1.Preliminary Study on Extraction and Separation of Anti-tumor Ingredients from Fresh Gekko Swinhonis
Hongxia LI ; Jiangong KANG ; Shizhuang ZHANG
China Pharmacist 2015;(11):1841-1843
Objective:To study the extraction and separation of anti-tumor active ingredients from fresh Gekko swinhonis. Meth-ods:The extraction was carried out with ethanol at different concentrations by various methods. The extract was purified by HPLC after deproteinization and degreasing using a repeated freezing and thawing method. MTT was used to detect the antitumor activity of the ex-tract. Results:The A value of extraction process groupⅢwith 85% ethanol ultrasonic extraction was (0. 548 ± 0. 045) with the high-est tumor inhibition rate, and compared with the control group, the difference was significant (P<0. 05). Conclusion:The results of pharmacodynamics show that the optimum extraction technology is ultrasonic extraction with 85% ethanol.
3.Protective effect of new adenosine analog B2 against serum deprivation-induced PC12 cell injury.
Jing SUN ; Min LI ; Ruixia KANG ; Jiangong SHI ; Jianjun ZHANG
Acta Pharmaceutica Sinica 2011;46(10):1199-203
This study is to investigate the effect of compound B2 on the damage of PC12 cells induced by serum deprivation and to explore its related mechanisms. The binding characteristics of B2 to rat striatum adenosine A2A receptor was studied by radioligand 3H-MSX-2 binding assay. Cell viability was detected by MTT assay. ROS formation was measured after DCFDA fluorescent staining. B2 has affinity to rat adenosine A2A receptor (K1 = 0.37 micromol x L(-1)). B2 remarkably increased PC12 cell survival rate in serum deprivation-induced PC12 cells. The percentage of serum deprivation-induced death of PC12 was 49.6%, and the treatment of B2 (0.1-100 micromol x L(-1)) increased the cell viability to 63.3%, 74.9%, 86.3% and 88.1%, respectively. Adenosine A2A receptor antagonist SCH 58261 could significantly block the protective effect of B2. The cell viability with 0.1 micromol x L(-1) SCH 58261 decreased by 16.1%, 24.0% and 19.8%, in the presence of B2 (0.1-10 micromol x L(-1)). Serum deprivation-induced ROS formation was 3.5 times more than that of control group, and treatment with B2 significantly and dose-dependently inhibited ROS over-formation. The protective effect of B2 may be related with adenosine A2A receptor. Decrease of serum-deprivation induced ROS formation may also be one of the mechanisms.