Irisin Ameliorates Oxidative Stress-Induced Injury in Pancreatic Beta-Cells by Inhibiting Txnip and Inducing Stat3-Trx2 Pathway Activation

Figure 3

Trx2 was activated by Irisin through Stat3 nuclear translocation and Txnip inhibition of PA at 0.2 mM, Irisin at 100 nM, and Irisin NA at 100 nM; BSA was used as the control. (a) Gene expression of Trx1, Trx2, Txnip, MafA, Pdx-1, and Stat3 was measured by qPCR after Irisin treatment of INS-1 cells. β-Actin was used as an internal standard ( independent experiments). (b) Protein expression of Trx2, Txnip, p-Stat3, and Stat3 was measured by immunoblotting after Irisin treatment in INS-1 cells and is presented in a histogram ( independent experiments). β-Actin was the internal standard. (c) Stat3 nuclear translocation in INS-1 cells was detected by immunofluorescence analysis and captured by fluorescence microscopy (×100) ( independent experiments). (d) Protein expression of Trx2, Txnip, p-Stat3, and Stat3 was detected after PA and Irisin cotreatment and is shown in the histogram ( independent experiments). (e) Mitochondria were separated and detected with an insulin disulfide reduction assay to determine Trx2 activity ( independent experiments). The data are expressed as the ; vs. the control; ^# vs. the PA treatment group; ^& vs. the PA and Irisin cotreatment group. BSA: bovine serum albumin; PA: palmitic acid; Irisin NA: anti-Irisin-neutralizing antibody.

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