OBJECTIVETo observe the effect of Huzhang on the progress of pulmonary fibrosis in rats, evaluate the role of Huzhang in this process and explore its mechanism.

METHODWistar male rats were randomized into 7 groups (normal control group, model group, positive control group, prophylactic group, 3rd day treatment group, 7th day treatment group and 14th day treatment group). Bleomycin was administered by intratracheal injection to produce pulmonary fibrosis groups except the normal control group. The positive control group began to be given DXM (4 mL x kg(-1) x d(-1)) on the day of the model-making. The normal control group and model group were given NS (4 mL x kg(-1) x d(-1)) on the day of the model-making. The prophylactic group was given reagent (4 mL x kg(-1) x d(-1)) 2 days ahead of the model-making, whereas the 3rd day treatment group, the 7th day treatment group and the 14th day treatment group given the same dose respectively on the third day, the seventh day and the fourth day behind of the model-making. Lung tissue was stained with hematoxylin-eosin (HE) and Masson's trichrome to determine the pathological grading. The lung fibroblast (LF) was cultured in vitro by way of pancreatic enzyme digestion, which was used to detect the contents of the expression of MMP-2 and TIMP-1mRNA with RT-PCR method.

RESULTCompared with those in the model group, the alveolitis, pulmonary fibrosis and collagen accumulation were significantly alleviated in the positive control group, Huzhang prophylactic group and each treatment groups. In the positive control group, Huzhang prophylactic group, the 3rd day treatment group, the 7th day treatment group and the 14th day treatment group, the expression of MMP-2 mRNA was weaker significantly than that in the BLM model group (P < 0.05 or P < 0.01) except that on the 42nd day. The expression of TIMP-1mRNA was also weaker significantly than that in the BLM model group at all set times in all treatment groups (P < 0.05 or P < 0.01). The inhibition of TIMP-1 lasted until the 42nd day.

CONCLUSIONHuzhang inhibited the expression of MMP-2mRNA and TIMP-1mRNA of lung fibroblast in different periods to reduce the alveolitis and pulmonary fibrosis, which was probably one of the anti-fulmonary fiborsis mechanisms of Huzhang.

Animals ; Disease Models, Animal ; Drugs, Chinese Herbal ; therapeutic use ; Fibroblasts ; drug effects ; metabolism ; Humans ; Male ; Matrix Metalloproteinase 2 ; genetics ; metabolism ; Pulmonary Fibrosis ; drug therapy ; genetics ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Tissue Inhibitor of Metalloproteinase-1 ; genetics ; metabolism