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ObjectiveSalidroside is the most abundant natural active compound in the famous Chinese herbal medicine Rhodiolae Crenulatae Radix et Rhizoma. This study aims to explore the effect of salidroside on the proliferation， migration， invasion， and apoptosis of human hepatoma （HepG2） cells. MethodThe HepG2 cells without any treatment were selected as the blank group， and the HepG2 cells in the salidroside groups were treated with salidroside at final concentrations of 20， 40， 80 μmol·L-1， respectively. A multifunctional cell analyzer， scratch assay， and Transwell assay were employed to determine the proliferation， migration， and invasion of HepG2 cells， respectively. An inverted microscope was used to observe the morphology， and a transmission electron microscope to observe the mitochondria of HepG2 cells. Flow cytometry was employed to determine the apoptosis and cycle distribution of HepG2 cells. Real-time fluorescent quantitative polymerase chain reaction ( Real-time PCR ) and Western blot were employed to determine the expression of apoptosis-associated genes and migration-， invasion-， and apoptosis-associated proteins， respectively， in HepG2 cells. ResultCompared with the blank group， salidroside （20， 40， 80 μmol·L-1） decreased the cell index and increased the healing area in a time- and dose-dependent manner （P<0.05）. Compared with that in the blank group， the HepG2 cells that could pass through Matrigel reduced in the salidroside （20， 80 μmol·L-1） groups. Compared with the blank group， salidroside （20， 40， 80 μmol·L-1） increased the total apoptosis rate in a dose dependence manner and blocked the cells in the G2/M phase （P<0.05）. Compared with the blank group， salidroside up-regulated the expression of epithelial-cadherin （E-cadherin） in a dose-dependent manner （P<0.05） and down-regulated that of nerve-cadherin （N-cadherin） in the 20 and 80 μmol·L-1 groups （P<0.05）. Compared with the blank group， salidroside （20， 40， 80 μmol·L-1） up-regulated the mRNA level of cysteine-containing aspartate-specific protease -3 （Caspase-3） and the protein levels of B-cell lymphoma-2 （Bcl-2） associated X protein （Bax）， Caspase-3， and cysteine-containing aspartate-specific protease-9 （Caspase-9） in a dose-dependent manner （P<0.05）， while it down-regulated the protein levels of the actin-binding protein Girdin and Bcl-2 in a dose-dependent manner （P<0.05）. ConclusionSalidroside inhibited the proliferation， migration， and invasion and induced the apoptosis of HepG2 cells through the mitochondrial pathway. The results suggest that salidroside can be used as a potential chemotherapy candidate for liver cancer.
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Purpose To evaluate the application value of ERCC2 gene polymorphism ( rs3916840 C/T, rs1799793 G/A and rs238416 G/A) detection in molecular pathological diagnosis of breast cancer. Methods The polymorphisms of ERCC2 ( rs3916840, rs1799793 and rs238416) were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay in 101 patients with breast cancer and in 101 cancer-free controls. Results Analysis of the data showed a 0. 287-fold increased risk of breast cancer due to the deletion of genotype GA at rs238416 (P0. 05). Furthermore, Heterozygous genotype of rs3916840 was significantly associated with tumor size (P=0. 049), heterozygous genotype of rs1799793 was significantly associated with PR sta-tus and triple negative breast cancer (P=0. 037). Remarkably, the genotype frequency of GA in p53-positive patients was lower than that in p53-negiative patients (P=0. 026). Conclusions These results indicate that the polymorphism of rs238416 of ERCC2 is sig-nificantly associated with breast cancer risk. Tumor size, PR status, triple negative breast cancer, and p53 protein expression are asso-ciated with polymorphisms of ERCC2 (rs3916840, rs1799793 and rs238416) respectively. ERCC2 gene polymorphism detection is useful for the early diagnosis and prognosis evaluation of breast cancer.
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Objective To explore the effects of different extracts of modified Siwu Siteng Decoction (TFT-Ⅰ, TFT-Ⅱ) on rat models with hyperuricemia. Methods Rat model with hyperuricemia was induced by hypoxanthine and oxonic acid potassium salt. Seventy rats were randomly divided into 7 groups:normal group, model group, allopurinol group, TFT-Ⅰ high and low dose groups, TFT-Ⅱhigh and low dose groups. Each dose group was given lavage with related medicine, and blank group and model group were given lavage with distilled water for one week, respectively. Uric acid in serum (SUA) was measured through fully automatic biochemical analyzer, and xanthine oxidase (XOD) activity in serum and liver tissue was measured through colorimetric method. Results Compared with model group, TFT-Ⅰ and TFT-Ⅱ high dose groups significantly reduced the level of SUA, serum and liver XOD activity (P0.05). Conclusion Alcohol soluble ingredients of astragalus membranaceus and Siwu decoction in modified Siwu Siteng Decoction can effectively reduce the level of blood uric acid.
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<p><b>OBJECTIVE</b>To investigate the effects of arsenic trioxide (As(2)O(3)) on the apoptosis and p-glycoprotein (P-gp) expression of multidrug-resistant human leukemia cells.</p><p><b>METHODS</b>Human multidrug-resistant leukemia cell line K562/ADM overexpressing the MDR1 gene, was used as the target cells. The cell proliferating activity was assessed using the MTT colorimetric assay. Cytomorphology was investigated under light, confocal and electron microscopes. DNA fragmentation was examined using agarose gel electrophoresis, while p-gp expression, cell cycle status and sub-G1 cells were determined using flow cytometry.</p><p><b>RESULTS</b>Zero point five to 20 micromol/L As(2)O(3) inhibited the proliferation of K562/ADM cells, and K562/ADM cells were more sensitive to As(2)O(3) than the parental K562 cells. As(2)O(3)-induced apoptosis of K562/ADM cells was determined by the observance of typical morphological changes and the appearance of DNA ladder and sub-G1 cell populations. As(2)O(3) significantly inhibited the P-gp expression of K562/ADM cells, and synergistically enhanced the sensitivity of the drug-resistant cells to adriamycin.</p><p><b>CONCLUSIONS</b>As(2)O(3) induces growth-inhibition and apoptosis, down-regulates P-gp expression and exerts a synergistic effect in combination with adriamycin in multidrug-resistant leukemia cells.</p>