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秦艽中龙胆苦苷对应激诱导的胃肠动力障碍的缓解作用

Attenuation of stress-induced gastrointestinal motility disorder by gentiopicroside, from Gentiana macrophylla Pall.

作者信息

Ruan Ming, Yu Bin, Xu Li, Zhang Liang, Long Jun, Shen Xiangchun

机构信息

Jiangsu Key Laboratory for Pharmacology and Safety Evaluation of Chinese Materia Medica, Nanjing University of Chinese Medicine, Nanjing 210023, PR China; School of Food Science, Nanjing Xiaozhuang University, Nanjing 211171, PR China.

Jiangsu Key Laboratory for Pharmacology and Safety Evaluation of Chinese Materia Medica, Nanjing University of Chinese Medicine, Nanjing 210023, PR China.

出版信息

Fitoterapia. 2015 Jun;103:265-76. doi: 10.1016/j.fitote.2015.04.015. Epub 2015 May 1.

Abstract

AIM

The current study was designed to explore the mechanism of the prokinetic activity of Gentiopicroside (Ge), from Gentiana macrophylla Pall which is widely used to strengthen gastric motility in clinic.

METHODS

Gastrointestinal motility disorder rats were induced by stress stimulation and the rats were treated with Ge. The functions of gastric emptying and intestinal propelling were measured after blood was obtained to assay the levels of plasmatic motilin (MTL), vasoactive intestinal peptide (VIP), somatostatin (SST), gastrin (GAS), neurotensin (NT) and substance of P (SP). The expressions of MTL receptor (MTLR), VIP receptor 2 (VIPR2) and SST receptor 2 (SSTR2) were measured also. In addition, an isolated guinea pig ileum was applied to evaluate the influences of Ge on M-R, H1-R, 5-HT4-R and D-R in vitro.

RESULTS

Ge increased gastric emptying and intestinal propelling obviously. It also decreased the level of SST and increased GAS in plasma significantly. Moreover, it promoted the expressions of MTLR in gastric antrum, duodenum, jejunum and ileum, and restrained the expression of VIPR2 in duodenum. Piboserod and loratadine had no obvious restrain to Ge' exciting ileum effect and Ge also didn't affect dopamine paralyzing ileum. However, Ge failed to improve the hypofunction of guinea pigs ileums pre-treated with atropine sulfate.

CONCLUSION

The mechanisms of Ge' prokinetic effect were associated with modulating the levels of SST and GAS in plasma, raising the expressions of MTLR in gastric antrum, duodenum, ileum and jejunum, reducing the expression of VIPR2 in duodenum and activating M-R.

摘要

目的

本研究旨在探讨临床广泛用于增强胃动力的秦艽中龙胆苦苷(Ge)促动力活性的机制。

方法

通过应激刺激诱导胃肠动力障碍大鼠,并给予Ge治疗。取血测定血浆胃动素(MTL)、血管活性肠肽(VIP)、生长抑素(SST)、胃泌素(GAS)、神经降压素(NT)和P物质(SP)水平后,检测胃排空和肠推进功能。同时检测MTL受体(MTLR)、VIP受体2(VIPR2)和SST受体2(SSTR2)的表达。此外,应用离体豚鼠回肠评价Ge在体外对M受体、H1受体、5-HT4受体和D受体的影响。

结果

Ge明显增加胃排空和肠推进。它还显著降低血浆中SST水平并增加GAS水平。此外,它促进胃窦、十二指肠、空肠和回肠中MTLR的表达,并抑制十二指肠中VIPR2的表达。匹维溴铵和氯雷他定对Ge兴奋回肠的作用无明显抑制作用,Ge也不影响多巴胺致回肠麻痹。然而,Ge未能改善预先用硫酸阿托品处理的豚鼠回肠的功能减退。

结论

Ge促动力作用的机制与调节血浆中SST和GAS水平、提高胃窦、十二指肠、回肠和空肠中MTLR的表达、降低十二指肠中VIPR2的表达以及激活M受体有关。

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