In vitro antiglycation, antioxidant and anti-inflammatory activities of Launaea taraxacifolia: inhibition of pentosidine- and vesperlysine-like advanced glycation end-products

Advanced Glycation End-Products (AGEs) induce metabolic memory, which in turn promotes oxidative stress and chronic inflammation, resulting in diabetic complications. AGEs formation, accumulation, oxidation, and inflammation have become common drug targets. Despite extensive research, orthodox agents have had safety concerns, limited efficacy, and are costly, underscoring the need for safer, more effective, multitargeted botanicals that modulate glycation, oxidation, and inflammation. West African ethnomedicine uses Launaea taraxacifolia ( L. taraxacifolia ) for its nutritional and medicinal advantages, including diabetes management. However, its antiglycation potential is unknown. Thus, this in vitro study investigated African lettuce’s antiglycation effects and its potential in modulating the associated glycoxidative and inflammatory processes. Qualitative and quantitative phytochemical analyses of a 70% ethanolic leaf extract of L. taraxacifolia (LTE) were conducted using standard methods. The antioxidant and anti-inflammatory activities were determined using DPPH free radical and protein denaturation assays, respectively. The antiglycation effect was evaluated by measuring inhibition of vesperlysine- and pentosidine-like AGE fluorescence induced by various reducing sugars in a Bovine-Serum Albumin (BSA) model. Qualitative analysis revealed the presence of phenolics, saponins, and flavonoids, among others. Quantitatively, the total phenolic content was 7.27 mg (GAE/100 mg), while the total flavonoid content was 11.03 mg (QE/100 mg). The extract scavenged DPPH radicals (IC 50 = 1.69 µg/mL) and reduced inflammation (protein denaturation IC 50 = 145.5 µg/mL). In general, LTE inhibited vesperlysine-like AGEs with IC 50 values of 0.538 and 0.580 mg/mL against glucose- and galactose-induced glycation, respectively, and demonstrated its strongest inhibition against fructose-induced pentosidine-like AGEs (IC 50 = 0.323 mg/mL). LTE demonstrated substantial antiglycoxidative and anti-inflammatory effects, supporting its potential as a natural regulator of metabolic memory and diabetes complications.