相关实验视频

Updated: Jul 2, 2025

Analysis of Raw and Processed Cyperi Rhizoma Samples Using Liquid Chromatography-Tandem Mass Spectrometry in Rats with Primary Dysmenorrhea

Analysis of Raw and Processed Cyperi Rhizoma Samples Using Liquid Chromatography-Tandem Mass Spectrometry in Rats with Primary Dysmenorrhea

Published on: December 23, 2022

多糖类作为天然的功能成分,用于酸诱导的小鼠胃

Miao Zhang^1,2, Liba Xu², Long Chen^2,3

¹School of Chemistry and Chemical Engineering, Guangxi Minzu University, Nanning 530006, China.

Molecules (Basel, Switzerland)

|February 24, 2024

概括

丹德罗 (Dendrobium officinale polysaccharide,DOP) 通过减少炎症和氧化应激,有效治疗大鼠的胃. 此外,DOP还抑制了细胞亡并促进了组织的修复,在某些方面表现优于奥梅普拉.

科学领域:

药理学药理学是指药理学的学科.
自然产品化学化学
胃肠病学胃肠病学

背景情况:

丁 officinale 多糖 (DOP) 是Dendrobium officinale的一个关键生物活性化合物,以其药用特性而闻名.
胃 (GUs) 是一个重大的健康问题,通常涉及氧化应激和炎症.
了解像DOP这样的天然化合物的治疗潜力对于开发新疗法至关重要.

研究的目的:

在大鼠模型中研究Dendrobium officinale多糖 (DOP) 对改善乙酸诱导的胃的疗效.
阐明DOP对胃粘膜损伤的保护作用的潜在机制.

主要方法:

提取和标识DOP的特征.
在老鼠中诱导胃,使用乙酸.
不同剂量DOP和梅的使用.
评估的愈合,食物摄入,体重,氧化应激标志物 (SOD,GSH,GSH-PX),炎症细胞因子 (IL-1β,IL-6,TNF-α),亡以及关键信号通路 (NF-κB,FoxO3a,Bim) 通过西斑和qRT-PCR.

主要成果:

DOP显著地保护了胃,改善了食物摄入量和体重.
通过增强抗氧化酶活性和降低对促炎性细胞因子的调节,DOP减轻了氧化应激和炎症.
DOP抑制了细胞亡,促进了胃组织的自我修复,并调节了NF-κB通路,在某些参数上显示了与奥梅普拉相似或更好的效果.

结论:

丹德罗 officinale 聚糖 (DOP) 在老鼠中表现出显著的胃保护作用,防止乙酸诱导的胃.
治疗机制包括抑制氧化应激,通过NF-κB途径抑制炎症反应,以及促进组织修复的同时促进细胞亡.
进一步的研究是有必要的,以充分了解DOP与增长因素的相互作用,如EGF和VEGF在GU治疗.

关键词:

丹德罗 (Dendrobium officinale) 的多糖是什么胃潰瘍胃潰瘍胃潰瘍氧化应激是一种氧化应激.结构特征结构的描述.

更多相关视频

Author Spotlight: Exploring the Mysteries of Sichuan's Herbal Medicine in Chinese Medicine Research

Author Spotlight: Exploring the Mysteries of Sichuan's Herbal Medicine in Chinese Medicine Research

Published on: March 1, 2024

Investigating the Alleviating Effects of Bacillus cereus Administration on Colitis through Gut Microbiota Modulation

Investigating the Alleviating Effects of Bacillus cereus Administration on Colitis through Gut Microbiota Modulation

Published on: July 27, 2022

相关概念视频

Drugs for Peptic Ulcer Disease: Sucralfate as Mucosal Protective Agents

Drugs for Peptic Ulcer Disease: Sucralfate as Mucosal Protective Agents

In the intricate landscape of the gastric lumen, excessive acid secretion disrupts the natural defense mechanisms, weakening the mucus-bicarbonate barrier. This vulnerability allows pepsin to infiltrate epithelial cells, digesting mucosal proteins and triggering erosion, leading to ulcer formation.
In this scenario, mucosal protective agents like sucralfate play an essential role. Sucralfate, a complex of sulfated sucrose and aluminum hydroxide, demonstrates its usefulness in acidic conditions,...

Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents

Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents

The gastric mucosa produces prostaglandins E2 (PGE2) and prostacyclin (PGI2), crucial in maintaining gastric health. They exert cytoprotective effects, including increasing bicarbonate secretion, releasing protective mucin, reducing gastric acid output, and preventing harmful vasoconstriction. These effects are mediated through various receptors, such as EP1, EP2, EP3, and EP4.
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...

Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists

Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists

Histamine H2 receptors, which are intricately located on the basolateral membrane of parietal cells, play a crucial role in modulating gastric acid secretion. When released from enterochromaffin-like cells, histamine engages H2 receptors, initiating the cyclic AMP (cAMP) pathway. In this pathway, adenylyl cyclase converts ATP into cAMP, elevating intracellular cAMP levels. The activation of protein kinase A follows, stimulating the proton pump. This stimulation prompts the secretion of hydrogen...