OBJECTIVE:To prepare aspirin-β-cyclodextrin-PLGA microspheres,and control its quality. METHODS:Aspirin-β-cy-clodextrin inclusion complexes were firstly prepared,and then aspirin-β-cyclodextrin-PLGA microspheres were prepared by emul-sion-solvent evaporation method. The morphology and particle size of microspheres were detected,and entrapment efficiency and accu-mulative release rate were calculated. With entrapment efficiency as index,orthogonal test was adopted to optimize stirring speed,PVA concentration,PVA volume and feed ratio. RESULTS:The optimal formulation was as follows as stirring speed of 4 000 r/min,PVA concentration of 3%(g/100 ml),PVA volume of 30 ml,feed ratio of 1∶10. Prepared microspheres were round and smooth in appear-ance. Entrapment efficiency of the microspheres was (41.79 ± 1.09)%. The diameter were regular and ranged 0.5-127.5 μm. As drug-loaded microspheres degraded,the release of aspirin was slow and its accumulative release rate was 83%within 600 h. CONCLU-SIONS:Aspirin-β-cyclodextrin-PLGA microspheres are prepared successfully with regular morphology and good sustained-release.

Objective:To observe the effects of Chaihu Jiedu decoction on human hepatic stellate LX-2 cells,and to explore the potential molecular mechanisms.Methods:The wistar rats were divided into the experimental group and the control group,respectively with Chaihu Jiedudecoction and saline lavage,then centrifugal and get the drug-containing serum and control serum.At the same time,trsuscitate cells.When we got the expected number of cells,we divided into the experimental group and the control group.The human hepatic stellate cells (LX-2) were with the drug serum for 24 h,36 h,48 h,72 h.Then the cell proliferation inhibition rate was measured by CCK-8,the apoptosis were detected by flow cytometry (Annexin V-FITC,PI staining method).Results:ChaihuJiedu decoction could inhibit proliferation of LX-2 cells 24 hours after dosing.The in hibition rate in 36 h,48 h,72 h were 0.37 ％,0.46 ％,0.44 ％ respectively.It could prevent LX-2 cells into proliferation and induce the apoptosis of LX-2 cells.The apoptosis rates in 48 h,72 h were (9.80±0.95)％,(36.40± 5.09)％ respectively,and there are difference of statistical significance(P＜0.05).Conclusion:Chaihu Jiedu decoction can inhibit the proliferation of LX-2 cells proliferation,and induce apoptosis,so as to interfere with course of the liver fibrosis.

Objective:To investigate the effects of methyltransferases like 3(METTL3)mediated m6A modification of double homology cassette A pseudogene8(DUXAP8)on the proliferation,migration and invasion of salivary adenoid cystic carcinoma SACC-LM cells and its potential molecular mechanisms.Methods:Whole-transcriptome sequencing showed that DUXAP8 was highly ex-pressed in SACC than in para-cancerous tissues(P＜0.05).The m6A modification sites on DUXAP8 were predicted using the SRAMP website,and the mRNA and protein expression of m6A-modified genes and the genes associated with the epithelial-mesen-chymal transition(EMT)was measured by qRT-PCR and Western blot,respectively.METTL3 and DUXAP8 was knocked down or overexpressed in SACC-LM cells,and the proliferation,migration,and invasion of the cells were assessed by CCK-8,scratch and Transwell assays.The correlation between METTL3 and DUXAP8 was evaluated using MeRIP-qPCR.Results:The expression of DUXAP8 in SACC tumor was higher than that in para-cancerous tissues(P＜0.05).Knockdown of DUXAP8 reduced proliferation,migration and invasion of SACC-LM cells,as well as the expression of EMT-related genes(P＜0.05).Multiple m6A modification sites of high confidence were found on DUXAP8.METTL3 was highly expressed in tumor tissues,more than other related genes(P＜0.05)and enzyme-encoding genes in SACC-LM cells(P＜0.05).METTL3 was found to function as a methyltransferase to regulate the expression of DUX-AP8,and downregulation of METTL3 inhibited prolifera-tion,migration and invasion of SACC-LM cells and partially reversed the promotion of these activities induced by DUX-AP8 overexpression(P＜0.05).Conclusion:METTL3-me-diated m6A modification upregulated DUXAP8 expression,which promotes the proliferation,migration and invasion of SACC cells.