Alzheimer Disease ; drug therapy ; genetics ; prevention & control ; Amyloid beta-Peptides ; genetics ; Animals ; Disease Models, Animal ; Mice ; Mice, Transgenic ; Phytotherapy ; Presenilin-1 ; genetics

Radiotherapy is an important treatment on gynecological tumors,especially for brachyther- apy.~(137)Cs,~(192)Ir were usually used in the past,but the local control and survival rates were not increased obvi- ously.The machines,that was made in China,of ~(252)Cf neutrons brachytherapy were used already by many hos- pitals in our country and played a preponderant role more and more.It can increase the local control and sur- vival rates effectively on gynecological tumors.

This study was to examine the mechanism of oleanolic acid (OA) induces G2/M phase arrest and apoptosis in human hepatocellular carcinoma Bel-7402 cells. MTT and trypan blue exclusion test assay were adopted to detect the proliferate status of cells treated with OA. We assayed the cell cycle by flow cytometry using PI staining. Apoptosis was determined by Annexin V-FITC staining and PI labeling. The expressions of cycle related proteins and apoptotic related proteins were determined by Western blot analysis. OA strongly inhibited human hepatoma cells proliferation. When Bel-7402 cells were pretreated with OA for 24 h, OA induced apoptosis and G₂/M phase cell cycle arrest in a concentration-dependent manner. Analysis of the cell cycle regulatory proteins demonstrated that OA decreased the protein levels of cyclin B1, but increased the protein levels of p-Cdk1 (Tyr15) and p-Cdc25C (Ser 216). Moreover, OA modulated the phosphorylation of protein kinases Chk1 and p2l. Western blotting assay also showed significant decrease of Bcl-2 protein expression and increase of Bax protein expression, the cytosol Cyt c level, cleaved-caspase-9 and cleaved-caspase-3 activity. These data suggest that OA produces anti-tumor effect via induction of G₂/M cell cycle arrest and apoptosis.
Apoptosis ; drug effects ; Carcinoma, Hepatocellular ; drug therapy ; pathology ; Cell Line, Tumor ; G2 Phase Cell Cycle Checkpoints ; drug effects ; Humans ; Liver Neoplasms ; drug therapy ; pathology ; M Phase Cell Cycle Checkpoints ; drug effects ; Oleanolic Acid ; pharmacology

Alzheimer Disease ; drug therapy ; enzymology ; Amyloid Precursor Protein Secretases ; antagonists & inhibitors ; Animals ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Humans ; Medicine, Chinese Traditional ; methods ; Membrane Glycoproteins ; antagonists & inhibitors ; Molecular Targeted Therapy ; Phytotherapy ; methods ; Presenilins ; antagonists & inhibitors

Objective To investigate the establishment of rabbit model of obstructive sleep apnea syndrome(OSAS) through hypobaric hypoxia and their changes in pathophysiology.Methods Twelve adult rabbits were randomly assigned to 2 groups,control group and experimental group.The rabbits of experimental group were placed in hypobaric hypoxia cabin,in which the altitude was 5 000 m,10 h daily,for 4 weeks.The rabbits of control group were raised normally.The airway were scanned by CT,arterial blood gas was analyzed and respiratory airflow was monitored.The rabbits were sacrificed after the experiment,and pharyngeal tissue and genioglossus were harvested for pathological examination.Results In hyoid bone plane of upper airway,the pharyngeal of experimental group showed significant thickened(P

OBJECTIVETo study the role of PI3K/Akt pathway in the neuroprotective effect of paeoniflorin on PC12 cells.

METHODThe paeoniflorin group (5, 10, 20 μmol · L(-1)) was pretreated for 30 min, and then added with Aβ25-35 (20 μmol · L(-1)) for interaction for 24 h. Inhibitor LY294002 (10 μmol · L(-1)) was pretreated for 30 min before the action of paeoniflorin (10 μmol · L(-1)). The MTT colorimetric method was used to detect the cell viability. The apoptosis rate was tested by the FITC-Annexin V/PI staining. The protein expression of p-AKT, Bax, Bcl-2 and cleaved caspase-3 protein were detected by Western blot analysis.

RESULTPaeoniflorin could significantly inhibit the Aβ25-35-induced PC12 cell toxicity and apoptosis. Its protection effect may be achieved by up- regulating AKT phosphorylation level, increasing Bcl-2 protein expression, reducing Bax protein expression, inhibiting the activation of caspase-3. Inhibitor LY294002 could weaken the above protective effects of paeoniflorin.

CONCLUSIONPaeoniflorin could activate PI3K/Akt signaling pathway to protect the PC12 cell injury induced by Aβ25-35.

Alzheimer Disease ; drug therapy ; genetics ; metabolism ; physiopathology ; Amyloid beta-Peptides ; toxicity ; Animals ; Apoptosis ; drug effects ; Cell Survival ; drug effects ; Drugs, Chinese Herbal ; pharmacology ; Glucosides ; pharmacology ; Humans ; Monoterpenes ; pharmacology ; Neurons ; cytology ; drug effects ; metabolism ; Neuroprotective Agents ; pharmacology ; PC12 Cells ; Peptide Fragments ; toxicity ; Phosphatidylinositol 3-Kinases ; genetics ; metabolism ; Proto-Oncogene Proteins c-akt ; genetics ; metabolism ; Proto-Oncogene Proteins c-bcl-2 ; genetics ; metabolism ; Rats ; Signal Transduction ; drug effects

Boronic Acids ; adverse effects ; Bortezomib ; Humans ; Peripheral Nervous System Diseases ; chemically induced ; Pyrazines ; adverse effects

Carcinoma ; complications ; Carcinoma, Papillary ; Female ; Histiocytosis, Langerhans-Cell ; complications ; Humans ; Middle Aged ; Thyroid Neoplasms ; complications

OBJECTIVETo observe the reconstruction features of adventitia in senescent rats, and to explore the intervention mechanism of Chinese herbs (CH, extracts from Radix Ginseng, Radix Notoginseng, and Rhizoma Chuanxiong).

