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Updated: Oct 14, 2025
Human Liver Microphysiological System for Assessing Drug-Induced Liver Toxicity In Vitro
Published on: January 31, 2022
miR-26a-5p protects against drug-induced liver injury via targeting bid
Qian Zhang1, Yan Liu1, Yujie Yuan2
1Department of Geriatrics, the third Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.
Backgrounds:
miR-26a-5p is a short noncoding RNA that is abnormally expressed in drug-induced liver injury (DILI), but its pathophysiologic role in the mechanism of disease in DILI is still vague.
Methods:
The expression of miR-26a-5p, viability of hepatic stellate cells (HSCs) proliferation, and apoptosis were explored via real-time PCR, CCK-8 assay, Tunel fluorescence, and flow cytometry. The expression of Bid was detected via Western blot assays, real-time PCR, and immunofluorescence. The apoptosis-associated proteins were determined through Western blot. The interaction between miR-26a-5p and Bid was measured via Dual luciferase reporter assay.
Results:
miR-26a-5p expression was greatly decreased in HSCs and serum treated with azithromycin, simvastatin and diclofenac sodium, respectively. Hepatocyte viability was largely suppressed while hepatocyte apoptosis was markedly increased in DILI. Correspondingly, the apoptosis-associated proteins including Bid, caspase-8 and cytochrome C in HSCs were significantly upregulated when treated with either of these drugs. Moreover, miR-26a-5p interacted with Bid, and hepatocyte proliferation and apoptosis influenced by miR-26a-5p mimics were obviously reversed when co-treated with overexpressed Bid plasmids.
Conclusions:
miR-26a-5p played a protective role against DILI via targeting Bid.
Insights
MicroRNA-26a-5p (miR-26a-5p) protects against drug-induced liver injury (DILI) by targeting the protein Bid. Decreased miR-26a-5p levels in liver cells correlate with increased apoptosis and injury in DILI.
Area of Science:
- Molecular Biology
- Hepatology
- RNA Biology
Background:
- MicroRNA-26a-5p (miR-26a-5p) is dysregulated in drug-induced liver injury (DILI).
- The precise role of miR-26a-5p in DILI pathogenesis remains unclear.
Purpose of the Study:
- To investigate the pathophysiological role of miR-26a-5p in DILI.
- To elucidate the molecular mechanism underlying miR-26a-5p's function in DILI.
Main Methods:
- Real-time PCR, CCK-8 assay, Tunel fluorescence, and flow cytometry were used to assess miR-26a-5p expression, cell viability, and apoptosis.
- Western blot, real-time PCR, and immunofluorescence detected Bid expression.
- Dual luciferase reporter assays confirmed the interaction between miR-26a-5p and Bid.
Main Results:
- miR-26a-5p expression decreased in hepatic stellate cells (HSCs) and serum exposed to DILI-inducing drugs.
- Hepatocyte viability was reduced, and apoptosis increased in DILI models.
- Bid and other apoptosis-related proteins were upregulated; miR-26a-5p directly targeted Bid, and its protective effects were reversed by Bid overexpression.
Conclusions:
- miR-26a-5p exerts a protective effect against DILI.
- This protective role is mediated through the targeting of Bid.
- Modulating miR-26a-5p may offer a therapeutic strategy for DILI.
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