The delivery mechanism of micro-porous osmotic pump tablets / 药学学报

To investigate the delivery mechanism of micro-porous osmotic pump tablets ( MPOP), taking tramadol hydrochloride ( TR) as the model drug, tramadol hydrochloride micro-porous osmotic pump tablets (TR MPOP) were prepared with compressible starch as diluent, cellulose acetate as coating material, polyethylene glycol 400 as pore-forming agents. The equilibrium solubility and osmolality of TR were determined. The effects of fillers in tablet cores, coating levels, and osmotic pressures of release media on expansion behavior of preparations were described. The influences of the category, osmolality, and pH value of release media, release methods, and release conditions on release curves of tablets were evaluated. Based on several models, the delivery pattern of TR MPOP was fitted. The equilibrium solubility in water and osmolality of TR were (775.8 +/- 17.7) g x L(-1) and 4.036 Osmol x kg(-1), respectively. During the drug-release period, it was observed that the tablets expanded markedly in response to the expansion characteristics of compressible starch and the osmotic pressure difference across the membrane. When osmotic pressure of release media increased, the significant change of the equilibrium solubility of TR was not found, but the release rates of TR MPOP decreased significantly. The delivery rate was not influenced by the pH of release mediums, dissolution methods and paddle stirring rates. The drug release profile conformed to the model of zero order in 8 h. The pore-forming agents were dissolved in release medium, which caused micro-pores. The expansion of tablets made the size of micropores bigger, and then the drug-releasing pores were obtained. It was proved that the drivers of drug delivering from TR MPOP were mainly the difference of osmotic pressure, and secondly the difference of solubility. TR MPOP were the controlled-release preparation.

Clinical study on Ganbi decoction in treating antituberculotic agent-caused liver injury / 中国结合医学杂志

<p><b>OBJECTIVE</b>To study the effect and mechanism of Ganbi decoction (GBD) in treating patients with antituberculotic agent caused liver injury (ATB-LI).</p><p><b>METHODS</b>One hundred and twenty-eight patients with ATB-LI were randomly assigned to the treated group (n = 66) and the control group (n = 62) with the envelop method. Meanwhile, 60 healthy persons were selected as the healthy control group. The treated group was treated by GBD one dose every day with the constituents modified depending on patients' symptoms, and the control group was treated with glucuronolactone tablets and inosine injection. One week was taken as one treatment course. The changes of clinical syndromes, physical signs, T-lymphycyte sub-groups and serum level of nitric oxide (NO) were observed before and after treatment and the recovery time of liver function was recorded. The outcome was compared with that in the healthy control group.</p><p><b>RESULTS</b>In the treated group, 28 patients (42.4%) were cured, 30 (45.5%) improved and 8 (12.1%) ineffectively cured, the total effective rate being 87.9% (58/66). In the control group, 17 patients (27.4%) were cured, 24 (38.7%) improved, and 21 (33.9%) ineffectively cured, the total effective rate being 66.1% (41/62). The total effective rate in the treated group was significantly higher than that in the control group (P < 0.05). Liver function was improved in both groups, recovery time in the treated group was 12.0 +/- 7.0 days, which was significantly shorter than that in the control group (16.0 +/- 8.0 days), showing significant difference between the two groups (P < 0.05). The levels of CD3, CD4 and CD8 were significantly higher and level of NO significantly lower in the two groups of patients than those in the healthy control group (P < 0.05), but these parameters were improved more significantly in the treated group after treatment, when compared with those before treatment or with those in the control group, all showing significant difference (P < 0.05).</p><p><b>CONCLUSION</b>GBD could prevent ATB-LI, and its mechanism could be by way of reducing NO production induced by endotoxin of macrophage and stimulating the proliferation of T-lymphycyte to elevate immunity.</p>

Pseudolaric acid B induces human melanoma A375-S2 cell apoptosis in vitro / 中国中药杂志

<p><b>OBJECTIVE</b>To study the mechanisms of pseudolaric acid B-induced apoptosis on A375-S2 cells.</p><p><b>METHOD</b>MTT, fluorescence microscope observation, DNA agarose gel electrophoresis and Western blot analysis wereused.</p><p><b>RESULT</b>Pseudolaric acid Binduces A375-S2 cell apoptosis in a time and dose-dependent manner. Apoptotic bodies and DNA ladder were observed in 5 micromol x L(-1) pseudolaric acid B-treated A375-S2 cells for 36 h. The expression of Bcl-2, Bcl-xL and ICAD was reduced time dependently, whereas the expression of Bax was increased.</p><p><b>CONCLUSION</b>The major cause of pseudolaric acid B induced cytotoxicity on A375-S2 cells was apoptosis. Mitochondria proteins and ICAD might be involved in the apoptotic pathways of pseudolaric acid B-treated A375-S2 cells.</p>

Mechanisms of capsaicin-induced apoptosis of human melanoma A375-S2 cells / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To study the mechanisms of capsaicin-induced apoptosis of human melanoma A375-S2 cells.</p><p><b>METHODS</b>MTT assay, fluorescence microscopy, DNA agarose gel electrophoresis, flow cytometry and Western blot analysis were carried out to assess the morphological and biochemical changes of A375-S2 cells after capsaicin treatment.</p><p><b>RESULTS</b>Capsaicin induced A375-S2 cell death in a time- and dose-dependent manner. Sub-diploid peak was seen at 24 h after 250 micromol/L capsaicin treatment, and apoptotic bodies and DNA ladder were observed at 36 h after capsaicin treatment. The expression of inhibitor of caspase activated DNase (ICAD) was reduced with the lapse of time.</p><p><b>CONCLUSION</b>Capsaicin induces A375-S2 cell apoptosis and down-regulation of ICAD contributes to this process.</p>