OBJECTIVE To investigate the improvement effects and potential mechanisms of Sangbaipi decoction （SBP） on mice with second-hand smoke-induced pulmonary fibrosis （PF）. METHODS Using network pharmacology methods， the common targets between the active components of SBP and PF-specific targets were screened， the protein-protein interaction network was constructed， the pathway enrichment analysis was performed using the Kyoto Encyclopedia of Genes and Genomes， and the molecular docking was conducted. Based on these results， the male Kunming mice were divided into a normal control group， a model control group， an SBP group （1.08 g/kg， calculated by crude drugs）， and a pirfenidone group （positive control， 90 mg/kg）， with eight mice in each group. Except for the normal control group， all other groups were exposed to second-hand smoke via the static respiratory tract smoking method （30 min of smoking twice daily for 20 consecutive days） to establish a mouse model of PF induced by second-hand smoke. Each drug group was administered the corresponding drug solution via gavage 0.5 h after the second daily smoke exposure； the normal control and model control groups were simultaneously administered an equal volume of water via gavage， once daily for 20 consecutive days. Twenty-four hours after the final administration， pathological changes in lung tissue were observed， and the levels of pro-inflammatory factors， injury markers， and the expression of proteins in related signaling pathways in lung tissue were detected. RESULTS A total of 2 448 common targets were identified， with core targets including protein kinase B1 （AKT1）， tumor necrosis factor-α （TNF-α）， and interleukin-6 （IL-6）， which were enriched in signaling pathways such as phosphoinositide 3-kinase （PI3K）/AKT. The bin ding energies of AKT1， PI3K， TNF-α， and IL-6 to the active compound chaksine were －11.0， －7.7， －9.0， and －9.4 kcal/mol， respectively. Compared with the model control group， pathological changes such as inflammatory cell infiltration and collagen deposition in lung tissue were alleviated in the administration groups. The expression of collagen Ⅲ in lung tissue was significantly downregulated， and the levels of IL-6， TNF-α， tissue inhibitor of metalloproteinase 1， and pulmonary surfactant-associated protein D， as well as the percentage of positive areas with pulmonary fibrosis and protein phosphorylation levels of PI3K and AKT， were all significantly downregulated or reduced （ P ＜0.05）. CONCLUSIONS The role of SBP in improving PF induced by second-hand smoke may be related to the regulation of multiple core targets， including AKT1， and the inhibition of the PI3K/AKT signaling pathway， thereby alleviating pulmonary inflammation and collagen deposition.

Objective To observe the long-term clinical effect of pars plana vitrectomy combined with fovea-sparing internal limiting peeling in the treatment of macular foveoschisis in pathologic myopic. Methods A prospective case series study. Fifteen patients (15 eyes) with pathological myopic macular foveoschisis who received treatment in Eye Hospital of Wenzhou Medical University from December 2015 to December 2016 were enrolled. There were 4 males (4 eyes) and 11 females (11eyes), with an average age of 55.33±8.34 years. All patients underwent BCVA, diopter, spectral domain OCT and axial length measurement. The mean logMAR BCVA was 0.95±0.64. The mean central fovea thickness (CFT) was 576.00±185.32 μm. All patients underwent vitrectomy combined with fovea-sparing internal limiting peeling. After gas-liquid exchange, 12％ C3F8 was filled and followed up at 1, 3, 6 and 12 months after surgery. Follow-up time was more than 12 months. The structural changes of BCVA and macular area were observed.Results The foveal internal limiting membranes was successfully preserved in all eyes using the techinique. At the final follow-up, the CFT was 258.60±175.22 μm and the BCVA was 0.46±0.43, which were significantly improved compared with preoperative measurements (t=4.90, 5.20;P<0.001). Macular foveoschisis was resovled in 13 eyes. BCVA increased in 14 eyes. Internal limiting membranes proliferation and contraction occurred in 5 eyes and full-thickness macular hole occurred in 1 eye.Conclusions Pars plana vitrectomy with fovea-sparing internal limiting peeling is effective in the treatment of myopic macular retinoschisis. It can improve BCVA and CFT.

Objective To explore the effects and possible mechanism of histone deacetylase inhibitor SAHA on the interstitial fibrosis induced by diabetes.Methods The SD rats were divided into three groups:control group (Con,n=9),diabetes mellitus (DM) group (n=9) and SAHA treatment group (n=9).The diabetic rat model was established by injecting streptozotocin (STZ) through tail vein.After 8 weeks,the SAHA treatment group rats were fed with a SAHA solution (25 mg· kg-1 · d-1) by gastric gavage.After 16 weeks,all rats were sacrificed to detect relevant biochemical parameters,and observe the changes of pathomorphology in kidney.In addition,immunohistochemistry staining and Western blotting were employed to detect the protein expressions of transforming growth factor-β1 (TGF-β1),Smad2,Smad3,p-Smad2,p-Smad3,Smad7,collagen-Ⅰ and collagen-Ⅲ,respectively.Results Compared with Con group,the levels of blood glucose (BG),urinary trace albumin/urinary creatinine (ACR),triglyceride (TG) and total cholesterol (TC) in the diabetic group were all increased significantly (all P ＜ 0.05),the protein expressions of TGF-β1,p-Smad2,p-Smad3,collagen-Ⅰ and collagen-Ⅲ in kidney were all increased in diabetic group (all P ＜ 0.05),and the expression of Smad7 was significantly reduced (P ＜ 0.05).Compared with DM group,the levels of ACR was reduced,the renal fibrosis was alleviated,the protein expressions of TGF-β1,p-Smad2,p-Smad3,collagen-Ⅰ and collagen-Ⅲ in SAHA group were all decreased (all P ＜ 0.05),and the expression of Smad7 was increased significantly (P ＜ 0.05).Conclusion SAHA may restore the protein level of Smad7 by enhancing protein stability,then promote the moderate transduction of TGF-β1/Smads signaling pathway,which reduce the fibrosis of renal tubules in diabetic rats.