RETRACTED: Tetramethylpyrazine relieves LPS-induced pancreatic β-cell Min6 injury via regulation of miR-101/MKP-1 (Retracted Article)

被引:7
|
作者
Chen, Dong [1 ]
Cao, Dong [2 ]
Sui, Ping [3 ]
机构
[1] Qingdao Municipal Hosp, Dept Nucl Med, Qingdao, Shandong, Peoples R China
[2] Qingdao Municipal Hosp, Dept Pharm, Qingdao, Shandong, Peoples R China
[3] Jining Med Univ, 133 Hehua Rd, Jining 272067, Peoples R China
关键词
Tetramethylpyrazine; T1MD; pancreatic beta-cell; miR-101; MKP-1; TYPE-1; DIABETES-MELLITUS; OXIDATIVE STRESS; MKP-1; EXPRESSION; LIPOPOLYSACCHARIDE; ADOLESCENTS; MICRORNAS; CHILDREN; PROTEIN; SYSTEM;
D O I
10.1080/21691401.2019.1628039
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Tetramethylpyrazine (TMP) is a traditional Chinese medicine with anti-inflammation and immunomodulatory effects. In this context, our purpose was to investigate the associated regulatory mechanisms of TMP against lipopolysaccharide (LPS)-caused pancreatic beta cell Min6 injury. The injury of Min6 cells was induced by 10 mu g/mL of LPS. Viability of Min6 cells was detected through CCK-8 assay, apoptosis process through flow cytometry, and the proteins involved in apoptosis through western blot. Insulin secretion was valued through the glucose-stimulated insulin secretion (GSIS) assay. microRNA-101 (miR-101) was measured through qRT-PCR. Mitogen-activated protein kinase phosphatase 1 (MKP-1) and signaling regulators was measured through western blot. We found that, TMP treatment effectively attenuated LPS-induced injury in Min6 cells by suppressing cell apoptosis and promoting insulin secretion. Further investigation revealed that TMP exerted protective effect through down-regulating miR-101, and MKP-1 was demonstrated as a target of miR-101. Moreover, TMP attenuated LPS-triggered inflammation by inactivating the JNK1/2 and NF-kappa B through the down-regulation of miR-101. In conclusion, our present study revealed that TMP alleviated LPS-induced injury in pancreatic beta-cell Min6 injury via regulation of miR-101/MKP-1 with the bluntness of JNK1/2 and NF-kappa B pathways.
引用
收藏
页码:2545 / 2552
页数:8
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