ABSTRACT
Objective: To investigate the wound-healing effect of Alocasia longiloba (A. longiloba) petiole extract on wounds in rats.Methods: Twenty-two male Sprague-dawley rats were randomly assigned to receive 10％ solcoseryl gel, phosphate buffer saline, 50％ ethanol, 95％ ethanol and hexane extracts of A. longiloba at 1.5％, 3％ and 6％ doses, respectively. A full thicknesses wound (6 mm) was created on the dorsal of the rat; and all rats were applied with the extract solutions, 10％ solcoseryl gel and phosphate buffer saline once a day topically until day 12. The wound was photographed on day 1, 6 and 12, and the percentage of wound contraction was calculated. On day 12, rats were sacrificed and histological examination of granulation tissue was carried out using haematoxylin & eosin and Masson's Trichrome stain to determine the wound healing effect.Results: In this study, 6％ of 50％ and 95％ ethanol extracts of A. longiloba showed 82.50％ and 82.32％ wound contraction, respectively, and were comparable with 10％ solcoseryl gel (82.30％). Meanwhile, phosphate buffer saline treated group showed the lowest wound contraction (69.86％). Histological assessment of wound treated with 6％ of 95％ ethanol extract of A. longiloba showed distinct epidermal and dermal layer, higher proliferation of fibroblast and more angiogenesis with collagen compared to other wound treated groups. Conclusions: A. longiloba petiole extracts have a wound healing potential and 6％ of 95％ ethanol extract of A. longiloba is more effective. Further studies are required to understand the wound healing mechanism of action of the extract.
ABSTRACT
Introduction: Critical time windows exert profound influences on foetal physiological and metabolic profiles, which predispose an individual to later diseases via a 'programming' effect. Obesity has been suggested to be 'programmed' during early life. Foetuses and infants who experience adverse growth are subjected to a higher risk of obesity. However, the key factors that link adverse foetal growth and obesity risk remain obscure. To date, there is considerable evidence showing that the overall balance between free radical damage and the antioxidative process being challenged occurs throughout gestation. With the view that pregnancy is a pro-inflammatory state confronted with enhanced oxidative stress, which possesses similar characteristics to obesity (a chronic inflammatory state with increased oxidative stress), oxidative stress is thus biologically plausibly be proposed as the underlying mechanism between this causal-disease relationship. Oxidative stress could act as a programming cue for the development of obesity by inducing complex functional and metabolic deregulations as well as inducing the alteration of the adipogenesis process. Thereby, oxidative stress promotes adipose tissue deposition from early life onwards. The enhancement of fat accumulation further exaggerates oxidative derangement and perpetuates the cycle of adiposity. This review focuses on the oxidative stress pathways in prenatal and early postnatal stages, from the aspects of various endogenous and exogenous oxidative insults. Because oxidative stress is a modifiable pathway, this modifiability suggests a potential therapeutic target to fight the obesity epidemic by understanding the causal factors of oxidant induction.