ArticleScientific reports2025
Baicalin inhibits infectious bronchitis virus replication via MAVS-dependent interferon-β upregulation and mitochondrial function preservation.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Baicalin Modulates Hepatic Lipid Metabolism and Improves Intestinal Health in White-Feathered Broilers.Biology · 2026Article
- Temporal Modulation of Type I Interferon and NF-κB Signaling by Baicalin Suppresses Infectious Bronchitis Virus Replication and Inflammatory Response.Animals : an open access journal from MDPI · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
The inhibitory effect of baicalin on infectious bronchitis virus (IBV) replication is closely related to expression of the mitochondrial antiviral signaling protein (MAVS) in chicken embryonic kidney (CEK) cells. Baicalin significantly upregulated MAVS expression dose-dependently and maintained mitochondrial function through MAVS. Baicalin increased expression of mitofusin-1 (Mfn1), anti-apoptotic mitochondrial import receptor subunit TOM70 (TOM70), voltage-dependent anion channel 1 (VDAC1), autophagy-related 5 (Atg5), and autophagy-related 12 (Atg12). Overexpression of Mfn1, VDAC1, TOM70, Atg5, and Atg12 enhanced baicalin-mediated interferon-β (IFN-β) expression, while knockdown of Mfn1, TOM70, VDAC1, TRADD, Atg5, or Atg12 significantly decreased IFN-β protein levels. In MAVS-knockdown cells, overexpression of Mfn1, mitofusin-2 (Mfn2), VDAC1, TNFR1-associated death domain protein (TRADD), Fas-associated death domain protein (FADD), Atg5, and Atg12 did not affect baicalin-mediated IFN-β expression. Thus, baicalin promotes mitochondrial fusion, permeability, metabolism, and autophagy. Baicalin upregulates IFN-β via Mfn1, VDAC1, TOM70, Atg5, and Atg12 dependent on MAVS. Moreover, baicalin inhibits key cytokines in the NF-κB pro-inflammatory pathway.
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Registered trials
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