Research Paper Volume 13, Issue 1 pp 525—536

Liraglutide improved the cognitive function of diabetic mice via the receptor of advanced glycation end products down-regulation

class="figure-viewer-img"

Figure 4. Liraglutide restored cells viability decline and up-regulated RAGE by AGEs in HT22 cells. Results in (AC) did showed lower cells viability HT22 cells with AGEs at different concentrations than those without AGEs. "*"of (D) cells viability is lower of HT22 cells with AGEs at a concentration of 400ug/ml, 600ug/ml or 800ug/ml than those without AGEs; "*" of (E) significant difference of RAGE levels between HT22 cells with AGEs at a concentration of 400ug/ml; "*" of (F) cells viability is higher of HT22 cells with AGEs at a concentration of 400ug/ml and liraglutide at a concentration of 200nM/ml than those with AGEs at a concentration of 400ug/ml but without liraglutide. "*" of (G, I) significant difference of RAGE levels between HT22 cells (with AGEs at a concentration of 400ug/ml) with liraglutide at a concentration of 200nM/ml and those without liraglutide. Results in (H) did not showed the direct interaction between GLP-1R and RAGE in HT22 cells.