Environmental Monitoring ; instrumentation

Humans ; Immunoglobulin E ; Mouth Diseases ; Syndrome

Objective To explore the function of fluorescent probe JC-1 in detecting the changes of mitochondrial membrane potential(△?m)in early apoptotic cells.Methods After 2-ME was used to induce MUTZ-1 cell apoptosis,cells were dyed with fluorescent probe JC-1,and then the changes of △?m in the early stage of apoptotic cells were analyzed by flow cytometry or detected under fluorescent microscope. Results The control cells with high △?m are those forming JC-1 aggregates in the inner membrane of mitochondria,thus showing orange-red fluorescence.2-ME caused decrease of △?m in MUTZ-1 cells,in which JC-1 maintains monomeric form,thus showing only green fluorescence.The decreases of △?m were in a time-dependent manner,which were significantly higher than those in control group(P

10.3969/j.issn.1007-3969.2013.05.008

This study is to investigate the effect of total flavonoids of Uygur medicine bugloss (BTF) on rats with myocardial ischemia/reperfusion injury, and to explore the mechanisms by which it acts. Left anterior descending (LAD) coronary artery in rats was occluded for 30 min followed by 4 h reperfusion. Meanwhile, BTF dissolved in saline was administered intraperitoneally at dosage of 10, 30 and 50 mg x kg(-1). Electrocardiograph, infarction index, serum myocardial enzymes and heart function were determined to evaluate the effect of BTF. Some other observations were carried out to explore whether inhibiting inflammation and apoptosis is involved in the mechanisms underlying BTF. Our results showed that in ischemia/reperfusion injured rats BTF could dose-dependently reduce myocardial infarction index and myocardial enzyme leakage, and enhance heart function, indicating that it possesses significant cardio protection. ELISA analysis showed that BTF could decrease the content of myocardial inflammatory cytokines such as IL-1beta, IL-6 and TNF-alpha. Western-blotting confirmed that BTF could increase the expression of anti-apoptotic protein Bcl-2 and reduce the expression of proapoptosis protein Bax. Further more, the phosphorylation level of PI3K and Akt was upregulated by BTF treatment. BTF can protect rat against myocardial ischemia/reperfusion injury. Anti-inflammation and inhibition of apoptosis through upregulating PI3K/Akt signal pathway may contribute to the protective effect of BTF.
Animals ; Apoptosis ; Apoptosis Regulatory Proteins ; Boraginaceae ; chemistry ; Flavonoids ; pharmacology ; Heart ; Interleukin-6 ; Myocardial Infarction ; Myocardial Reperfusion Injury ; drug therapy ; Myocardium ; Phosphatidylinositol 3-Kinases ; Phosphorylation ; Protective Agents ; Proto-Oncogene Proteins c-akt ; Rats ; Signal Transduction ; Tumor Necrosis Factor-alpha ; bcl-2-Associated X Protein

Objective To investigate the influence of CT-guided thermochemotherapy for pig's healthy pancreas and in turn to discuss the feasibility and efficacy on pancreatic tumors.Methods 9 healthy pigs were undergone CT-guided 80℃themochemotherapy with 18 G fine meedle injecting individually of 5-Fu 750mg(10 ml)into the pancreatic tail within 2min.CT,MRI and serum analyses test were carried out as the follow up study at 1h,3rd,7th and 14th day after the procedure;since the 3rd day,3 pigs were sacrificed right after every follow up and together with comparative study between diagnostic imagings and pathologic changes. Results The pig pancreatic tail necrotic lesions appeared to be most conspicuous at the 3rd day after thermochemotherapy and shrank gradually from 7th day to 14th day.Serum amylase level reached the highest at 3rd day after the treatment and lowered down at 7th day;and near approximately normal at 14th day.The outcomings of diagnostic imagings and macroscopic pathology were in accordance.Obvious pancreatitis occurred only in one pig and all others were nearly uneventful without serious complications of pancreatitis,intestinal adhesion and mortaligy.Conclusion CT-guided themochemotherapy can induce pancreatic,focal necrosis in healthy pig but with no serious complications;and these can further more establish the foundation for clinical practiee.(J Intervent Radiol,2007,16:844-846)

Objective To investigate the effects of high spermatic vessel dissection on testicular morphological alteration of SD rats in prepuberty,puberty and sexual maturity phases.Methods Thirty-day-old SD rats were divided into 2 groups underwent sham operation and left high spermatic vessel dissection as a simulation of Palomo′s maneuver.Detailed morphological investigations were made at 3 different postoperative intervals among the 3rd day,30th day and 56th day.Results High spermatic vessel dissection in prepubertal rats induced acute testicular ischemia in the operated testes on the 3rd day.Most of the operated testes on the 30th day showed testicular atrophy.And all the operated testes showed testicular atrophy and sperm disappearance in epididymis on the 56th day.Conclusion High dissection of spermatic vessel in prepubertal rats induced testicular ischemia in prepuberty and testicular growth failure in puberty,testicular atrophy completely and sperm production losing in sexual maturity phase.

OBJECTIVETo study the effect of 2-methoxyestradiol(2-ME) on telomerase activity expression and apoptosis in human myelodysplastic syndrome cells line MUTZ-1.

