AIM:To optimize the formulation of breviscapine oral disintegrating tablets and preparation process. METHODS: To adopt the multifactor and multilevel uniform design to optimize the preparation prescription,disintegrating time as the assessment index. RESULTS: The tablets prepared were finer in appearance,disintegrated within 35 s,with desirable taste.The dissolution rate was faster than breviscapine ordinary tablets. CONCLUSION: Breviscapine oral disintegrating tablets achieve the goal of design and it is easy to operate.

AIM:To establish quality control method for Breviscapine(Orally) Disintegrating Tablets. METHODS: Its main ingredient scutellarin was identified by TLC, the scutellarin in the tablets was determined by HPLC.And the disintegration, dissolution rate and tablet weights were determined. RESULTS: Breviscapine(Orally) Disintegrating Tablets could be disintegrated in 30 seconds,and the tablet weight was fit for the criterion.And the dissolution rate was more quick than the original Breviscapine tablets in the market.A good linearity was obtained within the range of 0.081 6 ?g-0.408 0 ?g with the correlation coefficient(0.999 9.) The recovery was(99.67%) and RSD was 0.47%. CONCLUSION: The method for identifying and determing Breviscapine Orally Disintegrating Tablets is simple,reproducible and practical.

OBJECTIVE: To explore the eff ect of pulchinenoside (PULC) on fi broblast-like synoviocytes (FLS) apoptosis in adjuvant arthritis (AA) rats. METHODS: A total of 60 SD rats were randomly divided into 8 groups: A normal control group, an AA group, a low PULC group (50 mg/kg), a middle PULC group (100 mg/kg) or a high PULC group (150 mg/kg) and an ibuprofen (8 mg/kg) group (n=10 per group). FLS from the AA rats was cultured. The expression of Bcl-2, Bax, caspase-3 and the FLS proliferation were detected by the real time qPCR and MTT, respectively. The expression of IL-6 and IL-8 in culture medium was detected by ELISA. RESULTS: Compared with the AA group, the Bcl-2 expression was down-regulated (all P<0.05), the Bax and caspase-3 expression was up-regulated (all P<0.05), and the FLS proliferation was inhibited (all P<0.05). The IL-6 and IL-8 expression was suppressed in the FLS in the PULC groups at different dosages (all P<0.05) as well as in the ibuprofen group (P<0.05). CONCLUSION PULC may inhibit the FLS proliferation in AA rats by increase in FLS apoptosis.
Animals ; Apoptosis ; drug effects ; Arthritis, Experimental ; Caspase 3 ; metabolism ; Fibroblasts ; cytology ; drug effects ; Interleukin-6 ; metabolism ; Interleukin-8 ; metabolism ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Pulsatilla ; chemistry ; Rats ; Rats, Sprague-Dawley ; Synovial Membrane ; cytology ; bcl-2-Associated X Protein ; metabolism