目的探讨紫丹银屑颗粒对银屑病样小鼠模型的治疗作用和作用机制,为临床应用提供参考。方法将试验动物随机分为正常对照组、模型对照组、紫丹银屑高、中、低剂量组及阳性对照组,每组10只,灌胃给药。采用流式细胞分析仪分析紫丹银屑颗粒对...目的探讨紫丹银屑颗粒对银屑病样小鼠模型的治疗作用和作用机制,为临床应用提供参考。方法将试验动物随机分为正常对照组、模型对照组、紫丹银屑高、中、低剂量组及阳性对照组,每组10只,灌胃给药。采用流式细胞分析仪分析紫丹银屑颗粒对Ha Ca T细胞周期的影响(在96孔板上依次设定紫丹银屑颗粒2、4、8、16、32g·L-1组,维A酸片8 g·L-1组,空白细胞组);采用动物体内实验,观察紫丹银屑颗粒对银屑病小鼠模型血清中白介素-2、肿瘤坏死因子含量的影响。结果体外试验显示,与模型组比较,紫丹银屑颗粒高、中剂量组细胞增殖数量显著减少,有显著性差异(P<0.05);体内试验显示,与模型组比较,紫丹银屑颗粒高、中剂量组S期细胞数量显著减少,有显著性差异(P<0.05)。结论紫丹银屑颗粒能够显著抑制人永生化表皮细胞增殖,并显著降低模型动物血清白介素-2、肿瘤坏死因子的含量,这可能是紫丹银屑颗粒治疗银屑病的作用机制之一。展开更多
Intracellular cAMP and Ca^2＋ are involved in the regulation of steroidogenic activity in Leydig cells, which coordinate responses to luteinizing hormone （LH） and human ehorionic gonadotropin （hCG）. However, the i...Intracellular cAMP and Ca^2＋ are involved in the regulation of steroidogenic activity in Leydig cells, which coordinate responses to luteinizing hormone （LH） and human ehorionic gonadotropin （hCG）. However, the identification of Ca^2＋ entry implicated in Leydig cell steroidogenesis is not well defined. The objective of this study was to identify the type of Ca^2＋ channel that affects Leydig cell steroidogenesis. In vitro steroidogenesis in the freshly dissociated Leydig cells of mice was induced by hCG incubation. The effects of mibefradil （a putative T-type Ca^2＋ channel blocker） on steroidogenesis were assessed using reverse transcription （RT）-polymerase chain reaction analysis for the steroidogenic acute regulatory protein （STAR） mRNA expression and testosterone production using radioimmunoassay. In the presence of 1.0 mmol L-1 extracellular Ca^2＋, hCG at 1 to 100 IU noticeably elevated both StAR mRNA level and testosterone secretion （P 〈 0.05）, and the stimulatory effects of hCG were markedly diminished by mibefradil in a dose-dependent manner （P 〈 0.05）. Moreover; the hCG-induced increase in testosterone production was completely removed when external Ca^2＋ was omitted, implying that Ca entry is needed for hCG-induced steroidogenesis. Furthermore, a patch-clamp study revealed the presence of mibefradil-sensitive Ca^24- currents seen at a concentration range that nearly paralleled those inhibiting steroidogenesis. Collectively, Our data provide evidence that hCG-stimulated steroidogenesis is mediated at least in part by Ca^2＋ entry carried out by the T-type Ca^2＋ channel in the Leydig cells of mice.展开更多
文摘目的探讨紫丹银屑颗粒对银屑病样小鼠模型的治疗作用和作用机制,为临床应用提供参考。方法将试验动物随机分为正常对照组、模型对照组、紫丹银屑高、中、低剂量组及阳性对照组,每组10只,灌胃给药。采用流式细胞分析仪分析紫丹银屑颗粒对Ha Ca T细胞周期的影响(在96孔板上依次设定紫丹银屑颗粒2、4、8、16、32g·L-1组,维A酸片8 g·L-1组,空白细胞组);采用动物体内实验,观察紫丹银屑颗粒对银屑病小鼠模型血清中白介素-2、肿瘤坏死因子含量的影响。结果体外试验显示,与模型组比较,紫丹银屑颗粒高、中剂量组细胞增殖数量显著减少,有显著性差异(P<0.05);体内试验显示,与模型组比较,紫丹银屑颗粒高、中剂量组S期细胞数量显著减少,有显著性差异(P<0.05)。结论紫丹银屑颗粒能够显著抑制人永生化表皮细胞增殖,并显著降低模型动物血清白介素-2、肿瘤坏死因子的含量,这可能是紫丹银屑颗粒治疗银屑病的作用机制之一。
文摘Intracellular cAMP and Ca^2＋ are involved in the regulation of steroidogenic activity in Leydig cells, which coordinate responses to luteinizing hormone （LH） and human ehorionic gonadotropin （hCG）. However, the identification of Ca^2＋ entry implicated in Leydig cell steroidogenesis is not well defined. The objective of this study was to identify the type of Ca^2＋ channel that affects Leydig cell steroidogenesis. In vitro steroidogenesis in the freshly dissociated Leydig cells of mice was induced by hCG incubation. The effects of mibefradil （a putative T-type Ca^2＋ channel blocker） on steroidogenesis were assessed using reverse transcription （RT）-polymerase chain reaction analysis for the steroidogenic acute regulatory protein （STAR） mRNA expression and testosterone production using radioimmunoassay. In the presence of 1.0 mmol L-1 extracellular Ca^2＋, hCG at 1 to 100 IU noticeably elevated both StAR mRNA level and testosterone secretion （P 〈 0.05）, and the stimulatory effects of hCG were markedly diminished by mibefradil in a dose-dependent manner （P 〈 0.05）. Moreover; the hCG-induced increase in testosterone production was completely removed when external Ca^2＋ was omitted, implying that Ca entry is needed for hCG-induced steroidogenesis. Furthermore, a patch-clamp study revealed the presence of mibefradil-sensitive Ca^24- currents seen at a concentration range that nearly paralleled those inhibiting steroidogenesis. Collectively, Our data provide evidence that hCG-stimulated steroidogenesis is mediated at least in part by Ca^2＋ entry carried out by the T-type Ca^2＋ channel in the Leydig cells of mice.
