摘要
目的观察三七总苷对应激大鼠胃黏膜损伤及胃壁细胞超微结构的影响。方法采用经典的水浸-束缚应激模型,应激6 h后,大鼠处死剖腹取胃,肉眼计数各组胃黏膜糜烂、出血情况并计算溃疡指数(UI);在透射电镜下观察各组胃黏膜壁细胞超微结构改变。结果肉眼观察正常对照组大鼠胃黏膜色泽红润,未见损伤性改变;模型组大鼠胃黏膜充血明显,腺胃部可见散在斑点状糜烂、出血,溃疡指数为(16.83±4.96);与模型组相比,三七总苷组和雷尼替丁组胃黏膜充血减少,UI值均明显下降(P<0.01)。电镜下,正常对照组大鼠胃壁细胞分泌小管少见,呈现明显的静息状态,模型组分泌小管增多呈现泌酸激活状态;与模型组比较,三七总苷组分泌小管扩张不明显或明显塌陷,细胞内囊泡样结构增多;雷尼替丁组则见大量囊泡样结构,分泌小管明显减少。结论三七总苷可明显减轻应激对胃黏膜的损伤,还可促进胃黏膜壁细胞从激活状态向静息状态转化,说明三七总苷对应激大鼠胃黏膜具有保护作用,可能通过调控壁细胞的泌酸功能而发挥其抗应激性胃黏膜损伤作用。
Objective To observe the effect of total saponins of Panax notognseng (PNS) on gastric mucosal lesion and uhrastructure of gastric mucosal parietal cells of stress rats. Methods Water - immersion restraint stress (WRS) was used to induce rat models of stress. Six hours after WRS, the rats were executed to obtain the gastric tissue. The erosion and hemorrhage of gastric mucosa in rats were observed by naked eyes, and then the ulceration index (UI) was calculated. The ultrastrncture of gastric mucosal parietal cells in rats was observed under transmission electron microscope. Results The results observed by naked eyes showed that no lesion was found in the normal group. However, in the model group, the gastric mucosal congestion was obvious, there existed scattered punctiform erosion and bleeding in the glandular stomach, and the UI was 16.83 ± 4.96; compared with the model group, gastric mucosal congestion was reduced and UI decreased in the PNS group and ranitidine group (P 〈 0.01 ). Under the electron microscope, there were less endocrine tubular villi in the parietal cells of the normal group, showing a static status. However, in the model group, the number of endocrine tubular villi increased, showing an activating status; compared with the model group, the expansion of endocrine tubular villi was not obvious but the number of cytoplasm interior vesicles in parietal cells increased in PNS group, and in ranitidine group, the number of endocrine tubular villi was decreased and the number of vesicular structure was increased. Conclusion PNS can reduce the stress - induced gastric nmeosal lesion, and promote the wall cells of gastric mucosa transforming from the activated status into static status. The protective mechanism of PNS is probably related with the regulation of acid secretion of Parietal cell.
出处
《时珍国医国药》
CAS
CSCD
北大核心
2008年第9期2143-2145,共3页
Lishizhen Medicine and Materia Medica Research
基金
广州中医药大学中医药科研创新项目(No.2006F31)
关键词
应激性溃疡
胃黏膜损伤
溃疡指数
壁细胞
超微结构
Stress ulcer
Gastric mueosal lesion
Ulceration index
Parietal cell
Ultrastructure