Anaphylactoid reaction induced by Qingkailing injection via basophils cells degranulation / 中国中药杂志

<p><b>OBJECTIVE</b>To observe the effects of Qingkailing injection on RBL-2H3 cell degranulation and histamine release, and discuss the possible mechanism of anaphylactoid reaction induced by Qingkailing injection.</p><p><b>METHOD</b>RBL-2H3 cells were incubated with Qingkailing injection for 30 min. Then the morphological changes of cells were observed by transmission electron microscopy. Cell degranulation rate was detected by Alcian blue dye assay, Annexin V binding assay and beta-hexosaminidase assay, and cell histamine release rate was detected by ELISA.</p><p><b>RESULT</b>Different concentration of Qingkailing injection can induce the typical morphological changes in RBL-2H3 cell with degranulation. The rates of degranulation and histamine release in Qingkailing injection treated cells were significantly increased and dose-dependent.</p><p><b>CONCLUSION</b>RBL-2H3 cell degranulation and histamine release can be induced by single administration of Qingkailing injection, and then induced anaphylactoid reaction, which may be one of the possible mechanisms of serious adverse induced by Qingkailing injection for the first administration in clinic.</p>

Study of effects and mechanism of phytosterols on chronic abacterial prostatitis / 中国中药杂志

<p><b>OBJECTIVE</b>To investigate the inhibitory effects of phytosterols on abacterial prostatitis and discuss the possible mechanism.</p><p><b>METHOD</b>Xiaozhiling-induced chronic prostatitis model were used to observe the inhibitory effect of phytosterols on abacterial prostatitis. The changes of serum IL-2, IL-1beta and TNF-alpha were evaluated by enzyme-linked immunosorbent assay (ELISA). The expression of COX-2 and 5-LOX were evaluated by Western blot and immunohistochemistry.</p><p><b>RESULT</b>Treated by phytosterols (150 mg x kg(-1)), the number of white blood cells in xiaozhiling-induced chronic abacterial prostatitis rats was obviously decreased, the density of lecithin corpuscle in prostatic secretion increased and closed to control group. The edema, inflammatory infiltration of prostate were partly recovered compared with model group. The proliferation of chronic prostatitis were obviously decreased in phytosterols groups compared with model group in histological sections. Phytosterols could obviously reduce the serum IL-1beta, TNF-alpha, prostate COX-2 and 5-LOX expression and improve IL-2 level.</p><p><b>CONCLUSION</b>These results demonstrated that phytosterols had good therapeutic effects on chronic abacterial prostatitis. Participation of immune regulation and inhibiting COX-2 and 5-LOX expression may be the mechanisms of action.</p>

Apoptosis induced by satraplatin in human ovarian carcinoma cells A2780 / 中国临床药理学与治疗学

AIM: To observe the growthinhibiting cell cycle-modifying and apoptosis-inducing effects of satraplatin on human ovarian carcinoma cell line A2780, and to explore its possible mechanism. METHODS: The effect of satraplatin on A2780 cells proliferation was determined using MTT, and the change in cell cycle was analyzed using PI staining. Morphologic change was visualized by fluorescence and electron microscopy. AnnexinV-FITC/PI staining multiparameter flow cytometry and immuno- histochemical TUNEL assay were used to detect apoptotic cells. The activity of caspase-3 and the effect of pan-caspase inhibitor on cell viability were measured as well. RESULTS: The growthinhibiting and apoptosis-inducing effects of satraplatin were dose-dependent and similar to those of cisplatin. Satraplatin mainly caused A2780 cell accumulation in S phase accompanied by minor accumulation in G2/M phase. Cells treated with satraplatin exhibited typical morphology of apoptosis. Satraplatin-induced increase in caspase-3 activity of A2780 cells was concentration-dependent. The viability of A2780 cells was affected by pan-caspase inhibitor z-VAD-fmk in a dose-dependent manner under certain concentration of z-VAD-fmk. CONCLUSION: Satraplatin-induced apoptosis in A2780 in vitro was observed. Caspase-dependent and independent pathways were involved in apoptosis induced by satraplatin, and the latter included caspase-3 dependent and non-caspase-3 dependent pathways.