OBJECTIVE:To study the safety of percutaneous administration of Hongzhi gutong cataplasm. METHODS:Rab-bits were taken for single dose in complete skin irritation test(n=4),single dose in damaged skin irritation test(n=4)and multi-ple doses in complete skin irritation test(n=4). The left and right sides of the skin respectively paste 3 cm×3 cm blank matrix and Hongzhi gutong cataplasm for 24 h(calculated by crude drug of 0.14 g). After removing tape 1,24,48,72 h,the erythema and edema in hair removal site of rabbits in the former 2 tests were observed;after 24 h of administration,the rabbits in the last group were administrated again after exposing the administration area for 1 h,repeated 3 times,the erythema and edema in hair removal site after removing tape the first,second time and 1,24,48,72 h in the third time were respectively observed. RESULTS:In the 3 experiments,the scores of erythema and edema of all rabbits were 0,and skin irritation was evaluated as no irritation. CONCLU-SIONS:Hongzhi gutong cataplasm has no skin irritation in rabbits.

OBJECTIVE:To study the chemical constituents of 70％ ethanol extract of Breynia fruticosa.METHODS:The 70％ ethanol extract of B.fruticosa were isolated and purified by D101 macroporous resin,silica gel column chromatography,RP-silica gel column chromatography,Sephadex LH-20 gel column chromatography,preparative HPLC.The structure of compound was analyzed and identified according to physicochemical characters and spectral data.RESULTS:10 compounds were separated from 70％ ethanol extract of B.fruticosa,such as Luteolin (1),Quercetin (2),Kaempferol (3),Tiliroside (4),(+)-Lyoniresinol (5),(+)-Isolariciresinol (6),(+)-Nortrachelogenin (7),(+)-Syringaresinol (8),Icariol A2 (9),5,5'-Dimethoxy-7-oxolariciresinol (10),respectively.CONCLUSIONS:Ten compounds are isolated from this plant for the first time.The study play the found for quality evaluation of 70 ％ ethanol extract of B.fruticosa.

Pulmonary fibrosis is the end-stage manifestation of a large class of lung diseases characterized by fibroblast proliferation and accumulation of a large amount of extracellular matrix accompanied by inflammatory injury and tissue structure destruction. Studies have shown that flavonoids have anti-pulmonary fibrosis effects through multiple paths， including dihydromyricetin， morin and fisetin can inhibit fibroblast differentiation； Trollius altaicus flavonoids， hesperidin and linarin can play an anti-inflammatory role； total flavonoids from Scutellaria baicalensis， scutellarin and chrysin can inhibit epithelial- mesenchymal transition； total flavonoids of Litchi chinensis， diosmin and silybin can play an anti-oxidative stress role； quercetin， baicalin and apigenin can regulate autophagy； total flavonoids of Oxytropis falcata， calycosin and dihydroquercetin can regulate apoptosis； naringin， scutellarin and total flavonoids of Dracocephalum moldavica can inhibit pyroptosis， thus exerting anti- pulmonary fibrosis effects.

OBJECTIVE To investigate the anti-pulmonary fibrosis effect of linarin in vivo and in vitro， and investigate its mechanism preliminarily. METHODS C57BL/6J mice were randomly divided into normal group （carboxymethylcellulose sodium）， model group （carboxymethylcellulose sodium）， positive control group （pirfenidone， 200 mg/kg）， linarin low-dose and high-dose groups （12.5， 25 mg/kg）， with 8 mice in each group. Except for normal group， pulmonary fibrosis model was induced in other groups. After modeling， they were given relevant medicine intragastrically， once a day， for consecutive 14 d. The general situation of mice was observed， and their lung indexes were measured； the levels of tumor necrosis factor-α （TNF-α） and transforming growth factor-β1（ TGF-β1） in serum and interleukin-6 （IL-6） in lung tissue were determined. Hematoxylin-eosin （HE） staining and Masson staining were used to observe the histopathological morphology of lung. The pulmonary fibrosis was scored according to Ashcroft score standard. The expressions of α-smooth muscle actin （α-SMA） and （type Ⅰ collagen， Collagen Ⅰ）， phosphorylated extracellular signal-regulated kinase （p-ERK1/2） and TGF-β1 in lung tissues were detected. HFL1 cells were stimulated by TGF- β1 to form pulmonary fibrosis model in vitro， which were divided into normal group， model group and linarin low-， medium- and high-concentration groups （3.7， 7.4， 14.8 mg/L）. After being cultured for 48 h， the protein expressions of α-SMA， Collagen Ⅰ and p-ERK1/2 in HFL1 cells were detected. RESULTS In vivo， compared with normal group， the lung index of model group and the levels of TNF- α， TGF- β1 and IL-6 were significantly increased （P＜0.01）. There were a large number of inflammatory infiltration and cellular fibrosis lesions in the alveoli， and a large number of collagen depositions. The scores of HE staining and Masson staining were significantly increased （P＜0.01）. The protein expressions of α-SMA， Collagen Ⅰ， p-ERK1/2 and TGF-β1 in lung tissue were up-regulated significantly （P＜0.01）. Compared with model group， above indexes of mice were improved significantly in linarin high-dose group （P＜0.05 or P＜0.01）， and most of indexes （except for lung index） were improved significantly in linarin low-dose group （P＜0.05 or P＜0.01）. In vitro， compared with blank group， the density of cells in the model group increased， and obvious proliferation and other changes occurred； protein expressions of α-SMA， Collagen Ⅰ and p-ERK1/2 were significantly up-regulated （P＜0.05 or P＜0.01）. Compared with model group， the cell density of each concentration group was decreased and the morphology gradually returned to normal； the expressions of above proteins in linarin high-concentration group and the protein expression of p-ERK1/2 in linarin medium-concentration group were down-regulated significantly（P＜0.05 or P＜0.01）. CONCLUSIONS Linarin may regulate ERK and inflammatory pathways to reduce the inflammatory response， thereby exerting anti-pulmonary fibrosis effect.