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Article in Chinese | WPRIM | ID: wpr-329958


<p><b>OBJECTIVE</b>To investigate the effects of cis-combretastatin-A1 phosphate (cis-CA1P) on tumor cell proliferation, and its effects on the blood vessel formations.</p><p><b>METHODS</b>MTT and IC50 values were used to assess the inhibitory effects of cis-CA1P on tumor cell proliferation. Chicken embryo chorioallantoic membrane and thoracic aorta annulations isolated from rats were used to investigate the effects of cis-CAIP on the blood vessel formation.</p><p><b>RESULTS</b>Cis-CA1P concentration-dependently inhibited the proliferations of several cancer cell lines, including human gastric carcinoma cell line MGC-803, human leukemic monocyte lymphoma cell line U937, human melanoma cell line A375, human colon cancer cell line HCT116, human breast carcinoma cell line MDA-MB-231, and human leukemia cell line K562. Cis-CAIP significantly decreased the formation of blood vessels in chicken embryo chorioallantoic membrane and in thoracic aorta annulations.</p><p><b>CONCLUSION</b>Cis-CA1P inhibits cancer cell proliferation and prevents blood vessel formation.</p>

Animals , Aorta , Cell Line, Tumor , Cell Proliferation , Chick Embryo , Chorioallantoic Membrane , Humans , In Vitro Techniques , Neovascularization, Pathologic , Phosphates , Pharmacology , Rats , Stilbenes , Chemistry , Pharmacology
Article in Chinese | WPRIM | ID: wpr-330095


<p><b>AIM</b>Using GeneChip to analyze the changes in genes expression of brain potassium, sodium and calcium channels after chronic treatment with nicotine.</p><p><b>METHODS</b>Animals were treated with nicotine at the doses of 2.4 mg/kg sc. twice a day for 14 days. RNA was extracted from the whole brain samples and converted to double-stranded cDNA and then to biotinylated cRNA. The biotinylated cRNA was fragmented, and hybridized to GeneChip (Affymetrix Rat Neurobiology U34). The chips were scanned with a probe array scanner, and the data were analyzed with the Affymetrix Microarray Analysis Suite (MAS). The GeneChip data were confirmed u sing RT-PCR.</p><p><b>RESULTS</b>After treatment with chronic nicotine, transcripts of potassium, sodium and calcium channels showed altered expression. K+ channel: outward rectifier K+ channel and Ca2(+)-activated K+ channel were down-regulated, other voltage-dependent K+ channel including Kv2.3r were up-regulated. Voltage-dependent Na+ channel: beta2 subunit was increased, alpha subunit and beta1 subunit were decreased. Beta3 subunit of Ca2+ channel was up-regulated.</p><p><b>CONCLUSION</b>Chronic exposure to nicotine not only desensitized nicotinic receptors, but also effected genes expression, of important ion channels, such as sodium channels, potassium channels and calcium channels.</p>

Animals , Brain , Metabolism , Calcium Channels , Metabolism , Gene Expression , Male , Nicotine , Pharmacology , Potassium Channels , Metabolism , Rats , Rats, Sprague-Dawley , Sodium Channels , Metabolism