ABSTRACT
Objective:To observe the expression of mammalian target of rapamycin (mTOR) that mediates autophagy in pulmonary fibrosis and the effect of autophagy in the formation of pulmonary fibrosis, in order to explore the treatment mechanism of Buyang Huanwu Tang on pulmonary fibrosis. Method:Totally 144 C57BL/6 mice were randomly divided into 6 groups:sham operation group, model group, prednisone group, high-dose Buyang Huanwu Tang group, medium-dose Buyang Huanwu Tang group and low-dose Buyang Huanwu Tang group, with 24 mice in each group. The sham operation group was injected with the same amount of 0.9% saline. The remaining groups were treated with bleomycin tracheal injection to replicate the pulmonary fibrosis model. After modeling, sham operation group and model group were given 0.9% normal saline (0.01 g·kg-1·d-1), group high-dose Buyang Huanwu Tang group was given Buyang Huanwu Tang (28.08 g·kg-1·d-1), medium-dose Buyang Huanwu Tang group was given Buyang Huanwu Tang (14.04 g·kg-1·d-1), low-dose Buyang Huanwu Tang group was given Buyang Huanwu Tang(7.02 g·kg-1·d-1), and P group was given prednisone (0.455 g·kg-1·d-1) by gavage. The samples were taken in batches on the 7th, 14th and 28th days after modeling; degrees of alveolitis and fibrosis in mice were observed by hematoxylin-eosin (HE) staining and Masson staining. The mTOR protein, ribosomal S6 protein and microtubule associate protein 1 hight chain3-Ⅱ(MAP1LC3-Ⅱ) of mouse lung tissue were detected by Western blot; electron microscopy was used to observe the autophagy of lung tissue in mice. Result:Compared with the sham-operated group, the degrees of alveolitis and pulmonary fibrosis were significantly severer in the model group on 7th, 14th and 28th days (PPPPConclusion:The mTOR protein is activated in mice lung tissue, autophagy is inhibited, mTOR protein participates in the pathogenesis of pulmonary fibrosis by inhibiting autophagy; Buyang Huanwu Tang has a certain therapeutic effect on BLM-induced pulmonary fibrosis in mice, and its mechanism may be related to the down-regulation of mTOR protein expression that mediates autophagy.
ABSTRACT
OBJECTIVE:To explore the effects of tamsulosin on proliferation and apoptosis in prostatic cancer PC-3 cells. METHODS:After treated with 0 (blank control group),12.5,25 and 50 μmol/L tamsulosin (tamsulosin low,medium and high-concentration groups)for 48 h,the viability of PC-3 cells was detected by MTT method. Hoechst 33258 staining was used to detect cell apoptosis rate. Western blot was used to determine the expression level of Bax and Bcl-2 protein,and the phosphoryla-tion level of protein kinase B(Akt),mammalian target rapamycin(mTOR),ribosomal S6 protein kinase(p70S6K)and 4E bind-ing protein 1(4E-BP1). RESULTS:Compared with blank control group,PC-3 cells viability and the phosphorylation level of Akt, p70S6K and 4E-BP1 decreased in tamsulosin low,medium and high-concentration groups,while expression level of Bax protein in-creased (P<0.05 or P<0.01);the apoptosis rate of PC-3 cells was increased in tamsulosin medium and high-concentration groups,while the expression level of Bcl-2 and phosphorylation level of mTOR were decreased(P<0.01),in concentration-depen-dent manner. CONCLUSIONS:Tamsulosin can inhibit PC-3 cells proliferation and induce cell apoptosis via blocking Akt/mTOR signal pathway.