RESUMEN
Cinnamon is the main component of Sanyangxuedai, which is one of the effective traditional Chinese medicines for treating malignancies. Leukemia is a prevalent malignant disease that Sanyangxuedai has been used to treat. Although successful in several studies, there is a lack of solid evidence as to why Sanyangxuedai has an effect on leukemia, and little is known about the underlying mechanisms. In this study, the active ingredients of cinnamon were isolated, purified, and identified. The transwell transport pool formed with the Caco-2 cell model was used to filter the active ingredients of cinnamon by simulating the gastrointestinal barrier in vitro. Moreover, the cell morphology, cell cycle status, apoptosis status, and antigenic variation of the cell surface antigens were observed and measured in K562 cells after treatment with the active ingredients of cinnamon. Our results showed that 50-75 µM was a safe concentration of cinnamon extract for treatment of K562 cells for 72 h. The cinnamon extract caused growth inhibition of K562 cells. Cinnamon extract seemed to arrest the cells at the G1 stage and increased the apoptosis rate significantly. Interestingly, cinnamon extract treatment upregulated the expression of erythroid and myeloid differentiation antigens and downregulated that of the megakaryocytic differentiation antigens in a dose-dependent manner. Our findings indicate that cinnamon extract from Sanyangxuedai may be effective for treating leukemia.
Asunto(s)
Cinnamomum zeylanicum/química , Leucemia/tratamiento farmacológico , Extractos Vegetales/farmacología , Células Madre/efectos de los fármacos , Apoptosis/efectos de los fármacos , Células CACO-2 , Ciclo Celular/efectos de los fármacos , Diferenciación Celular/efectos de los fármacos , Proliferación Celular/efectos de los fármacos , Humanos , Células K562 , Leucemia/patología , Células Madre/metabolismo , Células Madre/patologíaRESUMEN
Apolipoprotein B (apoB) gene 3' variable number of tandem repeat (VNTR) is highly variable, and therefore can be an informative marker for associative analysis of lipid metabolism. This is the first report focusing on a possible association of apoB VNTR polymorphism with nephrotic hyperlipidemia. Genomic DNA was extracted from 500 children with primary nephrotic syndrome (PNS) and 500 healthy controls. The apoB genotype was determined by PCR analysis. Allele size distribution followed a unimodal curve, with the main peak at the hypervariable element 35 (HVE35); the most prevalent genotype was HVE35/35 in both control and PNS children. The genotype and allele distributions of apoB variants in PNS children were not significantly different from controls. There was significant variation in serum lipid profiles among different genotypes in control children. Individuals with the long (L) allele exhibited significantly higher total cholesterol, low-density lipoprotein cholesterol (LDL-C) and apoB levels than those with the medium (M) or short (S) allele; consequently, M/L carriers had significantly higher total cholesterol, LDL-C and apoB concentrations than did S/S, S/M, S/L, or M/M carriers. However, in PNS children, no significant differences in serum lipid levels were observed among individuals with different genotypes and alleles of apoB 3' VNTR. We conclude that hyperlipidemia in nephrotic children is not associated with apoB 3' VNTR polymorphism.