中华医学杂志(英文版)
中華醫學雜誌(英文版)
중화의학잡지(영문판)
CHINESE MEDICAL JOURNAL
2004年
6期
913-916
,共4页
丁惠国%王宝恩%贾继东%夏华向%王振宇%赵春惠%徐燕琳
丁惠國%王寶恩%賈繼東%夏華嚮%王振宇%趙春惠%徐燕琳
정혜국%왕보은%가계동%하화향%왕진우%조춘혜%서연림
octreotide%hepatic stellate cell%intracellular Ca2+%L-VOCC%portal hypertension%endothelin-1%LSCM%immunocytochemistry
Background The contractility of hepatic stellate cells (HSCs) may play an important role in the pathogenesis of cirrhosis with portal hypertension. The aim of this study was to research the effects of octreotide, an analogue of somatostatin, on intracellular Ca2+ and on the expression of L-type voltage-operated calcium channels (L-VOCCs) in activated HSCs, and to try to survey the use of octreotide in treatment and prevention of cirrhosis with portal hypertension complications. Methods HSC-T6, an activated HSCs line, was plated on small glass coverslips in 35-mm culture dishes at a density of 1×105/ml, and incubated in DMEM media for 24 hours. After the cells were loaded with Fluo-3/AM, intracellular Ca2+ was measured by Laser Scanning Confocal Microscopy (LSCM). The dynamic changes in activated HSCs of intracellular Ca2+, stimulated by octreotide, endothelin-1, and KCl, respectively, were also determined by LSCM. Each experiment was repeated six times. L-VOCC expression in HSCs was estimated by immunocytochemistry. Results After octreotide stimulation, a signifcant decrease in the intracellular Ca2+ of activated HSCs was observed. However, octreotide did not inhibit the increases in intracellular Ca2+ after stimulation by KCl and endothelin-1. Moreover, octreotide did not significantly affect L-VOCC expression. These results suggest that neither L-VOCC nor endothelin-1 receptors in activated HSCs are inhibited by octreotide. Conclusions Octreotide may decrease portal hypertension and intrahepatic vascular tension by inhibiting activated HSCs contractility through decreases in intracellular Ca2+. The somatostatin receptors in activated HSCs may be inhibited by octreotide.