ABSTRACT
ObjectiveTo study the mechanism of Shenbai Jiedu prescription inhibiting the proliferation of HCT116 colorectal cancer （CRC） cells by regulating the phosphatase and tensin homolog deleted on chromosome ten （PTEN）/phosphatidylinositol 3-kinase （PI3K）/ protein kinase B （Akt） signaling pathway. MethodShenbai Jiedu prescription was extracted by water extraction and alcohol precipitation to prepare freeze-dried powder. HCT116 cells were cultured in vitro， and treated with different concentrations of Shenbai Jiedu prescription （2， 4， 8， 16 g·L-1）. The inhibitory effect of Shenbai Jiedu prescription on the proliferation of HCT116 cells was tested by methyl thiazolyl tetrazolium （MTT）. Real-time quantitative PCR was used to detect the mRNA expression levels of PTEN， PI3K， Akt， glycogen synthase kinase-3β （GSK-3β）， c-Myc， survivin and Cyclin D1. Western blot was employed to measure the protein expression levels of PTEN， phosphorylated PTEN （p-PTEN）， PI3K， Akt， phosphorylated Akt （p-Akt）， GSK-3β， phosphorylated GSK-3β （p-GSK-3β）， c-Myc， survivin and Cyclin D1， β-catenin nuclear import was explored by immunofluorescence assay. ResultCompared with the control group， Shenbai Jiedu prescription inhibited the proliferation of HCT116 cells in a dose-dependent manner （P<0.01）. Compared with the control group， the mRNA expression levels of PTEN and GSK-3β were up-regulated whereas those of PI3K， Akt， c-Myc， survivin and CyclinD1 were down-regulated after treatment with Shenbai Jiedu prescription （P<0.01）. The protein expression levels of PTEN， p-PTEN and GSK-3β were up-regulated whereas those of PI3K， Akt， p-Akt， GSK-3β， p-GSK-3β， c-Myc， survivin and CyclinD1 were down-regulated （P<0.05， P<0.01）. Immunofluorescence assay showed that Shenbai Jiedu prescription suppressed β-catenin nuclear import in HCT116 cells. ConclusionShenbai Jiedu prescription inhibited the proliferation of HCT116 cells via the mechanism of regulating the PTEN/PI3K/Akt signaling pathway.
ABSTRACT
ObjectiveTo investigate the mechanism by which Shenbai Jiedu prescription （SBJDF） inhibits the proliferation of colorectal cancer （CRC） HCT116 cells. MethodAfter 48 h treatment of HCT116 cells with SBJDF （0， 0.25， 0.5， 1， 2， 4 g·L-1）， the viability of HCT116 cells were determined by methyl thiazolyl tetrazolium （MTT） colorimetry. Following the classification of cells into blank control group and SBJDF （1， 2， 4 g·L-1） groups， the effect of SBJDF on HCT116 cell morphology was observed under an inverted microscope. The effects of SBJDF on the proliferation of HCT116 cells and mitochondrial membrane potential （Δψm） were detected by colony formation assay and JC-1 probe， respectively. The flow cytometry was then performed for determining cell cycle distribution and apoptosis. The effects of SBJDF on cell cycle-， apoptosis-， and nuclear factor kappa-B （NF-κB） signaling pathway-related proteins were determined by Western blot. ResultSBJDF effectively inhibited the vitality of HCT116 cells and changed their morphology in a concentration-dependent manner. Compared with the blank control group， SBJDF at 1， 2， 4 g·L-1 significantly reduced cell colony formation （P<0.05， P<0.01），and SBJDF at 2 and 4 g·L-1 arrested the HCT116 cell cycle at G0/G1 phase （P<0.05， P<0.01）. Compared with the blank control group， SBJDF at 1， 2， 4 g·L-1 remarkably down-regulated the protein expression of CyclinD1 （P<0.05， P<0.01）. SBJDF at 2 and 4 g·L-1 lowered the CyclinA2 and cyclin-dependent kinase 4 （CDK4） （P<0.05， P<0.01）. SBJDF at 4 g·L-1 reduced the cyclin-dependent kinase 1 （CDK1） （P<0.01）. Compared with the blank control group， SBJDF at 2 and 4 g·L-1 induced HCT116 cell apoptosis， down-regulated the protein expression of anti-apoptosis-related proteins Bcl-2 and Bcl-xl as well as the NF-κB signaling pathway-related proteins IκB kinase α （IKKα），inhibitor α of NF-κB （IκBα），and phospho-NF-κB p65 （p-p65） （P<0.05， P<0.01）， and diminished the mitochondrial membrane potential of HCT116 cells. ConclusionSBJDF inhibits the proliferation of HCT116 cells， which may be related to its inhibition of the activation of NF-κB signaling pathway and the induction of cell cycle arrest and apoptosis.
