ABSTRACT
The roles of intermediate conductance Ca(2+)-activated K(+) channel (IKCa1) in the pathogenesis of hepatocellular carcinoma (HCC) were investigated. Immunohistochemistry and Western blotting were used to detect the expression of IKCa1 protein in 50 HCC and 20 para-carcinoma tissue samples. Real-time PCR was used to detect the transcription level of IKCa1 mRNA in 13 HCC and 11 para-carcinoma tissue samples. The MTT assay was used to measure the function of IKCa1 in human HCC cell line HepG2 in vitro. TRAM-34, a specific blocker of IKCa1, was used to intervene with the function of IKCa1. As compared with para-carcinoma tissue, an over-expression of IKCa1 protein was detected in HCC tissue samples (P<0.05). The mRNA expression level of IKCa1 in HCC tissues was 2.17 times higher than that in para-carcinoma tissues. The proliferation of HepG2 cells was suppressed by TRAM-34 (0.5, 1.0, 2.0 and 4.0 μmol/L) in vitro (P<0.05). Our results suggested that IKCa1 may play a role in the proliferation of human HCC, and IKCa1 blockers may represent a potential therapeutic strategy for HCC.
ABSTRACT
The roles of intermediate conductance Ca(2+)-activated K(+) channel (IKCa1) in the pathogenesis of hepatocellular carcinoma (HCC) were investigated. Immunohistochemistry and Western blotting were used to detect the expression of IKCa1 protein in 50 HCC and 20 para-carcinoma tissue samples. Real-time PCR was used to detect the transcription level of IKCa1 mRNA in 13 HCC and 11 para-carcinoma tissue samples. The MTT assay was used to measure the function of IKCa1 in human HCC cell line HepG2 in vitro. TRAM-34, a specific blocker of IKCa1, was used to intervene with the function of IKCa1. As compared with para-carcinoma tissue, an over-expression of IKCa1 protein was detected in HCC tissue samples (P<0.05). The mRNA expression level of IKCa1 in HCC tissues was 2.17 times higher than that in para-carcinoma tissues. The proliferation of HepG2 cells was suppressed by TRAM-34 (0.5, 1.0, 2.0 and 4.0 μmol/L) in vitro (P<0.05). Our results suggested that IKCa1 may play a role in the proliferation of human HCC, and IKCa1 blockers may represent a potential therapeutic strategy for HCC.
Subject(s)
Humans , Calcium Channel Blockers , Pharmacology , Carcinoma, Hepatocellular , Pathology , Cell Proliferation , Hep G2 Cells , Intermediate-Conductance Calcium-Activated Potassium Channels , Metabolism , Ion Channel Gating , Liver Neoplasms , Pathology , Potassium , Metabolism , Pyrazoles , Pharmacology , Tumor Cells, CulturedABSTRACT
<p><b>OBJECTIVE</b>To investigate the amount of daily iodine intake in the diet of the target population in drinking water with areas of excessive iodine after stopping supply of iodized salt, to provide evidence for developing strategies on control and prevention of excessive iodine.</p><p><b>METHODS</b>335 objectives were selected by a two-stage sampling method in 4 administrative villages with different iodine contents in drinking water. The amount of drinking water intake and dietary survey for 335 people were done by a door-to-door survey,while the iodine contents in the drinking water of each selected family, local staple food and vegetable were measured.</p><p><b>RESULTS</b>The median level of iodine in drinking water was 431.5 microg/L while the daily amount of iodine intake among the three groups of waters with different iodine contents were all greater than RNI. The daily iodine intake of local people was all greater than UL in the areas where the water iodine contents were more than 300 microg/L. It was of statistical sense that the iodine mean intake per capita per day of the three groups differed at different water iodine levels (P < 0.01). The iodine mean intake per capita per day of the three groups of different water iodine levels increased along with water iodine and showed a uptrend (P < 0.01). 83.2%-98.7% of the daily iodine intake of the three groups was from drinking water and 1.3%-16.8% came from food. The iodine intake had high-positive correlation relation with the content of water iodine (P < 0.01).</p><p><b>CONCLUSION</b>It was concluded that drinking water was the main source of iodine intake in areas with iodine excessive water by the percentage of over 80%. It was necessary to adopt measures to improve the quality of water to decrease the iodine content other than just stopping supplies of iodized salt in the areas where the water iodine contents were greater than 300 microg/L, in order to prevent and control excessive intake of iodine.</p>