RESUMO
OBJECTIVE To optimize the extraction process of polysaccharides from Dendrobium officinale， and preliminarily study its effect on acute lung injury （ALI） in mice. METHODS Using D. officinale as raw material， the polysaccharides were extracted from D. officinale by ultrasonic-assisted hot water immersion. Using the extraction rate of D. officinale polysaccharides as response value， the single-factor experiments and Box-Behnken response surface method were used to optimize the ratio of material to liquid， extraction time and extraction temperature. ALI mice were induced by lipopolysaccharide. Using prednisone acetate （5 mg/kg） as the positive control， the effects on the mass ratio of wet and dry lung and pathological changes of lung tissue （HE staining and Masson staining） of low-dose， medium-dose and high-dose D. officinale polysaccharides （50，100，200 mg/kg） were investigated. RESULTS The optimal extraction technology of D. officinale polysaccharides was as follows： the ratio of material to liquid was 1∶25 （g/mL）， the extracting time was 1 h， and the extracting temperature was 58 ℃ . Under these conditions， the average extraction rate of D. officinale polysaccharides was 37.75% （RSD＝1.12%，n＝3）， the relative error of which with predicted value （38.63%） was 2.28%. Compared with the model group， the ratios of wet and dry lung in the positive control group and D. officinale polysaccharides groups were all decreased significantly （P＜0.05 or P＜0.01）， and the pathological changes in lung tissue （severe destruction of alveolar structure， significant widening of alveolar septa， extensive infiltration of inflammatory cells and proliferation of fibroblasts） were alleviated to varying degrees. CONCLUSIONS The optimal extraction process of D. officinale polysaccharides is feasible； the obtained polysaccharide extract has a certain improvement effect on ALI in mice.
RESUMO
Polysaccharides from Dendrobium officinale (PDO) have been found to elicit significant benefits for patients with fibrotic diseases. However, there are no reports on treatment of idiopathic pulmonary fibrosis (IPF) using PDO. The aim of this paper was to investigate the therapeutic effects of PDO on IPF and its underlying mechanisms. Our data showed that PDO significantly ameliorated indices for both pulmonary inflammation and fibrosis in a bleomycin (BLM)-induced pulmonary fibrosis model in rats, which was associated with inactivation of transforming growth factor ß1 (TGFß1)-Smad2/3 signaling pathway. Moreover, PDO effectively blocked TGFß1-induced transformation of rat alveolar epithelial type II cells into myofibroblasts, with the inhibition of total Smad2/3, pSmad2/3, collagen I and fibronectin protein expression in a dose-dependent manner in vitro. Therefore, PDO may represent as a promising candidate biomacromolecule drug for the safe and effective therapy of IPF.
