用检测平滑肌细胞电活动和张力技术，研究了大黄素对豚鼠结肠带平滑肌细胞电和收缩活动的影响并cromakalim，glybenclamide，四乙胺及BaCl2的作用进行比较。结果表明，大黄素加强平滑肌细胞电和收缩活动，作用效果与剂量有关；大黄素与cromakalim的作用相互抑制。其促进平滑肌细胞电和收缩活动的作用与glybenclamide相似，而与四乙胺和BaCl2有明显区别。提示大黄素的作用机制与抑制细胞膜KATP等钾通道的活性相关。

应用检测淀粉酶分泌和单细胞[Ca2+]i的技术，研究了Bt2-cGMP和GDP对柴胡皂甙(I) [SA(I)]和CCK-8促大鼠胰腺腺泡酶分泌和增加[Ca2+]i的抑制作用。Bt2-cGMP对SA(I)和CCK-8促酶分泌的抑制有相似的剂量依赖性。Bt2-cGMP对SA(I)刺激的酶分泌动力学的抑制较对CCK-8滞后并持续。SA(I)诱发的胰腺腺泡单细胞[Ca2+]i的变化与CCK-8 的作用有所不同: [Ca2+]i峰值上升较慢且持续较长，并在峰后[Ca2+]i再次升高。GDP亦抑制SA(I)刺激的酶分泌和[Ca2+]i增加的峰植。结果表明，SA(I)可激活胰腺腺泡细胞膜受体从而升高[Ca2+]i和促酶分泌。

为了解柴胡皂甙(I)[SA(I) ]刺激大鼠胰腺腺泡酶分泌的信号传导通路，研究了GTPγs对SA(I)刺激通透腺泡细胞酶分泌的影响。用SLO通透细胞的同时，加入GTPγs 在15min期间能诱发酶分泌，10-7mol·L-1GTPγs有最大促泌效应。GTPγs浓度依赖性的增强SA(I)促酶分泌作用，10-7mol·L-1GTPγs导致10- 5mol·L-1SA(I) 刺激酶分泌量增加到1.6倍。用SLO预通透腺泡10min后，加入GTPγs使SA(I)刺激酶分泌的量-效曲线左移，SA(I)的EC502.0×10-5mol·L-1减小到1.0×10- 5mol·L-1。以上结果提示，SA(I)活化受体偶联的G蛋白包括在其刺激酶分泌的信号传导通路中。

目的：研宽大黄影响正常的及内毒素细茵脂多糖（LPS）刺激的大鼠腹腔巨噬细胞（PMφ）分泌肿瘤坏死因子（TNF-α）的特征及其与细胞[Ca2+]i的变化关系。方法：利用TNF-α敏感细胞系L929，用MTT法检测PMφ分泌的TNF-α量；用荧光探针和荧光先谱法分别没定多细胞和单细胞的[Ca2+]i。结果：适宜浓度的大黄可轻度活化正常的PMφ分泌TNR-α和升高[Ca2+]i，天黄对LPS刺激的PMφ十分泌TNF-α和升高[Ca2+]i有剂量依赖性的抑制效应，1.0%大黄分刺抑制了LPS刺激的PMφTNF-α分泌量的92.5%和[Ca2+]i升高的90.5%。其押制作用主要表现在给药的早期阶段。结论：大黄对PMφ分泌TNF-α有双向调节作用，降低细胞[Ca2+]i是其抑制LPS刺激作用的细胞内信号传导的关键环节。

AIM: To investigate whether emodin has any effects on circular smooth muscle cells of rat colon and to examine the mechanism underlying its effect. METHODS: Smooth muscle cells were isolated from the circular muscle layer of Wistar rat colon and the cell length was measured by computerized image micrometry. Intracellular Ca2+ ([Ca2+]i) signalling was studied in smooth muscle cells using Ca2+ indicator Fluo-3AM on a laserscanning confocal microscope. RESULTS: Emodin dose-dependently induced smooth muscle cells contraction. The contractile responses induced by emodin were inhibited by preincubation of the cells with ML-7 (an inhibitor of MLCK). Emodin caused a large, transient increase in [Ca2+]i followed by a sustained elevation in [Ca2+]i. The emodin-induced increase in [Ca2+]i was unaffected by nifedipine, a voltage-gated Ca2+-channel antagonist, and thesustained phase of the rising of [Ca2+]i was attenuated by extracellular Ca2+ removal with EGTA solution. Inhibiting Ca2+ release from ryanodine-sensitive intracellular stores by ryanodine reduced the peak increase in [Ca2+]i. Using heparin, an antagonist of IP3R, almost abolished the peak increase in [Ca2+]i. CONCLUSION: Emodin has a direct excitatory effect on circular smooth muscle cells in rat colon mediated via Ca2+/CaM dependent pathways. Furthermore, emodin-induced peak [Ca2+]i increase may be attributable to the Ca2+ release from IP3 sensitive stores, which further promote Ca2+ release from ryanodine-sensitive stores through CICR mechanism. Additionally, Ca2+ influx from extracellular medium contributes to the sustained increase in [Ca2+]i.

