Influence Of Compound Panax NotoginsenosideGranules(CPNG) On Bleomycin-induced Pulmonary Fibrosis In Rats

Objective：To explore the effects of compound panax notoginsenoside granules（CPNG） onbleomycin-induced pulmonary fibrosis in rats and its mechanisms.Methods：Sixty male Sprague-Dawley rats were randomly divided into6groups, includingcontrol normal group，model group, prednisolone group(3.33mg·kg^-1·d^-1)and CPNGhigh-dose, middle-dose and low-dose group(100、50、25mg·kg^-1·d^-1)，10Sprague-Dawleyrats in each group. Except the control normal group, pulmonary fibrosis models werereproduced by intratracheal injection of bleomycin（5mg/kg）. On the second day ofinjection of bleomycin, the rats in each treatment group were intragastric administratedprednisolone and corresponding dose of CPNG daily; control normal group and modelgroup were intragastric administrated the equal volume distilled water daily. After28days,all rats were executed to be observed the pulmonary index. Hydroxyproline （HYP） in lungtissue was assessed. Fixed parts of the lung tissue was obtained for HE and Masson stainfor histopathological examination. Malondialdehyde （MDA）, glutathion （GSH）, superoxidedismutase（SOD） and total antioxidant capacity （T-AOC） in blood and lung tissue wererespectively assessed by means of Thibabituric Acid（TBA）, chemical colorimetry,xanthine oxidase and chemical colorimetry. The expressions of transforming growth factorβ1（TGF-β1）, Smad2, Smad3, α-smooth muscle actin （α-SMA） and collagen I （Col-I）protein were analyzed by immunohistochemistry. The expressions of TGF-β1, Smad2,Smad7protein were analyzed by western-blotting. Results:Compared with model group, the pulmonary index and lung tissue HYP weredecreased （P<0.05，P<0.01）, MDA level in blood and lung tissue was also decreased（P<0.001）, but GSH, SOD, T-AOC level in blood and lung tissue were significantlyincreased （P<0.05，P<0.01，P<0.001）in all of CPNG groups. The histopathology of lungtissue with HE and Masson staining demonstrated that CPNG dramatically decreased thelung inflammation and lung fibrosis in rats（P<0.01，P<0.01）. Munohistochemistry andwestern-blotting demonstrated that CPNG could inhibite the expressions of TGF-β1,Smad2, Smad3, α-SMA and Col-I protein（P<0.05，P<0.01，P<0.01）, and increase theexpression of Smad7protein in lung tissue of rats（P<0.01）.Conclusion:CPNG has a therapeutic effect on bleomycin-induced pulmonary fibrosis in rats,which maybe relate to antioxidative damage, intervention TGF-β1/Smads signalingpathway, and restraining the formation and deposition of collagen.