Chronic hyperglycemia favours the formation of advanced glycation end products (AGEs) which are responsible
of many diabetic vascular complications. Keeping in view the medicinal properties of the1,2,3-triazole-
conjugated analogs, the present study was designed to evaluate the possible effect of carbazole-linked 1,2,3-tri-
azoles 2–16 against glucose- and methylglyoxal-AGEs-induced inflammation in human THP-1 monocytes. In vitro
antiglycation, and metabolic assays were used to determine antiglycation, and cytotoxicity activities. DCFH-DA,
immunostaining, immunoblotting, and ELISA techniques were employed to study the ROS and levels of proin-
flammatory mediators in THP-1 monocytes. Among all the synthesized carbazole-linked 1,2,3 triazoles, com-
pounds 2, 7, 8, and 11–16 showed antiglycation activity in glucose- and MGO-modified bovine serum albumin
models, whereas parent compound 1 only exhibited activity in glucose-BSA model. The metabolic assay
demonstrated the non-toxic profile of compounds 1–2, 11–13, and 15 up to 100 μM concentration in both HepG2
and THP-1 cell lines. We found that compounds 11–13, and 15 attenuated AGEs-induced ROS formation (P <
0.001), and halted NF-ĸB translocation (P < 0.001), likewise standard drugs, PDTC, rutin, and quercetin, in THP-
1 monocytes. Among the derivatives, compounds 12, and 13 also suppressed the AGEs-induced elevation of COX-
2 (P < 0.001) and PGE2 (P < 0.001). Our data show that the carbazole-linked triazoles 12, and 13 hampering the
formation of glycation products, prevent the activation of AGEs-ROS-NF-κB signaling pathway, and limit the
proinflammatory COX-2 protein, and PGE2 induction in human THP-1 monocytes. Both these compounds can
thus serve as leads for further studies towards the treatment and prevention of diabetic vascular complications