) and neuropeptide Y (NPY) genes in the Han and Hui ethnic groups. METHODS: All subjects for this case-control study matched strict enrollment criteria (nationality, gender and age) and lived in the city of Wu Zhong of Ningxia Province in China. The enrolled group contained 102 matched pairs of Hui ethnic individuals and 98 matched pairs of Han ethnic individuals. Enrolled subjects completed the general Symptom Checklist-90 (SCL-90). The TNFα-308G/A variant and NPYrs16147 polymorphism were detected in case (81 males, 119 females) and control (81 males, 119 females) groups by polymerase chain reaction (PCR) amplification. RESULTS: Nine factors of the SCL-90 were found to be statistically different (p<0.05) between case and control groups. The homozygous mutant genotype (AA) and the mutant allele (A) of the TNFα-308G/A gene were less frequently observed in the control population compared to the case group. The odds ratio (95% confidence interval) in "Allele" for MS was 2.28 (1.47-3.53), p=0.0001, while "OR" was 1.11 (0.83-1.47), p=0.15, for the NPYrs16147 gene polymorphism. CONCLUSIONS: Psychological stress has been positively associated with MS. A previous study from our group suggested there were differences in the level of psychological stress between Hui and Han ethnic groups. Furthermore, we found that the stress-related TNFα gene was associated with MS for both Han and Hui ethnic groups. In contrast, NPY may be a possible contributor to MS and associated cancer for the Han ethnic group.