Solanum melongena L. Extract Promotes Intestinal Tight Junction Re-Assembly via SIRT-1-Dependent Mechanisms

IF 4.5 2区 农林科学 Q1 FOOD SCIENCE & TECHNOLOGY
Pichayapa Sukmak, Purisha Kulworasreth, Supisara Treveeravoot, Apiwan Arinno, Supitcha Anuwongworavet, Wanapas Wachiradejkul, Purit Kulworasreth, Natnicha Teansuk, Laongdao Thongnak, Doungporn Amonlerdpison, Jakkapong Inchai, Chaiwet Jakrachai, Nattaphong Akrimajirachoote, Chanat Aonbangkhen, Chatchai Muanprasat, Wanangkan Poolsri, Chutima S. Vaddhanaphuti, Pawin Pongkorpsakol
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Abstract

Tight junction disruption can lead to pathogenesis of various diseases without therapeutic strategy to recover intestinal barrier integrity. The main objective of this study is to demonstrate the effect of Solanum melongena L. extract (SMLE) on intestinal tight junction recovery and its underlying mechanism. Intestinal barrier function is attenuated by Ca2+ depletion. SMLE treatment increased TER value across T84 cell monolayers. Permeability assay reveals that Ca2+ depletion promotes 4-kDa FITC-dextran permeability, but not 70-kDa FITC-dextran. SMLE suppresses the rate of 4-kDa FITC-dextran permeability, indicating that SMLE inhibits paracellular leak pathway permeability. SMLE-mediated TER increase and leak pathway suppression are abolished by neither calcium/calmodulin-dependent protein kinase kinase β (CaMKKβ) inhibitor nor AMP-activated protein kinase (AMPK) inhibitor. Furthermore, mammalian target of rapamycin (mTOR) and extracellular signal-regulated kinase (ERK) inhibitors have no effects on SMLE-mediated TER increase and leak pathway suppression. Interestingly, SMLE is unable to enhance TER value and diminish leak pathway permeability in T84 cell monolayers pre-treated with sirtuin-1 (SIRT-1) inhibitor. Immunofluorescence staining reveals that SMLE enhances re-assembly of tight junction proteins, including occludin and ZO-1 to intercellular space but this effect is abolished by SIRT-1 inhibitor. These data suggest that SMLE promotes intestinal tight junction re-assembly via SIRT-1-dependent manner.

Abstract Image

茄属植物提取物通过 SIRT-1 依赖性机制促进肠道紧密连接的重新组装
如果没有恢复肠道屏障完整性的治疗策略,紧密连接破坏会导致各种疾病的发病。本研究的主要目的是证明茄红素提取物(SMLE)对肠道紧密连接恢复的影响及其内在机制。肠屏障功能会因 Ca2+ 耗竭而减弱。SMLE 处理可增加 T84 细胞单层的 TER 值。渗透性测定显示,Ca2+耗竭会促进4-kDa FITC-葡聚糖的渗透性,但不会促进70-kDa FITC-葡聚糖的渗透性。SMLE 可抑制 4-kDa FITC-葡聚糖的通透率,这表明 SMLE 可抑制细胞旁漏途径的通透性。无论是钙/钙调蛋白依赖性蛋白激酶激酶β(CaMKKβ)抑制剂还是AMP激活蛋白激酶(AMPK)抑制剂都不能抑制SMLE介导的TER增加和渗漏途径抑制。此外,哺乳动物雷帕霉素靶标(mTOR)和细胞外信号调节激酶(ERK)抑制剂对 SMLE 介导的 TER 增加和泄漏途径抑制没有影响。有趣的是,SMLE 无法提高 TER 值,也无法降低预先用 sirtuin-1 (SIRT-1)抑制剂处理的 T84 细胞单层的泄漏通路通透性。免疫荧光染色显示,SMLE 能增强紧密连接蛋白(包括 occludin 和 ZO-1 )向细胞间隙的重新组装,但 SIRT-1 抑制剂会取消这种作用。这些数据表明,SMLE 通过 SIRT-1 依赖性方式促进肠道紧密连接的重新组装。
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来源期刊
Molecular Nutrition & Food Research
Molecular Nutrition & Food Research 工程技术-食品科技
CiteScore
8.70
自引率
1.90%
发文量
250
审稿时长
1.7 months
期刊介绍: Molecular Nutrition & Food Research is a primary research journal devoted to health, safety and all aspects of molecular nutrition such as nutritional biochemistry, nutrigenomics and metabolomics aiming to link the information arising from related disciplines: Bioactivity: Nutritional and medical effects of food constituents including bioavailability and kinetics. Immunology: Understanding the interactions of food and the immune system. Microbiology: Food spoilage, food pathogens, chemical and physical approaches of fermented foods and novel microbial processes. Chemistry: Isolation and analysis of bioactive food ingredients while considering environmental aspects.
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