联合应用平滑肌肌力张力测量技术和细胞内微电极记录技术，同步地观测脬鼠结肠带平滑肌自发的肌源性电活动和力学活动，研究了大黄素的药物作用。太黄素能缩短膜电位的波动周期，从而缩短峰电位集簇发放的周期；相应地，可使平滑肌的分节律收缩加快，幅值指敷升高。大黄素又能促使细胞膜电位自发的周期性波动的出现，导致峰电位的集簇发放；相应地，可使强直收缩转化为分节律收缩，即促进收缩形式向有利于肠道推进功能的方向转化。以上结果表明，大黄素能有效地提高豚鼠结肠带平滑肌细胞的电兴奋性和收缩功能，并且对其电学和力学活动的影响之间有明确的对应关系。

The effects of Daehengqi decoction (DCQ) and rhubarb (Rb) on the spontaneous cellular electrical activities of guinea pig taenia coU have been studied by intracellular microelectrode technique. DCQ and Rb both improve the depolarization of cell membrane, speed up the burst of slow wave and spike potentials (when the drug concentration was 1%, P>0.05, 10% or 20%, P<0.03), which were dose de pendent. At the same concentration the effects of Rb were more significant than those of DCQ. These results suggest DCQ and Rb directly enhance the cellular electrical excitability so as to strengthen the con traction of the colon, is one of the mechanisms of the purgative action of these drugs at the cellular level. The ionic basis of the effects might be that DCQ and Rb reduce the K+ conductance of the cell membranes in a resting state.

This investigation was to reveal the characteristics and mechanism of enzyme secretion and increase in [Ca2+], stimulated by saikosaponin (I) [SA(I)] in rat pancreatic acini. METHODS: Pancreatic acini were prepared from male Wistar rats Isolated acinar cells were suspended in Eagle's MEM solution After adding drugs, the incubation was performed at 37℃ for a set period of time, Amylase of supematant was assyayed using starch iodide reaction Isolated acinar single cell was incubated with Fura-2/AM at 37℃, then cells were washed and resuspanded in fresh solution and attached to he chamber Cytoplasm [Ca2+], of a sngle cell was expressed by fluorescence ratio F340/F380 recorded in a Nikon Pl Ca2+ mesurement systm. RESULTS: Rate couse of amylase secretion stimulated by SA (I) in rat pancreatic acini appeared in bell-like shape The peak amplitude increased depended on SA (I) concentration The maximum rate responded to 1×10-5mol/L SAC (I) was 13. I-fold of basal and the rate decreased to basal level at 30min CCK-8 receptor antagonist Bt2-cGmp markedly inhibited amylse secretion stimulated by SA (I) and the dose effect relationship was sirrdlar to that by CCK-8[Ca2+]i in a single acinar cell to the peak at 5 min after adding 5×10-6mol/L SA (I) and was 5.1-fold of basal level. In addition, there was a secondary increase after the initial peak CDP could inhibit both the rote of amylase secretion and rising of [Ca2+] stimulated by SA (I) in a single pancreatic acinar ce11. CONCLUSION: SA(I)) is highly efficient in promting the secetion of enzymes synthesized in rat pancreatie acini and raising intracellular [Ca2+]i. Signaling transduction pathway of SA (I) involves activating special membrane receptor and increase in cytoplasm [Ca2+]i sequentially

目的：研究鸟苷二磷酸（GDP）对柴胡皂甙（I）[SA（I）]刺激大鼠胰腺腺泡酶分泌和胞内钙离子升高的影响。方法：分离大鼠胰腺腺泡细胞，用链球菌溶血素-O（SLO）通透细胞膜。检浊腺泡分泌蛋白量标志腺泡酶分泌功能。用钙离子荧光指示剂Fluo-3和荧光光谱测定胞山钙离子浓度。结果：GDP可抑制SA（I）促胰腺腺泡的酶分泌作用。抑制作用随剂量增加而加强：SA（I）10μmol/L以双峰值为特征使[Ca2+]i显著上升；GDP5mmol/L。导致[Ca2+]逐步升高且两个峰值消失。细胞通透以后、与正常细胞相比，SA（I）刺激的30lmin酶分泌的累积量下降了57%；GDP5mmol/L他SA（I）刺激的早期酶分泌速率进一步降低。结论：GDP通过抑制细胞[Ca+]i的升高抑制了SA（I）刺激的胰腺腺泡酶分泌作用。