METHODSMUTZ-1 cells were incubated with different concentrations of 2-ME, apoptosis rate and cell cycle were measured by flow cytometry (FCM). Telomerase activity in MUTZ-1 cells was examined by telomeric repeat amplification protocol-Enzyme linked immunosorbent assay (TRAP-ELISA).

RESULTSThe FCM analysis showed that cells in G0/G1 phase and S phase were decreased, while in G2/M phase increased after exposed to 1,2 and 4 micromol/L of 2-ME for 12 hours (P < 0.05). 1 and 2 micromol/L of 2-ME had no notable effect on MUTZ-1 cells as compared with the control group (P > 0. 05). Cells incubated with 1, 2 and 4 micromol/L of 2-ME for 36 hours were induced apoptosis, the percentage of apoptosis was between (12.87 +/- 0.86)% and (21.82 +/- 1.71)% with a dose- and time- dependent manner. Telomerase activity was significantly inhibited in these concentration and negatively correlated with cell number in G2/M phase (r = -0.979, P = 0.021) and increased apoptosis (r = -0.970, P = 0.030 ), respectively. Moreover, the inhibition effect of telomerase activity was enhanced in a dose- and time- dependent manner.

CONCLUSIONS2-ME-induced apoptosis and inhibition of telomerase activity provide a possible mechanism for explaining the 2-ME's anticancer activity.

Apoptosis ; drug effects ; Cell Cycle ; drug effects ; Cell Line ; Estradiol ; analogs & derivatives ; pharmacology ; Humans ; Myelodysplastic Syndromes ; enzymology ; pathology ; Telomerase ; metabolism

To study the effects and possible mechanism of Vitamin K(2) (VK(2)) in the treatment of MDS-JSN04 cells, the changes of morphologic features of MDS-JSN04 cells were investigated by cytomorphology, the apoptosis of MDS-JSN04 cells was observed by transmission electron microscope; cellular proliferation was determined by the MTT assay; cell apoptosis, cell cycle shift and expression of myeloid-specific differentiation antigen (CD11b, CD13) were analyzed by flow cytometry (FCM). The expression of apoptosis-related genes bcl-2, survivin and bax were detected by retrotranscriptase polymerase chain reaction (RT-PCR); the activity of caspase-3 was determined by chemiluminescence assay. The results showed that the typical apoptotic morphological features appeared in cells treated with VK(2) for 72 hours; VK(2) induced apoptosis of MDS-JSN04 cells and in a dose-and-time-dependent manner, G(0)/G(1) cell arrest and significantly down-regulated the expression of bcl-2 and survivin, but had no effect on the expression of bax; the activity of caspase-3 significantly increased. It is concluded that VK(2) induces apoptosis of MDS-JSN04 cells through activating caspase-3 pathways and the apoptosis-related genes bcl-2, survivin may play an important role in this process.
Apoptosis ; drug effects ; CD11b Antigen ; analysis ; CD13 Antigens ; analysis ; Caspase 3 ; metabolism ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Flow Cytometry ; Gene Expression Regulation, Neoplastic ; Humans ; Inhibitor of Apoptosis Proteins ; Luminescent Measurements ; methods ; Microscopy, Electron, Transmission ; Microtubule-Associated Proteins ; genetics ; Myelodysplastic Syndromes ; genetics ; metabolism ; pathology ; Neoplasm Proteins ; genetics ; Proto-Oncogene Proteins c-bcl-2 ; genetics ; Reverse Transcriptase Polymerase Chain Reaction ; methods ; Vitamin K 2 ; pharmacology ; bcl-2-Associated X Protein ; genetics

OBJECTIVETo study effects of soy extract on lipid metabolims in ovariectomized rats.

METHOD90 Wistar rats were randomly divided into 9 groups: control group, sham group, model group, estrogen group, soy isoflavone group of high dose, soy isoflavone group of low dose, soy extract of high dose, soy extract of low dose, and soy polysaccharde group, 10 rats in each group. Except fer of control and sham groups, the test rats were ovariectomized. One week after operation, the rats were treated with different drugs. Six weeks after operation, the rats were killed, with serum and liver taken, and serumglycerol(sGT), cholesterol(sGC), LDL, HDL and liver homogenate hGT, hGC, measured.

RESULTThe level of sGC, LDL in ovariectmized rats increased significantly, compared with that in control and sham groups. In liver both the level of hGT and hGC were higher than that in liver from control and sham groups. Administration of estrogen or soy extract or soy isoflavone could attenuate these in ovariectomized rats, but soy polysacchardes did not have any effects.

CONCLUSIONOvariectomized rats have an imbalance of lipid metabolism, the level of hGT and hGC were increased, and administration of estrogen, soy extracts or soy isoflavone could decrease these changes induced by ovariectomizing.

Animals ; Cholesterol ; blood ; metabolism ; Estriol ; analogs & derivatives ; pharmacology ; Female ; Isoflavones ; isolation & purification ; pharmacology ; Lipoproteins, LDL ; blood ; Liver ; metabolism ; pathology ; Ovariectomy ; Plant Extracts ; isolation & purification ; pharmacology ; Quinestrol ; analogs & derivatives ; Random Allocation ; Rats ; Rats, Wistar ; Soybeans ; chemistry ; Triglycerides ; blood ; metabolism