Baicalin relieves inflammation stimulated by lipopolysaccharide via upregulating TUG1 in liver cells
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ORIGINAL ARTICLE
Baicalin relieves inflammation stimulated by lipopolysaccharide via upregulating TUG1 in liver cells Yanqiu Huang 1 & Mengyan Sun 2 & Xuefang Yang 2 & Aiyu Ma 1 & Yujie Ma 1 & Aiying Zhao 1 Received: 27 May 2019 / Accepted: 26 July 2019 # University of Navarra 2019
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. Keywords Hepatitis . Baicalin . Lipopolysaccharide . LncRNATUG1 . p38MAPK pathway . JNK pathway
Introduction Hepatitis is collectively referred as inflammation of liver, which is caused by viruses, bacteria or parasite infection, 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. * Aiying Zhao [email protected] 1
Department of Infectious Diseases, Heze Municipal Hospital, No2888 Caozhou Road, Heze 274000, Shandong, China
2
Department of Clinical Laboratory, Heze Municipal Hospital, Heze 274000, China
chemical poisons, drug or alcohol ingestion, and influence of autoimmune factors [1, 26, 29]. The main clinical features of hepatitis are loss of appetite, bloating, tired of greasy food, nausea and vomiting, which are accompanied with abnormal expression levels of aspartate aminotransferase (AST), alanine aminotransferas
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