Study on chromatography-efficacy relation of Zanthoxylum nitidum on gastric cancer cells / 中国中药杂志

<p><b>OBJECTIVE</b>To develop a method for elucidating " chromatography-efficacy" relation of the extract of Zanthoxylum nitidum on the gastric cancer cells.</p><p><b>METHOD</b>After obtaining the tumor inhibition rate and fingerprint peak data through MTT and HPLC, "chromatography-efficacy" relation was established by an appropriate statistical method.</p><p><b>RESULT</b>The gastric cancer "chromatography-efficacy" relation of Z. nitidum was established by step-back technique.</p><p><b>CONCLUSION</b>The "chromatography-efficacy" relation has statistically significant and practical significance, so it has reference value in some way.</p>

Characteristic chromatographic profile of Zanthoxylum niridum / 中国中药杂志

<p><b>OBJECTIVE</b>To establish the characteristic fingerprint of Zanthoxylum nitidum by HPLC, and to provide a reference for the quality control of Z. nitidum in the market.</p><p><b>METHOD</b>The established HPLC characteristic fingerprint of Z. nitidum, combined with similarity evaluation and system clustering analysis method, were applied to distinguish 25 batches of samples purchased from market preliminarily, to identify the authenticity and quality of Z. nitidum ingredients.</p><p><b>RESULT</b>In the 25 batches of samples purchased from market, only 8 batches were identified as genuine with good quality, 7 batches were identified as defective, 7 batches were identified as common counterfeit Toddalia asiatica, and 3 batches were identified as counterfeit.</p><p><b>CONCLUSION</b>This method is accurate, convenient and reliable. It can be used for identification and quality control of Z. nitidum ingredients.</p>

A novel sesquiterpene Hirsutanol A induces autophagical cell death in human hepatocellular carcinoma cells by increasing reactive oxygen species / 癌症

<p><b>BACKGROUND AND OBJECTIVE</b>Hirsutanol A is a novel sesquiterpene compound purified from fungus chondrostereum sp in Sarcophyton tortuosum. Its pharmacologic effect has not been reported yet. This study aimed to investigate cytotoxic effect of Hirsutanol A on hepatocellular carcinoma (HCC) cells and its mechanism.</p><p><b>METHODS</b>Hep3B cells were treated with different concentrations of Hirsutanol A. Cell proliferation was detected by MTT assay. The protein expression of LC3 was determined by Western blot. The generation of reactive oxygen species (ROS) was monitored by flow cytometry.</p><p><b>RESULTS</b>Hirsutanol A significantly inhibited proliferation of Hep3B cells with 50% inhibition concentrations (IC50) of 14.54, 6.71, and 3.59 micromol/L when exposed to Hirsutanol A for 24, 48, and 72 h, respectively. Incubation of Hep3B cells with Hirsutanol A markedly increased the level of ROS and the autophagy marker MAP-LC3 conversion from type I to type II. Pre-incubation with an antioxidant N-acetyl cystein (NAC) decreased the level of ROS, and reduced MAP-LC3 I-II conversion, and suppressed cell death. Blocking autophagy with a specific autophagy inhibitor 3-methyladenine (3-MA), the cytotoxic effect of this compound was attenuated.</p><p><b>CONCLUSION</b>Hirsutanol A has potent cytotoxic effect, and can induce autophagic cell death via increasing ROS production.</p>

Apoptosis induced by DNA primase inhibitor 3,3'-diethyl-9-methylthia-carbocyanine iodide in human leukemia HL-60 cells / 药学学报

<p><b>AIM</b>To investigate apoptosis induced by 3,3'-diethyl-9-methylthia-carbocyanine iodide (DMTCCI), an inhibitor of DNA primase found in our previous study, and the mechanism of DMTCCI in human myelogenous leukemia HL-60 cells.</p><p><b>METHODS</b>HL-60 cells were cultured in RPMI-1640 medium and treated with different concentrations of DMTCCI. MTT assay was used to detect growth inhibition. Flow cytometry and DNA ladders were used to detect apoptosis. Western blotting was used to observe the expression of survivin, Bcl-xL, Bad, Bax, Bcl-2, caspase-9, caspase-3, caspase-6, PARP, DFF45 and lamin B protein. Caspase-3 activity was measured by ApoAlert Caspase-3 Assay Kit.</p><p><b>RESULTS</b>DMTCCI inhibited proliferation of human leukemia HL-60 cells with IC50 value of 0.24 micromol x L(-1). The results of flow cytometry and DNA ladders showed that DMTCCI could induce apoptosis of HL-60 cells. The expression levels of protein survivin and Bcl-xL were down-regulated, Bad and Bax were up-regulated, while Bcl-2 protein had no change in response to DMTCCI treatment in HL-60 cells. Treatment of HL-60 cells with DMTCCI induced the proteolytic cleavage of caspase-9, caspase-3, caspase-6, PARP, DFF45 and lamin B protein. Caspase-3 activity apparently increased at 3 h and reached a peak at 12 h after exposure to 1 micromol x L(-1) of DMTCCI in HL-60 cells.</p><p><b>CONCLUSION</b>DMTCCI inhibited proliferation and induced apoptosis of human leukemia HL-60 cells. Bcl-2 family proteins, survivin and caspases family proteins might play a role in the apoptosis process induced by DMTCCI.</p>