Background
Acemannan is an acetylated polysaccharide of Aloe vera extract with antimicrobial, antitumor, antiviral, and antioxidant activities. This study aims to optimize the synthesis of acemannan from methacrylate powder using a simple method and characterize it for potential use as a wound-healing agent.
Conclusion
Our study provides a suitable technique for effective acemannan production and presents acemannan as a potential agent for use in accelerating wound healing through its antioxidant properties, as well as cell proliferation- and migration-inducing activities.
Methods
Acemannan was purified from methacrylated acemannan and characterized using high-performance liquid chromatography (HPLC), Fourier-transform infrared spectroscopy (FTIR), and 1H-nuclear magnetic resonance (NMR). 2,2-diphenyl-1-picrylhydrazyl (DPPH) and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assays were performed to investigate the antioxidant activity of acemannan and its effects on cell proliferation and oxidative stress damage, respectively. Further, a migration assay was conducted to determine the wound healing properties of acemannan.
Results
We successfully optimized the synthesis of acemannan from methacrylate powder using a simple method. Our results demonstrated that methacrylated acemannan was identified as a polysaccharide with an acetylation degree similar to that in A. vera, with the FTIR revealing peaks at 1739.94 cm-1 (C = O stretching vibration), 1370 cm-1 (deformation of the H-C-OH bonds), and 1370 cm-1 (C-O-C asymmetric stretching vibration); 1H NMR showed an acetylation degree of 1.202. The DPPH results showed the highest antioxidant activity of acemannan with a 45% radical clearance rate, compared to malvidin, CoQ10, and water. Moreover, 2000 µg/mL acemannan showed the most optimal concentration for inducing cell proliferation, while 5 µg/mL acemannan induced the highest cell migration after 3 h. In addition, MTT assay findings showed that after 24 h, acemannan treatment successfully recovered cell damage due to H2O2 pre-treatment.