[The mechanisms and effects of panax notoginside and methylprednisolone in a rat model of pulmonary fibrosis].
OBJECTIVE
To study the effects of panax notoginside (PNS) and methylprednisolone (solu-medrol) on the development of pulmonary fibrosis and the possible underlining mechanisms.


METHODS
Rats were divided into 3 groups: pulmonary fibrosis group, PNS treated group and solu-medrol treated group. On days 1, 3, 7, 14, and 28 after bleomycin treatment, 5 rats in each group were killed and the lungs and plasma were harvested for histopathological studies, immunohistochemical determination of collagen I and III and ELISA detection of MIP-1alpha and MCP-1.


RESULTS
The degrees of fibrosis, the levels of collagen I and III, and the levels of MIP-1alpha and MCP-1 decreased significantly in the PNS and solu-medrol treated groups as compared with the fibrosis group (P < 0.05).


CONCLUSIONS
Both PNS and solu-medrol are effective in modulating the process of pulmonary fibrosis induced by bleomycin in rats.
Li
Xuejun
X
Department of Respiratory Medicine, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.
Cui
Shehuai
S
D000818:Animals; D018932:Chemokine CCL2 / Q000097:blood; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D003094:Collagen / Q000096:biosynthesis; D004195:Disease Models, Animal; D006909:Hydroxyproline / Q000032:analysis; D008168:Lung / Q000473:pathology; D019402:Macrophage Inflammatory Proteins / Q000097:blood; D008297:Male; D008775:Methylprednisolone / Q000627:therapeutic use*; D005894:Panax; D008517:Phytotherapy; D011658:Pulmonary Fibrosis / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar
D018932:Chemokine CCL2; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D019402:Macrophage Inflammatory Proteins; D003094:Collagen; D006909:Hydroxyproline; D008775:Methylprednisolone