Article Publish Status: FREE
Abstract Title:

Tetramethylpyrazine relieves LPS-induced pancreaticβ-cell Min6 injury via regulation of miR-101/MKP-1.

Abstract Source:

Artif Cells Nanomed Biotechnol. 2019 Dec ;47(1):2545-2552. PMID: 31213095

Abstract Author(s):

Dong Chen, Dong Cao, Ping Sui

Article Affiliation:

Dong Chen


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 pancreaticβ cell Min6 injury. The injury of Min6 cells was induced by 10 μg/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-κB through the down-regulation of miR-101. In conclusion, our present study revealed that TMP alleviated LPS-induced injury in pancreatic β-cell Min6 injury via regulation of miR-101/MKP-1 with the bluntness of JNK1/2 and NF-κB pathways.

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