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RETRACTED ARTICLE: Baicalin relieves inflammation stimulated by lipopolysaccharide via upregulating TUG1 in liver cells

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This article was retracted on 23 February 2023

An Editorial Expression of Concern to this article was published on 17 March 2021

30 September 2020 An Editorial Expression of Concern on this article has now been published: https://doi.org/10.1007/s13105-021-00803-2

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Abstract

Hepatitis has become a major social, health, and economic problem worldwide. Herein, we tested the beneficial influence of baicalin, a flavonoid extracted from the roots of Scutellaria baicalensis, on human normal liver L-02 and THLE2 cell apoptosis and inflammatory reaction stimulated by lipopolysaccharide (LPS) and possible molecular mechanisms. L-02 and THLE2 cell viability and apoptosis after LPS and/or baicalin treatment were tested using CCK-8 assay and Annexin V-FITC/PI apoptosis kit, respectively. qRT-PCR was used to measure the MCP-1, IL-6, TNF-α, and lncRNA taurine upregulated gene 1 (TUG1) expressions in L-02 and THLE2 cells. sh-TUG1 was transfected to knockdown TUG1. SB203580 was used as inhibitor of p38MAPK pathway, while SP600125 was used as inhibitor of JNK pathway. We discovered that LPS stimulation caused L-02 and THLE2 cell apoptosis and inflammatory reaction. Baicalin relieved the L-02 and THLE2 cell apoptosis and inflammatory reaction stimulated by LPS. Moreover, LPS lowered the TUG1 expression in L-02 cells, while baicalin promoted the TUG1 expression in L-02 and L-02 and THLE2 cells, as well as inactivated p38MAPK and JNK pathways in LPS-stimulated L-02 cells. Besides, knockdown of TUG1 activated p38MAPK and JNK pathways and promoted inflammatory cytokine expression in L-02 cells. In conclusion, this study further affirmed the beneficial influences of baicalin on LPS-stimulated human normal liver cell apoptosis and inflammatory reaction. Baicalin relived liver cell inflammation stimulated by LPS might be via upregulating TUG1 and then inactivating p38MAPK and JNK pathways.

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Data availability

The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.

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Authors and Affiliations

Authors

Contributions

Yanqiu Huang, Aiying Zhao: conceived and designed the experiments.

Yanqiu Huang, Mengyan Sun, Xuefang Yang, Aiyu Ma, Yujie Ma: data collection.

Yanqiu Huang, Aiying Zhao: manuscript writing.

Corresponding author

Correspondence to Aiying Zhao.

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The authors declare that there is no conflict of interest.

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Highlights

1. Baicalin relieves L-02 cell apoptosis and inflammatory reaction stimulated by LPS.

2. Baicalin promotes TUG1 expression in L-02 cells.

3. Baicalin mitigates LPS-stimulated activation of p38MAPK and JNK pathways.

4. TUG1 knockdown activates p38MAPK and JNK pathways.

5. Baicalin also relieves LPS-caused THLE2 cell apoptosis and inflammatory reaction.

This article has been retracted. Please see the retraction notice for more detail: https://doi.org/10.1007/s13105-023-00951-7

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Huang, Y., Sun, M., Yang, X. et al. RETRACTED ARTICLE: Baicalin relieves inflammation stimulated by lipopolysaccharide via upregulating TUG1 in liver cells. J Physiol Biochem 75, 463–473 (2019). https://doi.org/10.1007/s13105-019-00698-0

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  • DOI: https://doi.org/10.1007/s13105-019-00698-0

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