[Research on the features of DNA damage in nasopharyngeal carcinoma patients of normal constitution and abnormal constitution and in high-risk population of nasopharyngeal carcinoma].

OBJECTIVE: To explore the features of DNA damage in nasopharyngeal carcinoma (NPC) patients of normal constitution and abnormal constitution and in high-risk population of NPC. METHODS: Using single cell gel electrophoresis technique, the DNA damage of peripheral blood lymphocytes was detected in 28 healthy subjects, 27 in high-risk population of NPC, and 13 NPC patients at their first visits. The DNA damage was detected in the populations of normal constitution and of abnormal constitution. The tail length, the tail moment, and the tail DNA% were taken as the indices of DNA damage. RESULTS: The tail length was (35.77 +/- 4.22) microm, the tail moment was (8.10 +/- 1.63) microm, and the tail DNA% was 57.48% +/- 4.63% in NPC patients. They were (15.25 +/- 4.15) microm, (5.01 +/- 1.92) microm, and 31.99% +/- 4. 11% in high-risk population of NPC. They were (14.31 +/- 3.64) microm, (4. 37 +/- 1.80) microm, and 29. 89% +/- 3. 15% in healthy subjects. There was statistical difference in the three indices among the three populations (P <0.05). In all the three populations, more DNA damage existed in those of abnormal constitution than in those of normal constitution (P <0.05). CONCLUSIONS: Obvious instability of genetic materials exists in NPC patients, manifested as severe DNA damage of lymphocytes. In all the three populations, more DNA damage existed in those of abnormal constitution than in those of normal constitution.

Enhancements of skin cell proliferations and migrations via 6-dehydrogingerdione.

Human skin protects the body from mechanical and chemical damages, and skin wound healing is a costly procedure and worldwide issue. A Zingiber officinale compound, 6-dehydrogingerdione (6-DG), is presented as a novel biofunctional healing agent for human skin wound repair. The effectiveness on cell growth/migration, growth factor, collagen amount, and enzymatic activity was assessed. 6-DG treatment accelerated cellular proliferation and migration dose-dependently. Enzyme-linked immunosorbent assay (ELISA) showed that 6-DG brought about higher growth factor productions on transforming growth factor-ß (TGF-ß), platelet-derived growth factor-αß (PDGF-αß), and vascular endothelial growth factors (VEGF). Under phorbol 12-myristate 13-acetate (PMA) incubation, 6-DG increased fibroblast collagen yield obviously, reduced matrix metalloproteinase-1 (MMP-1) protein expression, and recovered tissue inhibitor of metalloproteinase-1 (TIMP-1) secretion. 6-DG also blocked the mitogen-activated protein kinase (MAPK) pathway by suppressing c-Jun protein levels and extracellular signal-regulated kinases (ERK) phosphorylation in fibroblasts. From all of the above, 6-DG has potential to be a novel agent for human skin repair.

Green tea epigallocatechin gallate inhibits insulin stimulation of adipocyte glucose uptake via the 67-kilodalton laminin receptor and AMP-activated protein kinase pathways.

Insulin and (-)-epigallocatechin gallate (EGCG) are reported to regulate obesity and fat accumulation, respectively. This study investigated the pathways involved in EGCG modulation of insulin-stimulated glucose uptake in 3T3-L1 and C3H10T1/2 adipocytes. EGCG inhibited insulin stimulation of adipocyte glucose uptake in a dose- and time-dependent manner. The concentration of EGCG that decreased insulin-stimulated glucose uptake by 50-60% was approximately 5-10 µM for a period of 2 h. At 10 µM, EGCG and gallic acid were more effective than (-)-epicatechin, (-)-epigallocatechin, and (-)-epicatechin 3-gallate. We identified the EGCG receptor [also known as the 67-kDa laminin receptor (67LR)] in fat cells and extended the findings for this study to clarify whether EGCG-induced changes in insulin-stimulated glucose uptake in adipocytes could be mediated through the 67LR. Pretreatment of adipocytes with a 67LR antibody, but not normal rabbit immunoglobulin, prevented the effects of EGCG on insulin-increased glucose uptake. This suggests that the 67LR mediates the effect of EGCG on insulin-stimulated glucose uptake in adipocytes. Moreover, pretreatment with an AMP-activated protein kinase (AMPK) inhibitor, such as compound C, but not with a glutathione (GSH) activator, such as N-acetyl-L-cysteine (NAC), blocked the antiinsulin effect of EGCG on adipocyte glucose uptake. These data suggest that EGCG exerts its anti-insulin action on adipocyte glucose uptake via the AMPK, but not the GSH, pathway. The results of this study possibly support that EGCG mediates fat content.