Lu Jin-song, Liu Yu-qing, Li Ming, Li Bao-sheng, Xu Yan
Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Beijing 100700, China.
Zhongguo Zhong Yao Za Zhi. 2007 Jul;32(13):1333-6.
To study the effects and its possible mechanisms of total alkaloids (TA) from rhizoma Coptis chinensis on H. pylori LPS induced gastric lesion in rats.
H. pylori lipopolysaccharide was applied to rat intragastrically for 4 days to induce a pattern of mucosal responses resembling that of acute gastritis. After treatment with 50, 100, 200 mg x kg(-1) TA, we identified the changes on gastric histopathology, the effects on the activities of cNOS and NOS-2, the contents of TNF-alpha and the gastric mucus epithelial cell apoptosis.
H. pylori LPS could significantly induce the epithelial cell apoptosis of gastric mucus, increase the expression of NOS-2 and decline the expression of cNOS, and enhance the content of TNF-alpha in serum. Treatment with 50, 100, 200 mg x kg(-1) TA led to reduction in the extent of mucosal inflammatory changes elicited by H. pylori LPS and decrease in epithelial cell apoptosis. Furthermore, this effect of TA was associated with decrease in content of TNF-alpha in serum, decline in NOS-2, and increase in cNOS.
The findings suggest that TA is a potent protective agent against H. pylori LPS induced gastric mucosal inflammation. The concerned mechanisms may be related to its inhibition on epithelial cell apoptosis, and the suppression of the inflammatory responses by upregulating cNOS and interfering with the events propagated by NOS-2, and reducing the content of TNF-alpha.
研究黄连总生物碱（TA）对幽门螺杆菌脂多糖（H. pylori LPS）诱导的大鼠胃损伤的影响及其可能机制。
采用幽门螺杆菌脂多糖灌胃大鼠4天，诱导其产生类似急性胃炎的黏膜反应模式。给予50、100、200 mg·kg⁻¹的TA治疗后，观察胃组织病理学变化、对cNOS和NOS-2活性的影响、TNF-α含量以及胃黏液上皮细胞凋亡情况。
幽门螺杆菌脂多糖可显著诱导胃黏液上皮细胞凋亡，增加NOS-2表达，降低cNOS表达，并提高血清TNF-α含量。给予50、100、200 mg·kg⁻¹的TA治疗可减轻幽门螺杆菌脂多糖引起的黏膜炎症程度，减少上皮细胞凋亡。此外，TA的这种作用与血清TNF-α含量降低、NOS-2表达下降以及cNOS表达增加有关。
研究结果表明，TA是一种有效的抗幽门螺杆菌脂多糖诱导的胃黏膜炎症的保护剂。其相关机制可能与其抑制上皮细胞凋亡、上调cNOS并干扰NOS-2介导的炎症反应以及降低TNF-α含量有关。
