摘要
目的 :检测脾虚模型大鼠胃壁细胞胞内 [Ca2 +]i及黄芪对 [Ca2 +]i的调节作用。方法 :SD大鼠用大黄造成脾虚模型 ,并用黄芪注射液治疗 4日 ,用Fura 2 /AM荧光分光光度法检测壁细胞静息状态下和胃泌素刺激下 [Ca2 +]i。结果 :脾虚模型大鼠壁细胞静息状态下 [Ca2 +]i明显低于正常大鼠 ,胃泌素刺激后 [Ca2 +]i升高幅度亦明显低于正常组 ;脾虚黄芪治疗组大鼠静息状态下[Ca2 +]i有一定升高 ,胃泌素刺激下黄芪治疗组壁细胞 [Ca2 +]i升高幅度明显高于模型组并与正常组比较无明显差异。结论 :脾虚大鼠胃壁细胞静息状态下和胃泌素刺激下 [Ca2 +]i明显低于正常大鼠 ,说明脾虚证时壁细胞功能处于一种低代谢状态 ,推测胞内钙库容量可能降低 ,而且壁细胞表面胃泌素受体数下调或 /和功能下降 ,不能正常介导胞外信号。黄芪能够使低下的胞内代谢水平有一定程度恢复 ,胞内钙库容量有一定增大 ,并能使胃泌素受体数上调和 /或功能加强 。
Aims: Measuring gastric parietal cells [Ca 2+ ]i of Pi deficiency rat model and the regulating effects of Huangqi. [WT5”HZ]Methods:[WT5”BZ] SD rats were randomly divided into three groups: Pi deficiency model group, treating group Injected with Huangqi Injection, normal group. [Ca 2+ ]i was measured using fura 2/AM fluorescence method. [WT5”HZ]Results:[WT5”BZ] (1) The resting [Ca 2+ ]i of the model and its elevating percentage under gastrin stimulation were significantly lower than those of normal rats (P<0.01); (2) [Ca 2+ ]i of treating group was increased in a degree, but had no statistically significance compared with that of the model, and lower than that of the normal (P<0.01). The percentage of increased [Ca 2+ ]i of the treating group stimulating by gastrin was significantly higher than that of the model (P<0.01), and had no significant difference compared with the normal group. [WT5”HZ]Conclutions:[WT5”BZ] The results indicate that gastric parietal cells was in a lower metabolic condition when Pi deficiency syndroms occurs, and we speculates that calcium pool volume was lowed, or gastrin receptor number or its function were lowed which cannot mediated extracellular signals. The Chinese herbal Huangqi Injection, which function is replenishing Qi and invigorating Pi, can elevate intracellular calcium pool volume or upregulate gastrin receptor of gastric parietal cells, these may be the cellular mechanism of Huangqi's function.
出处
《中药药理与临床》
CAS
CSCD
2001年第2期15-17,共3页
Pharmacology and Clinics of Chinese Materia Medica
基金
广东省自然科学基金项目 !课题编号 980 640
关键词
胞浆游离钙离子
脾虚证
胃壁细胞
黄芪注射液
Pi deficicency syndrom model
[Ca 2+ ]i
gastric parietal cell
Huangqi