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Updated: Jan 1, 2026
In Vitro and In Vivo Approaches to Determine Intestinal Epithelial Cell Permeability
Published on: October 19, 2018
Methamphetamine-induced alterations in intestinal mucosal barrier function occur via the microRNA-181c/ TNF-α/tight
Simin Shen1, Jingjiao Zhao1, Yicong Dai1
1NHC Key Laboratory of Drug Addiction Medicine, The First Affiliated Hospital of Kunming Medical University, Kunming, 650032, Yunnan, China.
Abstract:
An enterogenic infection occurs when intestinal mucosal disruption is followed by the invasion of intestinal bacteria into the blood and distant organs, which can result in severe diseases or even death. Our previous study using Rhesus monkeys as an in vivo model revealed that methamphetamine (MA) induced intestinal mucosal barrier damage, which poses a high risk of enterogenic infection. However, how methamphetamine causes intestinal mucosal barrier damage remains largely unknown. In this study, we employed an in vitro model, and found that MA treatment could inhibit the expression of miR-181c, which directly targets and regulates TNF-α, and ultimately induces apoptosis and damages the intestinal barrier. Moreover, we measured TNF-α serum levels as well as the intestinal mucosal barrier damage indicators (diamine oxidase, d-lactic acid, and exotoxin) and found that their levels were significantly higher in MA-dependents than in healthy controls (P < 0.001). To the best of our knowledge, this is the first report evidencing that miR-181c is involved in MA-induced intestinal barrier injury via TNF-α regulation, which introduces novel potential therapeutic targets for MA-dependent intestinal diseases.
Insights
Methamphetamine disrupts the intestinal barrier by inhibiting miR-181c, leading to increased TNF-α. This mechanism explains methamphetamine-induced intestinal damage and suggests new therapeutic targets for related diseases.
Area of Science:
- Gastroenterology
- Microbiology
- Pharmacology
Background:
- Enterogenic infections arise from intestinal barrier damage and bacterial translocation.
- Methamphetamine (MA) use is linked to intestinal mucosal damage and increased infection risk.
- The precise mechanisms underlying MA-induced intestinal barrier dysfunction are not fully understood.
Purpose of the Study:
- To investigate the molecular mechanisms by which methamphetamine causes intestinal mucosal barrier damage.
- To identify potential therapeutic targets for MA-associated intestinal diseases.
Main Methods:
- Utilized an in vitro model to study the effects of MA on intestinal cells.
- Assessed the expression of miR-181c and its regulation of TNF-α.
- Measured serum levels of TNF-α and intestinal barrier integrity markers (diamine oxidase, d-lactic acid, exotoxin) in MA-dependent individuals and controls.
Main Results:
- MA treatment inhibited miR-181c expression in vitro.
- miR-181c directly targets and regulates TNF-α, leading to apoptosis and barrier damage.
- MA-dependent individuals exhibited significantly elevated serum TNF-α and barrier damage indicators compared to healthy controls.
Conclusions:
- This study is the first to demonstrate miR-181c's role in MA-induced intestinal barrier injury through TNF-α regulation.
- The findings highlight a novel pathway contributing to MA-related gastrointestinal pathology.
- miR-181c and TNF-α represent potential therapeutic targets for methamphetamine-dependent intestinal diseases.
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