METHODSTotally 85 20-month senescent rats were randomly divided into 5 groups according to body weight, i.e., the aging model group, the high dose CH group, the middle dose CH group, the low dose CH group, the Losartan group, 17 in each group. Another 14 2-month old Wistar rats were selected as a young group. Extracts of CH at the daily dose of 1493. 4, 746. 7, and 373. 4 mg/kg were administered to rats in the 3 CH groups respectively by gastrogavage. Losartan suspension at the daily dose of 10 mg/kg was administered to rats in the Losartan group by gastrogavage. Equal volume of distilled water was administered to rats in the aging model group and the young group. All medication was performed once daily. After 15-week intervention, morphological changes of thoracic aorta were observed by HE staining. The types, distribution, and contents of vessel wall collagens were determined using picric acid picrosirius red staining. The plasma renin activity (PRA) , the concentration of rennin angiotensin II (Ang II), and the content of Ang II in adventitia were detected by radioimmunoassay. The content of hydroxyproline ( Hyp) was detected by biochemical analysis. mRNA contents and protein expressions of angiotensin II receptor 1 (AT1R) and angiotensin II receptor 2 (AT2R) were detected by real-time PCR (RT-PCR) and Western blot.

RESULTSCompared with the young group, thickened adventitia, increased adventitia thickness/caliber, accumulated collagen fiber, increased area of type I collagen, decreased area of type III collagen, decreased type III/I collagen area ratio (P <0. 05), decreased plasma PRA and Ang II (P < 0.01, P < 0.05), increased contents of Ang II and Hyp in adventitia, down-regulated mRNA and protein expressions of AT1R, and up-regulated mRNA and protein expression of AT2R could be seen in the aging model group (P < 0.05). Compared with the aging model group, morphological changes could be improved in the 3 CH groups. Adventitia thickness/caliber was reduced in middle and high dose CH groups, as well as the Losartan group. The area of type I collagen was reduced and the area of type III collagen was enlarged, type III/I collagen area ratio obviously increased, contents of adventitia Hyp was obviously lowered in the high dose CH groups and the Losartan group (P < 0.05, P < 0.01). Ang II levels in adventitia decreased in middle and high dose CH groups and the Losartan group (P < 0.05, P < 0.01). There was no statistical difference in PAR among all groups (P > 0.05). Compared with the aging model group, mRNA expression of AT1R all increased in each treatment group (P < 0.01); mRNA expression of AT2R also increased in middle and high dose CH groups (P < 0.05). Protein expression of AT1R increased in the high dose CH group and the Losartan group (P < 0.01, P < 0.05); protein expression of AT2R also increased in middle and high dose CH groups (P < 0.05).

CONCLUSIONSAdventitia remodeling occurred in aged rats, manifested as thickened adventitia and accumulated collagens, disordered ratios of collagen I and III. Its mechanism might be possibly associated with aactivation of renin-angiotensin system (RAS). Extracts from Radix Ginseng, Radix Notoginseng, and Rhizoma Chuanxiong could improve adventitial remodeling possibly by interfering multi-targets, such as Ang II and AT1R, thereby delaying vascular aging.

Adventitia ; drug effects ; Aging ; Angiotensin II ; Animals ; Aorta, Thoracic ; Drugs, Chinese Herbal ; pharmacology ; Losartan ; Panax ; Plant Roots ; RNA, Messenger ; Rats ; Rats, Wistar ; Renin-Angiotensin System ; Rhizome

OBJECTIVE To investigate the regulation of {O2 (2,4-dinitrophenyl)1-〔(4-ethoxycarbonyl) piperazin-1-yl〕diazen-1-ium-1,2-diolate}(JS-K), anitric oxide donor, on tumor energy metabolism in H22 tumor- bearing mice. METHODS The hepatoma animal model in BALB/c mice was established with H22 cell line. The JS-K group and model group were received JS-K (0.75 and 1.5 mg?kg-1) and saline via tail intravenous once every 3 d for 14 d, received 5 injections, respectively. The positive group was received 5-FU 20 mg·kg- 1 by intraperitoneal injection once a day for 14 d. On the 15th day mice were sacrificed. The tumor growth inhibition rate were calculated. The activities of hexokinase (HK), phospho?fructo kinase (PFK), pyruvate kinase (PK), succinate dehydrogenase (SDH), adenosine triphosphatase (ATPase), and the levels of lactic acid (LD) and adenosine triphosphate (ATP) in tumor tissues were de?termined by colorimetric method. RESULTS Compared with model group, the tumor mass of JS- K 0.75 and 1.5 mg·kg- 1group was significantly reduced (P<0.01),and the tumor growth inhibition rate was 23.9% and 50.3%, respectively. The activity of HK, PFK, PK, SDH and ATPase of tumor tissue in model group was (22.6±3.7, 14.4±2.6, 12.9±3.2 and 10.5±2.6)U·g-1 protein and (0.70±0.10)μmolPi·mg-1 protein per hour, respectively; which in JS-K 1.5 mg?kg-1 group was dropped by 42.0%, 26.6%, 22.7%, 23.3% and 21.7% (P<0.01, P<0.05). Compared with the model group, the level of ATP and LD in JS-K group was dropped (P<0.01). CONCLUSION JS-K can inhibit the growth of tumor in H22 tumor-bearing mice and its mechanism may be related to regulating the tumor energy metabolism with inhibition of glycolysis and aerobic oxidation.