[Effects of hydroxyl acetylated curcumin induced sonodynamic therapy on viability, apoptosis and necrosis of THP-1 macrophages].

OBJECTIVE: We aim to investigate the sonodynamic effect induced by hydroxyl acetylated curcumin (HAC) on THP-1 macrophages. METHODS: THP-1 derived macrophages (1 x 10(5) per milliliter) were cultured with HAC at a concentration of 5 µg/mL for 4 h and then exposed to pulse ultrasound treatment (0.5 W/cm2) for 5 min. Six hours later, cell viability analysis was performed with CCK-8 assay, apoptosis and necrosis analysis were detected with Annexin V/PI staining by flow cytometery. RESULTS: The cell viability of THP-1 macrophage decreased significantly in the group treated with the combination of HAC and ultrasound (P < 0.01), and HAC-SDT induced both apoptosis and necrosis in THP-1 macrophages, the apoptotic rate was higher than the necrotic rate with appropriate conditions, the maximum apoptosis/necrosis ratio was detected in sonodynamic therapy (SDT) group (P < 0.01). CONCLUSION: hAC-SDT was effective to induce THP-1 macrophages apoptosis.

Professor Dong Gui-rong's experiences in treatment of child cerebral palsy / 中国针灸

According to the characteristics of the etiology and pathogenesis of child cerebral palsy, on the basis of "regulating the mind in treatment of all kinds of diseases" and "regulating the functions of five zang organs with back-shu points", Professor DONG Gui-rong applied the penetrating needling technique on the scalp points and acupuncture at back-shu points of five zang organs in the treatment of child cerebral palsy. The valuable clinical experiences have been summarized as "regulating the mind with scalp needling technique, benefiting the brain and opening the orifice", "regulating five zang organs with back-shu points" and "integration of acupuncture and rehabilitation, and function reconstruction". Two effective cases were introduced.

Anti-apoptotic action of hydrogen sulfide is associated with early JNK inhibition.

The mechanism of action of Hydrogen sulfide (H(2)S) as a novel endogenous gaseous messenger and potential cardioprotectant is not fully understood. We therefore investigated the prevention of cardiomyocyte apoptosis by exogenous H(2)S and the signaling pathways leading to cardioprotection. Using a simulated ischemia-reperfusion (I/Re) model with primary cultured rat neonatal cardiomyocytes, I/Re induced a rapid, time-dependent phosphorylation of c-Jun N-terminal kinase (JNK), with significant elevation at 0.25 h and a peak at 0.5h during reperfusion. NaHS (H(2)S donor) significantly inhibited the early phosphorylation of JNK, especially at 0.5h. Both NaHS and SP600125 (specific JNK inhibitor) decreased the number of apoptotic cells, lowered cytochrome C release and enhanced Bcl-2 expression. When NaHS application was delayed 1h after reperfusion, the inhibition of apoptosis by H(2)S was negated. In conclusion, this is novel evidence that early JNK inhibition during reperfusion is associated with H(2)S-mediated protection against cardiomyocyte apoptosis.

Effects of pravastatin on the function of dendritic cells in patients with coronary heart disease.

The aim of the study was to investigate the functional profile of dendritic cells in patients with coronary heart disease and the effects of pravastatin on this. Forty-eight patients with coronary heart disease were divided into three groups: 16 treated with pravastatin 10 mg/day, 16 treated with pravastatin 20 mg/day and 16 not treated with pravastatin. Dendritic cells from 48 patients with coronary heart disease (before and 4 weeks after the treatment) and 16 healthy individuals were derived from peripheral blood. CD86 of dendritic cells was assessed by flow cytometry. Immunostimulatory capacity of dendritic cells was measured by mixed lymphocyte reaction. The levels of cytokines in the medium of mixed lymphocyte reaction were analysed. Blood lipids and high-sensitivity C-reactive protein were measured. Compared to normal group, more CD86+ dendritic cells were expressed in coronary heart disease and greater immunostimulatory capacity of dendritic cells in coronary heart disease was demonstrated. T lymphocytes in coronary heart disease in mixed lymphocyte reaction secreted higher levels of pro-inflammation cytokines and lower levels of anti-inflammation cytokines. CD86 expression significantly correlated with C-reactive protein, but did not correlate with low-density lipoprotein cholesterol. Both dosages of pravastatin markedly inhibited the function of dendritic cells and lowered C-reactive protein, which is independent of plasma cholesterol lowering. The anti-inflammatory effect of pravastatin showed no obvious difference between the two dosage groups. In conclusion, dendritic cells were activated in coronary heart disease and dendritic cell-mediated immune mechanisms may be involved in the pathogenesis of coronary heart disease. Pravastatin can inhibit dendritic cell activation, which is independent of plasma cholesterol lowering. Pravastatin in different doses showed no apparent differences in the inhibition of dendritic cell functions.