Berberine inhibits norepinephrine-induced apoptosis in neonatal rat cardiomyocytes via inhibiting ROS-TNF-α-caspase signaling pathway / 中国结合医学杂志

<p><b>OBJECTIVE</b>To determine the effect of berberine (Ber) on norepinephrine (NE)-induced apoptosis in neonatal rat cardiomyocytes.</p><p><b>METHODS</b>The cultured neonatal rat cardiomyocytes were treated with NE in the presence or absence of Ber. The activity of lactate dehydrogenase (LDH) in the culture medium was examined, and apoptosis of cardiomyocytes was assessed by Hoechst 33258, isothiocyanate (FITC)-conjugated annexin-V, and propidine iodide (PI) staining. In addition, the activities of caspases-2 and-3 were measured by a fluorescent assay kit. The level of secreted tumor necrosis factor α (TNF-α) and production of intracellular reactive oxygen species (ROS) were also determined.</p><p><b>RESULTS</b>NE at a concentration of 50 μ mol/L induced an obvious increase in the activity of LDH in the culture medium (P<0.05), which was inhibited by coincubation with 0.5, 1.0, or 2.0 μ mol/L Ber (P<0.05). Ber also significantly attenuated NE-induced apoptosis in a dose-dependent manner (P<0.01). Moreover, Ber at a dose of 2 μ mol/L markedly decreased the ROS and TNF-α productions (P <0.05) and inhibited the activation of caspases-2 and -3 in cardiomyocytes exposed to NE (P<0.05)h.</p><p><b>CONCLUSION</b>The present study suggested that Ber could reduce NE-induced apoptosis in neonatal rat cardiomyocytes through inhibiting the ROS-TNF-α-caspase signaling pathway.</p>

Sodium valproate induces mitochondria-dependent apoptosis in human hepatoblastoma cells / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Sodium valproate inhibits proliferation in neuroblastoma and glioma cells, and inhibits proliferation and induces apoptosis in hepatoblastoma cells. Information describing the molecular pathways of the antitumor effects of sodium valproate is limited; therefore, we explored the mechanisms of action of sodium valproate in the human hepatoblastoma cell line, HepG2.</p><p><b>METHODS</b>The effects of sodium valproate on the proliferation of HepG2 cells were evaluated by the Walsh-schema transform and colony formation assays. Sodium valproate-induced apoptosis in HepG2 cells was investigated with fluorescence microscopy to detect morphological changes; by flow cytometry to calculate DNA ploidy and apoptotic cell percentages; with Western blotting analyses to determine c-Jun N-terminal kinases (JNK), p-JNK, Bcl-2, Bax, and caspase-3 and -9 protein expression levels; and using JC-1 fluorescence microscopy to detect the membrane potential of mitochondria. Statistical analyses were performed using one-way analysis of variance by SPSS 13.0 software.</p><p><b>RESULTS</b>Our results indicated that sodium valproate treatment inhibited the proliferation of HepG2 cells in a dose-dependent manner. Sodium valproate induced apoptosis in HepG2 cells as it: caused morphologic changes associated with apoptosis, including condensed and fragmented chromatin; increased the percentage of hypodiploid cells in a dose-dependent manner; increased the percentage of annexin V-positive/propidium iodide-negative cells from 9.52% to 74.87%; decreased JNK and increased phosphate-JNK protein expression levels; reduced the membrane potential of mitochondria; decreased the ratio of Bcl-2/Bax; and activated caspases-3 and -9.</p><p><b>CONCLUSION</b>Sodium valproate inhibited the proliferation of HepG2 cells, triggered mitochondria-dependent HepG2 cell apoptosis and activated JNK.</p>

Antisense oligonucleotides targeting protein kinase C alpha inhibits the proliferation of A549 cells / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the effects of antisense oligonucleotides (ASODN) targeting protein kinase C alpha (PKCalpha) on the proliferation of A549 cells.</p><p><b>METHODS</b>PKCalpha ASODN and random oligonucleotides (RODN) were transfected into A549 cells mediated by polyethyleneimine, and the proliferation and clone formation of A549 cells were detected by CCK-8 and clone formation assay, respectively. The expression of PKCalpha in the transfected cells was analyzed by RT-PCR and Western blotting.</p><p><b>RESULTS</b>Compared with those in the control group, PEI group and PEI-RODN group, the proliferation and clone formation of A549 cells treated with ASODN targeting PKCalpha were significantly inhibited (P<0.05). The expressions of PKCalpha mRNA and protein in PKCalpha ASODN-transfected A549 cells were significantly lower than those in the other 3 groups (P<0.05).</p><p><b>CONCLUSION</b>The PKCalpha ASODN mediated by PEI down-regutates the expression of PKCalpha gene and suppress the proliferation and clone formation of A549 cells.</p>

Psychological anxiety evaluation and analysis of graduates at a medical university under employment pressure / 南方医科大学学报

<p><b>OBJECTIVE</b>To evaluate the psychological anxiety of graduates at a medical university under the ever-increasing employment pressure, so as to provide ground work for psychological intervention on college students.</p><p><b>METHODS</b>Subjects were randomly drawn from the students who majored in clinical medicine, biomedical engineering, nursing and integrated Chinese and western medicine and graduated in the year of 2008 and 2009, with 25 subjects from each major each year, totaling up to 200. In March of their graduation year, they were evaluated by Hamilton Anxiety Scale (HAMA). A general analysis into their anxiety was first made and then the comparative analysis of anxiety on the basis of gender, year group and major of the subjects.</p><p><b>RESULTS</b>Female students showed a significantly higher anxiety than male students. Graduates in 2009 showed a significantly higher anxiety than those in 2008. In terms of the major difference, the anxiety was in a falling curve from integrated Chinese and western medicine, clinical medicine, biomedical engineering and nursing. There was no major difference in the students majoring integrated Chinese and western medicine, clinical medicine and biomedical engineering, but nursing students showed significantly low anxiety.</p><p><b>CONCLUSIONS</b>The increasing employment pressure has caused the significant increase in the anxiety of college students. The employment rate in different majors may play a positive role in anxiety. Generally, female students showed a higher degree of anxiety than male students.</p>