Objective To investigate the mechanism of CD34+ progenitor cell differentiation in rat by observing the change relations between the eosinophils (EOS) and the content of Eotaxin and IL-5 in blood and the CD34+/CCR3+,CD34+/IL-5Rα+ in bone marrow after occupational asthma (OA) model rats are simulated,and to observe the effect of WTKYD Trraitioual Chinese Medicine intervention.Methods A total of 40 healthy male SD model rats (200 ～ 250 g weight) were randomly divided into model contrast Group,prednisone acetate intervention Group,WTKYD+1/2 prednisone acetate intervention Group and WTKYD intervention Group,10 in each group,and set a Group for blank contrast.Give them saline (20 ml/kg),prednisone acetate (8.22 mg/kg),WTKYD (20g/kg) +1/2 prednisone acetate (4.11 mg/kg) and WTKYD (20 g/kg) intervention respectively.By means of cell count,immunohistochemical,ELISA,flow cytometry technique,situ hybridization and so on,to observe EOS anti the expression of Eotaxin in lung tissue,the EOS in peripheral blood,the content of Eotaxin and IL-5 in blood as well as the expression of CD34+/CCR3 + and CD34+/IL-5Ra+ in bone marrow respectively.Results The number of EOS,the content of Eotaxin and IL-5,the expression of CD34+/CCR3+ and CD34+/IL-5Ra+ in Model Contrast Group were higher in Blank Contrast Group,the difference was statistically significant (P＜0.01),while they were lower in mnedical intervention Groups when comparing to Model Contrast Group,the difference was statistically significant (P＜0.01 or P＜0.05),and the above items in WTKYD +1/2 Prednisone Acetate Intervention Group were even lower thau in Prednisone Acetate Intervention Group and WTKYD Intervention Group,the difference was statistically significant (P＜0.05).EOS in lung tissue is highly positive related to the content of Eotaxin and IL-5 in peripheral blood as well as the expression of CD34+/CCR3 and CD34+/IL-5Rα in bone marrow (0.9666,0.9829,0.9142,0.8874).Conclusion The increase of internnd EOS in lung tissue is related to the up-regulated expression of CD34+/CCR3+ and CD34+/IL-5Ra+ in bone marrow after antigens in Occupational Asthma model rats are stimulated.Through down-regulating it's expression to restrain the differentiation of CD34 + progenitor cells towards EOS,meanwhile,the collaboration of WTKYD and prednisone acetate possess a certain synergistic action.

Objective To investigate the mechanism of CD34+ progenitor cell differentiation in rat by observing the change relations between the eosinophils (EOS) and the content of Eotaxin and IL-5 in blood and the CD34+/CCR3+,CD34+/IL-5Rα+ in bone marrow after occupational asthma (OA) model rats are simulated,and to observe the effect of WTKYD Trraitioual Chinese Medicine intervention.Methods A total of 40 healthy male SD model rats (200 ～ 250 g weight) were randomly divided into model contrast Group,prednisone acetate intervention Group,WTKYD+1/2 prednisone acetate intervention Group and WTKYD intervention Group,10 in each group,and set a Group for blank contrast.Give them saline (20 ml/kg),prednisone acetate (8.22 mg/kg),WTKYD (20g/kg) +1/2 prednisone acetate (4.11 mg/kg) and WTKYD (20 g/kg) intervention respectively.By means of cell count,immunohistochemical,ELISA,flow cytometry technique,situ hybridization and so on,to observe EOS anti the expression of Eotaxin in lung tissue,the EOS in peripheral blood,the content of Eotaxin and IL-5 in blood as well as the expression of CD34+/CCR3 + and CD34+/IL-5Ra+ in bone marrow respectively.Results The number of EOS,the content of Eotaxin and IL-5,the expression of CD34+/CCR3+ and CD34+/IL-5Ra+ in Model Contrast Group were higher in Blank Contrast Group,the difference was statistically significant (P＜0.01),while they were lower in mnedical intervention Groups when comparing to Model Contrast Group,the difference was statistically significant (P＜0.01 or P＜0.05),and the above items in WTKYD +1/2 Prednisone Acetate Intervention Group were even lower thau in Prednisone Acetate Intervention Group and WTKYD Intervention Group,the difference was statistically significant (P＜0.05).EOS in lung tissue is highly positive related to the content of Eotaxin and IL-5 in peripheral blood as well as the expression of CD34+/CCR3 and CD34+/IL-5Rα in bone marrow (0.9666,0.9829,0.9142,0.8874).Conclusion The increase of internnd EOS in lung tissue is related to the up-regulated expression of CD34+/CCR3+ and CD34+/IL-5Ra+ in bone marrow after antigens in Occupational Asthma model rats are stimulated.Through down-regulating it's expression to restrain the differentiation of CD34 + progenitor cells towards EOS,meanwhile,the collaboration of WTKYD and prednisone acetate possess a certain synergistic action.

Objective: To observe the expression of alpha smooth muscle actin (α-SMA) and high mo-bility group protein B1 (HMGB1) in silicosis model rats interfered by lumbricus. Methods: 45 rats were ran-domly divided into the control group, model group and group interfered by lumbricus. The silicosis model rats were established. The group interfered by lumbricus were intragastric administered with lumbricus decoction by the 4 ml/kg dose. The control group and model group were ig administered with the equal amount of normal saline. Each group were killed 5 rats on the 7^th, 14^th and 28^th day. The lung tissues were stained with HE and Sirius red methods. The mRNA expressions of α-SMA and HMGB1 were determined with RT-PCR; The pro-tein levels of α-SMA and HMGB1 were determined with Western blotting. Results: Compared with the control group, the expression levels of α-SMA and HMGB1mRNA and protein in lung tissue of model group were grad-ually increased in the 7^th, 14^th and 28^th days, the difference was statistically significant (P< 0.01) . Compared with model group, the levels of α-SMA and HMGB1mRNA and protein in lung tissue of group interfered by lumbricus were gradually lowered in the 7th, 14th and 28th days, the difference was statistically significant (P<0.05, P<0.01) . Conclusion Lumbricus inhibits the collagen deposition and the formation of silicosis pulmo-nary fibrosis, which may be related to the inhibition of HMGB1 expression and activation of α-SMA in lung tis-sue.