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Objective To explore the relationship of zearalenone (ZEA) and precocious puberty in girls.Methods The peripheral serums from 71 cases of precocious puberty girls and 50 cases of healthy girls were collected respectively and concentrations of ZEA were detected by high performance liquid chromatography.Bone age,body mass index (BMI),volume of uterus and ovaries,concentrations of estradiol (E2),luteinizing hormone (LH) and folliclestimulating hormone (FSH) were detected,and the residence of each subject was recorded as well.Results (1) In 71 patients,52 patients were diagnosed as idiopathic central precocious puberty,others were diagnosed as premature thelarche.(2) In 71 patients,serum ZEA was detected from 51 patients,and undetected in 20 patients.(3)Concentration of ZEA in precocious puberty girls [(318 ±34) ng/L]was significantly increased than that in healthy girls [(143 ± 35) ng/L,P =0.002],but no distinct difference existed between ICPP group and PT group(P =0.326).(4)Compared with uterus volume of ZEA in the undetected patients (1.975 ±0.150) cm3,the uterus volume of ZEA detected patients (2.972 ±0.180) cm3,which was significantly enlarged,there was significant difference (P =0.01) ; Percentage of overweight girls in ZEA detected patients (31.4％,16/51 cases) was lower than which in ZEA undetected patients (65.0％,13/20 cases,P =0.01) ; Although there was no statistical differences in the breast diameter,bone age,value of E2,LH and FSH between ZEA detected patients and undetected patients (all P ＞ 0.05),but the increased tendency in ZEA detected patients existed.(5) ZEA in serum was detected in 53.3％ (16/30 cases) patients living in the cities,and the rate was obviously lower than 82.9％ of the patients (34/41 cases) living in the countryside,there was significant difference (P =0.007).Conclusions ZEA is correlated with precocious puberty in girls.ZEA pollution might be one of reasons for precocious puberty occurrence.
ABSTRACT
As one of endocrine dysfunction related diseases among children,precocious puberty has trend for increased rates in recent years.Widespread children exposure to known or suspected endocrine disrupting chemicals has been documented in worldwide,in which exogenous estrogen chemicals trigger precocious puberty onset have been attracting more and more attentions.Zearalenone widely contaminates foods such as grain,milk,meat and eggs,which displayed its estrogen effect to disrupt organism development.In this review,Zearalenone is suspected as triggering factor for precocious pubertal to be discussed,will lead to people pay more attentions to food safety and the prevention of precocious puberty.
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Objective To study the prevention,diagnosis and treatment of the pulmonary embolism after abdominal surgery.Methods The clinical data of patients with acute pulmonary embolism(PE) after abdominal surgery between July 2008 and June 2012 were analyzed retrospectively.The high-risk patients received D-dimer,deep venous ultrasound and pulmonary CT examination to confirm the diagnosis postoperatively.Anticoagulation,thrombolysis,inferior vena cava filter placement were carried out in these patients.The high-risk patients received low molecular weight heparin(LMWH) to prevent PE from January 2010.Results 5 patients with PE survived and 3 patients died.The incidence of venous thromboembolism event was 0.43％ (13/3012) before January 2010 and PE was 0.20％ (6/3012).The incidence of venous thromboembolism event was 0.15％ (7/4803) after taking preventive measures and PE was 0.04％ (2/4803).There was no PE within 1 week since using LMWH after 2010.Lower limb DVT was found in 7 patients including 2 patients with PE after LMWH discontinuance within 2-3 weeks postoperatively.Conclusions Early prevention,diagnosis and treatment of postoperative PE are important for high-risk patients.