相关实验视频
Updated: May 22, 2025
07:32
Murine Fecal Isolation and Microbiota Transplantation
Published on: May 26, 2023
3.8K
高盐驱动的肠道微生物群功能障碍通过促进AHR/SGK1/FOXO1轴介导的Th17细胞分化来加剧前列腺炎
Jing Chen1, Rui Feng2, Bin-Bin Gong1
1Department of Urology, the First Affiliated Hospital of Anhui Medical University, Institute of Urology, and Anhui Province Key Laboratory of Urological and Andrological Diseases Research and Medical Transformation, Anhui Medical University, Hefei, 230022, China.
Military Medical Research
|May 18, 2025
概括
高盐摄入量会通过通过5-HIAA/AHR/SGK1/FOXO1通路促进炎症T助手17 (Th17) 细胞分化,从而恶化慢性前列腺炎/慢性骨盆疼痛综合征 (CP/CPPS),这表明它是一种潜在的治疗标.
科学领域:
- 免疫学 免疫学 免疫学
- 胃肠病学 胃肠病学
- 泌尿器科 泌尿器科 泌尿器科 泌尿器科
背景情况:
- 慢性前列腺炎/慢性盆腔疼痛综合征 (CP/CPPS) 涉及空腹症状和盆腔疼痛,由由炎症性T辅助细胞17 (Th17) 驱动.
- 高盐饮食 (HSD) 可以通过Th17细胞轴诱导自身免疫反应,但其在CP/CPPS中的作用尚不清楚.
研究的目的:
- 调查HSD和CP/CPPS患者症状之间的相关性.
- 在小鼠模型中探索HSD对CP/CPPS发育和机制的影响.
- 为了确定HSD加重的CP/CPPS的潜在治疗点.
主要方法:
- 对CP/CPPS患者的临床评估和HSD相关性的分析.
- 建立一个实验性自身免疫性前列腺炎 (EAP) 鼠标模型,食正常盐饮食 (NSD) 或HSD.
- 肠道微生物群和代谢分析,便微生物群移植,5-氨酸 (5-HIAA) 补充,氨酸受体 (AHR) 抑制,以及体外Th17差异化试验.
主要成果:
- 通过促进Th17细胞分化,HSD与CP/CPPS症状以及EAP小鼠的前列腺炎症和疼痛恶化正相关.
- HSD降低了有益的肠道细菌和5-HIAA水平,加剧了EAP.
- 5-HIAA补充剂通过抑制Th17分化改善了HSD诱导的EAP症状,而AHR抑制逆转了这一效应,突出了5-HIAA/AHR/SGK1/FOXO1轴.
结论:
- 高盐摄入量是CP/CPPS的危险因素,促进Th17细胞分化.
- 5-HIAA/AHR/SGK1/FOXO1通路与HSD加重的CP/CPPS有关.
- 这一途径代表了管理CP/CPPS的潜在治疗目标.
相关概念视频
01:17Irritable Bowel Syndrome I: Introduction
213
Irritable Bowel Syndrome (IBS) is characterized by functional disturbances in the gastrointestinal system, presenting a cluster of symptoms without evident structural or biochemical abnormalities. It primarily affects the large intestine and may cause abdominal pain, bloating, excessive gas, diarrhea, constipation, or both.
IBS is a chronic condition that can persist over a long period or recur frequently.
The pathogenesis of IBS involves a complex interplay of the following factors:
Altered...
IBS is a chronic condition that can persist over a long period or recur frequently.
The pathogenesis of IBS involves a complex interplay of the following factors:
Altered...
213
01:09GPCRs Regulate Adenylyl Cylase Activity
5.1K
Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of...
5.1K
01:24Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors
329
Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI) tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining.
329
01:17Gastritis-II: Pathophysiology
202
Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
202