This study aimed to explore the capacity of immobilized lipases on the acetylation of six aglycon flavonoids, namely myricetin, quercetin, luteolin, naringenin, fisetin and morin. For this purpose, lipase B from Candida antarctica (CaLB) and lipase from Thermomyces lanuginosus (TLL) were immobilized onto the surface of ZnOFe nanoparticles derived from an aqueous olive leaf extract. Various factors affecting the conversion of substrates and the formation of monoesterified and diesterified products, such as the amount of biocatalyst and the molar ratio of the substrates and reaction solvents were investigated. Both CaLB and TLL-ZnOFe achieved 100% conversion yield of naringenin to naringenin acetate after 72 h of reaction time, while TLL-ZnOFe achieved higher conversion yields of quercetin, morin and fisetin (73, 85 and 72% respectively). Notably, CaLB-ZnOFe displayed significantly lower conversion yields for morin compared with TLL-ZnOFe. Molecular docking analysis was used to elucidate this discrepancy, and it was revealed that the position of the hydroxyl groups of the B ring on morin introduced hindrances on the active site of CaLB. Finally, selected flavonoid esters showed significantly higher antimicrobial activity compared with the original compound. This work indicated that these lipase-based nanobiocatalysts can be successfully applied to produce lipophilic derivatives of aglycon flavonoids with improved antimicrobial activity.

Abstract Infliximab (IFX) is widely used in the treatment of inflammatory bowel diseases (IBD) such as ulcerative colitis (UC) and Crohn's disease (CD). Still, long-term use may be ineffective or suggest some side effects. This study investigated the role of Myricetin, a flavonoid, alone and its complementary therapeutic potential in combination with IFX against UC, CH, and cancerization. DSS triggered the development of acute UC syndromes in Wistar albino rats, while TNBS treatment triggered some of the symptoms seen in CD. The effectiveness of IFX, Myricetin, and their combination against UC and CD was determined by the disease activity index and changes in TNF-α secretion. The effect of IFX and Myricetin on tumor aggressiveness was evaluated by in vitro wound healing and colony formation analysis and expression of NF-κB and COX2 genes in a colon cancer cell line. Myricetin strongly reduced NF-κB expression in the DSS-induced UC model (p < 0.0001), but this effect was weaker in the TNBS-induced CD model, while COX2 expression was the opposite. Myricetin was beneficial as a complement to IFX in the CD model, while also promoting the improvement of clinical symptoms of the acute UC model (p < 0.05). Myricetin slowed down wound healing and colony formation of HT-29 cells and attenuated NF-κB expression. Myricetin may promise an alternative treatment approach in acute UC. Additionally, CD cases may benefit from Myricetin only when used in conjunction with IFX.