Maltodextrin/ascorbic acid stimulates wound closure by increasing collagen turnover and TGF-β1 expression in vitro and changing the stage of inflammation from chronic to acute in vivo.
It has been reported that carbohydrates confer physicochemical properties to the wound environment that improves tissue repair. We evaluated in vitro and in vivo wound healing during maltodextrin/ascorbic acid treatment. In a fibroblast monolayer scratch assay, we demonstrated that maltodextrin/ascorbic acid stimulated monolayer repair by increasing collagen turnover coordinately with TGF-β1 expression (rising TGF-β1 and MMP-1 expression, as well as gelatinase activity, while TIMP-1 was diminished), similar to in vivo trends. On the other hand, we observed that venous leg ulcers treated with maltodextrin/ascorbic acid diminished microorganism population and improved wound repair during a 12 week period. When maltodextrin/ascorbic acid treatment was compared with zinc oxide, almost four fold wound closure was evidenced. Tissue architecture and granulation were improved after the carbohydrate treatment also, since patients that received maltodextrin/ascorbic acid showed lower type I collagen fiber levels and increased extracellular alkaline phosphatase activity and blood vessels than those treated with zinc oxide. We hypothesize that maltodextrin/ascorbic acid treatment stimulated tissue repair of chronic wounds by changing the stage of inflammation and modifying collagen turnover directly through fibroblast response.
Laboratory of Connective Tissue, Centro Nacional de Investigación y Atención de Quemados, Instituto Nacional de Rehabilitación, Mexico City, Mexico.
Rosa M
RM
Salgado
Wound Care Clinic, Hospital Regional "General Ignacio Zaragoza", Mexico City, Mexico.
Otilia
O
Cruz-Castañeda
Wound Care Clinic, Hospital Regional "General Ignacio Zaragoza", Mexico City, Mexico.
Francisco
F
Elizondo-Vázquez
Wound Care Clinic, Hospital Regional "General Ignacio Zaragoza", Mexico City, Mexico.
Lucia
L
Pat
UCSF Benioff Children's Hospital, Oakland, USA.
Anabel
A
De la Garza
Unidad de Biología Molecular y Medicina Genómica, Instituto de Investigaciones Biomédicas, UNAM/Instituto de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico.
Saúl
S
Cano-Colín
Department of Pathology, Hospital Ángeles Acoxpa, Mexico City, Mexico.
Leticia
L
Baena-Ocampo
Laboratory of Connective Tissue, Centro Nacional de Investigación y Atención de Quemados, Instituto Nacional de Rehabilitación, Mexico City, Mexico. Electronic address: kroted@yahoo.com.mx.
Edgar
E
Krötzsch
D000279:Administration, Cutaneous; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000975:Antioxidants / Q000008:administration & dosage*; D001205:Ascorbic Acid / Q000008:administration & dosage*; D016022:Case-Control Studies; D024061:Collagen Type III / Q000187:drug effects; D004338:Drug Combinations; D005260:Female; D006801:Humans; D008137:Longitudinal Studies; D035002:Lower Extremity; D008297:Male; D008875:Middle Aged; D010865:Pilot Projects; D011134:Polysaccharides / Q000008:administration & dosage*; D011446:Prospective Studies; D011897:Random Allocation; D019715:Tissue Inhibitor of Metalloproteinase-1 / Q000187:drug effects; D053773:Transforming Growth Factor beta1 / Q000187:drug effects; D014647:Varicose Ulcer / Q000188:drug therapy* / Q000382:microbiology / Q000473:pathology; D014945:Wound Healing / Q000187:drug effects*; D015034:Zinc Oxide / Q000008:administration & dosage
D000975:Antioxidants; D024061:Collagen Type III; D004338:Drug Combinations; D011134:Polysaccharides; C560822:TIMP1 protein, human; D019715:Tissue Inhibitor of Metalloproteinase-1; D053773:Transforming Growth Factor beta1; C008315:maltodextrin; D001205:Ascorbic Acid; D015034:Zinc Oxide
Cytokines; Extracellular matrix; Neutrophils; Tissue repair