Molecular characterization of thioredoxin-interacting protein (TXNIP) from Megalobrama amblycephala and its potential roles in high glucose-induced inflammatory response

This study aimed to characterize the full-length cDNA of thioredoxin-interacting protein (TXNIP) from Megalobrama amblycephala, and investigate its roles in high glucose (HC)-induced inflammatory response. The cDNA obtained covered 2706-bp with an open reading frame of 1203-bp encoding 400 amino acids, compared to Cyprinus carpio, it showed 89.96% homology. The highest expression of txnip was observed in head kidney followed by spleen and liver. After a 12-week feeding trial, high-carbohydrate diet remarkably increased txnip expression in liver and white muscle. Glucose administration resulted in a remarkably increased liver txnip expression, which peaked at 1 h. Thereafter, the expression decreased remarkably to the basal value at 12 h. However, insulin injection resulted in a significant decrease in txnip expression with minimum values attained at 2 h. Subsequently, it gradually increased to the normal values. Moreover, in the in-vitro study, over-expression of txnip along with remarkably increased il-1 beta and il-6 expression in hepatocytes, and its knockdown led to remarkably reduced il-1 beta expression. Furthermore, metformin treatment remarkably increased the cell viability and trx expression of hepatocytes under high glucose, while the opposite was true for ROS levels, LDH activity, the ALT/AST ratio, Txnip protein content and the transcriptions of txnip, tnf alpha and il-1 beta.

Automated summary

This study characterized the full-length cDNA of thioredoxin-interacting protein (TXNIP) from Megalobrama amblycephala and investigated its roles in high glucose-induced inflammatory response. Txnip expression was found to increase in liver and white muscle under a high-carbohydrate diet, while insulin injection led to a decrease in txnip expression. In vitro studies showed that over-expression of txnip increased il-1 beta and il-6 expression in hepatocytes, while knockdown reduced il-1 beta expression. Metformin treatment increased cell viability and trx expression, and decreased ROS levels and other factors under high glucose conditions.