Objective: To observe the effect of glucagon-like peptide-1 (GLP-1) on interleukin-1β (IL-1β)-induced damage in INS-1 cells and explore its possible mechanisms.
Methods: INS-1 cells were divided into normal control group, IL-1β group, and GLP-1+IL-1β group with corresponding treatments. The cell viability was determined by MTT assay, the expression of IKKβ mRNA was detected by real-time PCR, and that of the protein p65 was detected by Western blotting.
Results: In comparison with the normal control group, the cells in the IL-1β group showed a significantly decreased viability by 29% (P < 0.01); compared with those in IL-1β group, the cells in GLP-1+IL-1β group exhibited an significant increase in the cell viability by 30% (P < 0.01). In comparison with the normal control group, the cells in IL-1β group showed an significantly increased expression of IKKβ mRNA (1.967 ± 0.091 vs 1 ± 0, P < 0.05); GLP-1 significantly reduced IL-1β-induced increment of IKKβ mRNA expression to 1.287 ± 0.084 (P < 0.05). IL-1β treatment significantly increased NF-κB protein expression as compared to the control level (0.814 ± 0.111 vs 0.396 ± 0.026, P < 0.01), and GLP-1 significantly inhibited such effect (0.622 ± 0.059, P < 0.05).
Conclusions: GLP-1 inhibits IL-1β-induced β-cell damage probably by inhibiting the NF-κB pathway.