Shexiang Tongxin Dropping Pill () Protects against NaSO-Induced Hypoxia-Reoxygenation Injury in H9c2 Cells / 中国结合医学杂志

OBJECTIVES@#To investigate the protective effects of Shexiang Tongxin Dropping Pill (, STP) on NaSO-induced hypoxia-reoxygenation injury in cardiomyoblast H9c2 cells.@*METHODS@#The cell viability and levels of mRNA and protein expression in H9c2 cells were determined following NaSO-induced hypoxia using Hoechst staining, annexin V/propidium iodide (PI) flow cytometry, real-time polymerase chain reaction and Western blot analysis.@*RESULTS@#STP pretreatment significantly increased the viability and inhibited aberrant morphological changes in H9c2 cardiomyoblast cells induced by NaSO treatment (P<0.05). In addition, STP pretreatment attenuated NaSO-induced hypoxic damage, down-regulated the expression of pro-apoptotic Bax, and up-regulated the expression of anti-apoptotic Bcl-2 in H9c2 cells (P<0.05).@*CONCLUSIONS@#STP was strongly cardioprotective in hypoxia-reoxygenation injury by preventing hypoxic damage and inhibiting cellular apoptosis. These results further support the use of STP as an effective drug for the treatment of ischemic heart disease.

Pien Tze Huang () Overcomes Doxorubicin Resistance and Inhibits Epithelial-Mesenchymal Transition in MCF-7/ADR Cells / 中国结合医学杂志

OBJECTIVE@#To evaluate the effect of Pien Tze Huang (, PZH) on breast cancer chemoresistance and related epithelial-mesenchymal transition (EMT) and investigate the underlying mechanisms.@*METHODS@#3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay was used to determine the cell viability. Adriamycin (ADR) staining observed by fluorescence microscope was performed to detect the accumulation of ADR. Transwell assay was used to analyze the cell migration and invasion. Western-blot was performed to detect the protein expression of related genes.@*RESULTS@#MCF-7/ADR cells were resistant to ADR treatment, and PZH treatment inhibited the viability of MCF-7/ADR cells in a dose-dependent manner. PZH treatment also increased the intercellular accumulation of ADR and down-regulated the expression of ABCG2 and ABCB1 in MCF-7/ADR cells (P<0.05). In addition, PZH treatment inhibited EMT, migration and invasion of MCF-7/ADR cells (P<0.05). Moreover, PZH suppressed activation of transforming growth factor β1 (TGF-β) signaling in MCF-7/ADR cells (P<0.05).@*CONCLUSION@#PZH treatment can effectively overcome chemoresistance via down regulating ABCG2, ABCB1 and inhibit EMT in ADR resistant human breast cancer cells via suppression of the TGF-β1 pathway.

Qinghuachang Decoction Inhibited NF-kappaB Activation in LPS-induced Human Enterocytes / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To explore anti-inflammation and mechanism of Qinghuachang Decoction (QD) by using LPS stimulated differentiated colon cancer Caco-2 cells (as an inflammation model of human enterocytes).</p><p><b>METHODS</b>QD was prepared. Human colonic epithelial Caco-2 cells were cultured. Expressions of TNF-alpha and IL-8 were determined using ELISA. Expressions of inhibitory Kaba protein (IkappaB-alpha), phosphorylated inhibitory Kaba protein (p-lkappaB-alpha), nuclear transcription factor p50 (p50), and nuclear transcription factor ReIA (ReIA) protein were determined by Western blot.</p><p><b>RESULTS</b>Compared with the negative control group (without LPS stimulation), LPS stimulated the release of IL-8 and TNF-alpha in Caco-2 cells (P < 0.05). QD treatment could reduce the secretion of TNF-alpha and IL-8 induced by LPS in a dose dependent manner (P < 0.05). QD at 0, 5, 10, and 50 microg/mL had no significant effect on Caco-2 cell survival rates (P > 0.05), with no statistical difference among various concentrations (P > 0.05). QD could significantly suppress nuclear factor-kappa B (NF-kappaB) phosphorylation stimulated by LPS. The expression of p-IKappaB-alpha was decreased with increasing concentrations of QD (P < 0.05). There was no obvious change in IKB-alphaB expressions (P > 0.05). Expressions of p50 and ReIA decreased with increasing concentrations of QD (P < 0.05). Both of them were in a dose dependent manner.</p><p><b>CONCLUSION</b>QD inhibited LPS mediated NF-kappaB activation, which might be one of its mechanisms for treating inflammatory bowel disease (IBD).</p>

Pien Tze Huang induced apoptosis in human colon cancer HT-29 cells is associated with regulation of the Bcl-2 family and activation of caspase 3 / 中国结合医学杂志

<p><b>OBJECTIVE</b>To investigate the cellular effects of Pien Tze Huang (PZH) in the HT-29 human colon carcinoma cell line.</p><p><b>METHODS</b>The viability of HT-29 cells was determined by MTT assay. A fluorescence-activated cell sorting (FACS) analysis with annexin-V/propidium iodide (PI) and JC-1 staining were performed to determine cell apoptosis and the loss of mitochondrial membrane potential, respectively. Activation of caspase 3 was evaluated by a colorimetric assay. The mRNA expression levels of Bcl-2 and Bax were measured by reverse transcription polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>PZH, in a dose- and time-dependent manner, reduced viability and induced apoptosis of HT-29 cells. Moreover, PZH treatment resulted in the collapse of the mitochondrial membrane potential, activation of caspase 3, and an increase in the Bax/Bcl-2 ratio.</p><p><b>CONCLUSION</b>PZH inhibits the growth of HT-29 cells by inducing cancer cell apoptosis via regulation of the Bcl-2 family and activation of caspase 3, which may, in part, explain its anticancer activity.</p>