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三七白及粉对大鼠脑出血致应激性溃疡的治疗作用及其机制研究
Therapeutic effects and underlying mechanism of Panax notoginseng powder in rat models with post-cerebral hemorrhage stress ulcer
【摘要】 目的 观察三七白及粉对脑出血致应激性溃疡(SU)模型大鼠的治疗作用,并探讨其作用机制。方法 将30只雄性SD大鼠随机分为对照组、模型组、三七白及粉组,每组10只。适应性饲养1周后,模型组、三七白及粉组采用自体血定位注射法建立大鼠基底节脑出血致SU模型。在造模完成3天后,三七白及粉组予三七白及粉2.5 g/kg灌胃,对照组、模型组予等容积0.9%氯化钠注射液灌胃,每日1次,连续灌胃14天后,将大鼠麻醉后取血,检测大鼠血清一氧化氮(NO)、丙二醛(MDA)、超氧化物歧化酶(SOD)、前列腺素E2(PGE2)水平。取完整胃组织观察形态学改变,取脑组织和胃溃疡组织进行切片,并采用苏木素-伊红(HE)染色法观察脑组织和胃组织病理变化,并测定溃疡指数。结果 与对照组比较,模型组大鼠血清NO、SOD和PGE2水平均降低(P<0.05),MDA升高(P<0.05);与模型组比较,三七白及粉组大鼠血清NO、SOD和PGE2水平均升高(P<0.05),MDA降低(P<0.05)。脑组织病理学观察:基底节区细胞排列不规则,细胞核形态不规则,部分出现核皱缩现象,血肿及周围神经元减少,胶质细胞、毛细血管增生明显。胃组织形态观察:对照组大鼠胃黏膜表面光滑,色淡红,并覆盖有大量黏液,黏膜表面及浆膜面完整,未见水肿、充血等病理变化;模型组可见大量散在点、线状出血或糜烂,并伴有炎性渗出;三七白及粉组大部分可以找到溃疡灶,但面积较小,部分可见充血点及炎性渗出物。胃组织病理观察:对照组胃黏膜组织形态正常,结构完整;模型组胃黏膜镜下可见胃黏膜上皮细胞坏死、脱落,腺体结构破坏,黏膜间质明显充血、水肿和出血;三七白及粉组胃黏膜表面未见糜烂,间质充血、水肿程度较模型组明显减轻。三七白及粉组大鼠溃疡指数低于模型组(P<0.05)。结论 三七白及粉能促进脑出血致SU胃黏膜愈合修复,其作用机制可能是经过提高消化道黏膜保护因子PGE2、NO水平,增强SOD活性,降低MDA水平,增强抗氧化应激作用,进而加强胃黏膜的防御修复能力实现的。
【Abstract】 Objective To explore the therapeutic effects and underlying mechanism ofPanax notoginseng powder(PNP)in rat modelswith post-cerebral hemorrhage stress ulcer(SU). Methods Thirty male SD rats were randomly assigned in a 1∶1∶1 ratioto control group, model group, PNP group. After one week of adaptive feeding, the SU model was established by injecting autologous blood in rats of model group and PNP group.After 3 days of modeling, rats of PNP group and the other two groups were respectively given gastric irrigation of 2.5 g/kg/d of gastric irrigation and equal dose of 0.9% sodium chloride injection for 14 days.The rats were anesthetized and taken blood, andthe serum levels of nitric oxide(NO), malondialdehyde(MDA), superoxide dismutase(SOD), and prostaglandin E2(PGE2) were measured by nitrate reductase assay, complete stomach tissue were collected to observe morphological changes. Brain and ulcer tissues were sectioned, and hematoxylin-eosin(HE) staining was performed to observe pathological changes in brain and stomach tissues. Additionally, the ulcer index was determined. Results Compared with the control group, the serum NO, SOD and PGE2 levels of rats in the model group and PNP group decreased significantly(P<0.05), and MDA increased significantly(P<0.05). Compared with the model group, the serum NO, SOD and PGE2 levels of rats in PNP group increased significantly(P<0.05), and MDA decreased significantly(P<0.05). The evaluation of gross brain pathology specimens exhibited that in the basal ganglia, nuclear shape was irregular, with shrinkage, hematoma and less surrounding neurons in some, as well as significant proliferation of glial cells and capillaries.The gastric tissue morphology presented thatthe gastric mucosal surfaces of the rats in the control group were smooth, with light red color, more mucus, perfect mucosal surface and serosal surface, without pathological changes of edema and congestion. A large number of scattered bleeding or erosion in dots and lineswere seen in the model group, and with inflammatory exudate. A large number of ulceration could be found in the PNP group, but the area was small, accompanied by less congestion and inflammatory exudate. Pathological observation of gastric tissue indicated that the morphology of the gastric mucosa and serosal structure were normal in the control group. The necrosis and detachment of gastric mucosal epithelial cells were seen by HE pathological sections of gastric tissuein the model group, with poor glandular structure, and obvious interstitial congestion, edema, and hemorrhage in the mucosal interstitium.There was no erosion on the gastric mucosal surface in PNP group, and the degrees of interstitial congestion and edema, and the ulcer index of rats in PNP group were significantly lower than those of the model group(P<0.05).Conclusion PNP powder has a good effect to improve the healing of post-cerebral hemorrhage stress ulcer. The mechanism is likely to enhance SOD activity, reduce MDA level, and increase oxidative stress, and strengthen the gastric mucosal defense by increasing the levels of protective factors PGE2 and NO in the digestive tract mucosa. It may be improved the repair ability of gastric mucosa at further.
【Key words】 Panax notoginseng; Cerebral hemorrhage; Gastric ulcer; Rat; Animal model; Animal experiment; Nitric oxide; Superoxide dismutase; Malondialdehyde; Prostaglandin E2;
- 【文献出处】 河北中医 ,Hebei Journal of Traditional Chinese Medicine , 编辑部邮箱 ,2024年02期
- 【分类号】R285.5
- 【下载频次】177