Deacetylation affects the physical properties and bioactivity of acemannan, an extracted polysaccharide from Aloe vera.

Acemannan, an acetylated polymannose from Aloe vera, induces tissue repair. We investigated the role of acemannan's acetyl-groups on its physical and biological properties. Deacetylated acemannan (DeAcAM) was prepared and characterized. The physical properties and microscopic structure of DeAcAM were evaluated using water solubility, contact angle, X-ray diffraction, and scanning-electron microscopy. The activity of DeAcAM on cell proliferation and gene expression were assessed. Acemannan and DeAcAM structures were simulated and the acemannan tetramer diad and its completely deacetylated structure were also determined. Increased acemannan deacetylation reduced its water solubility and hydrophilicity. Complete deacetylation altered acemannan's conformation to a partial crystal structure. The bioactivity of acemannan was reduced corresponding to its deacetylation. Acemannan induced cell proliferation, and VEGF and Collagen I expression; however, 100% DeAcAM did not. The simulated structures of the acemannan diad and the completely deacetylated diad were different. We conclude acetyl-groups affect acemannan's structure and physical/biological properties.

Acemannan stimulates gingival fibroblast proliferation; expressions of keratinocyte growth factor-1, vascular endothelial growth factor, and type I collagen; and wound healing.

Aloe vera has long been used as a traditional medicine for inducing wound healing. Gingival fibroblasts (GFs) play an important role in oral wound healing. In this study, we investigated the effects of acemannan, a polysaccharide extracted from Aloe vera gel, on GF proliferation; keratinocyte growth factor-1 (KGF-1), vascular endothelial growth factor (VEGF), and type I collagen production; and oral wound healing in rats. [(3)H]-Thymidine incorporation assay and ELISA were used. Punch biopsy wounds were created at the hard palate of male Sprague Dawley rats. All treatments (normal saline; 0.1% triamcinolone acetonide; plain 1% Carbopol; and Carbopol containing 0.5%, 1%, and 2% acemannan (w/w)) were applied daily. Wounded areas and histological features were observed at day 7 after treatment. From our studies, acemannan at concentrations of 2, 4, 8, and 16 mg/ml significantly induced cell proliferation (P<0.05). Acemannan concentrations between 2 - 16 mg/ml significantly stimulated KGF-1, VEGF, and type I collagen expressions (P<0.05). Wound healing of animals receiving Carbopol containing 0.5% acemannan (w/w) was significantly better than that of the other groups (P<0.05). These findings suggest that acemannan plays a significant role in the oral wound healing process via the induction of fibroblast proliferation and stimulation of KGF-1, VEGF, and type I collagen expressions.