RETRACTED: Baicalin relieves inflammation stimulated by lipopolysaccharide via upregulating TUG1 in liver cells (Publication with Expression of Concern. See vol. 77, pg. 491, 2021) (Retracted Article)

被引:11
作者
Huang, Yanqiu [1 ]
Sun, Mengyan [2 ]
Yang, Xuefang [2 ]
Ma, Aiyu [1 ]
Ma, Yujie [1 ]
Zhao, Aiying [1 ]
机构
[1] Heze Municipal Hosp, Dept Infect Dis, 2888 Caozhou Rd, Heze 274000, Shandong, Peoples R China
[2] Heze Municipal Hosp, Dept Clin Lab, Heze 274000, Peoples R China
关键词
Hepatitis; Baicalin; Lipopolysaccharide; LncRNA TUG1; p38MAPK pathway; JNK pathway; NONALCOHOLIC STEATOHEPATITIS; OXIDATIVE STRESS; VIRAL-HEPATITIS; DOWN-REGULATION; APOPTOSIS; DIAGNOSIS; LPS; FLAVONOIDS; MANAGEMENT; PROTECTS;
D O I
暂无
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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-alpha, 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.
引用
收藏
页码:463 / 473
页数:11
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