Objective To investigate the impact on the endothelial cell function and renal blood flow through effective treatment for elderly patients with hypertension. Methods 64 cases of elderly hypertensive patients over 70years old with effective treatment, according to pre-treatment blood pressure, were divided into two groups: hyptension level-2 group(30cases) and hypertension level-3 group(34cases), and 30 cases of elderly people with health physical examination during the same period were setlected as the control group. Endothelial cell function was detected, including the endothelin-1 (ET-1)、 nitrous oxide (NO), thromboxane B2 (TXB2)、 6-keto-prostaglandinF1α (6-K-PDGF1α) in plasma. Renal blood flow was explored by color doppler ultrasonic instrument ,involving peak velocity in systole(PSV) and lowest velocity in end-diastole(EDV) of renal arteries, segmental arteries and interlobar arteries.After indicators had reached the standard 1 month in the hypertension level-2 and hypertension leve1-3 patients with effective antihypertensive therapy, the difference of ET-1, NO, TXB2,6-k-PGF1o and PSV, EDV among the three groups were compared. Results The differences were statistically significant in ET-1, NO, TXB2,6-k-PGF1α, PSV and EDV before treatment among three groups (P ＜ 0.05). After blood pressure treated had reached the standard 1 month,indicators were no statistically meaningful difference among the three groups (P ＞ 0.05). Conclusion After effective clinical treatments, the endothelial cell function and renal blood flow of the elderly hypertensive patients can be improved. At the same time, to delay renal damage in elderly patients with hypertension provide a theoretical basis.

Objective To investigate the expression of neuron-specific enolase(NSE) and bone morphogenic protein 4(BMP4) in different hippocampal areas of pentylenetetrazol(PTZ) kindled epilepsy rats and explore their relationship with the pathogenesis of epilepsy and brain injury.Methods Fifty male SD rats were divided into experimental group(n=40) and control group(n=10).The rats in experimental group were kindled into epilepsy by chemical method,and according to the kindling process,subdivided into four groups(grade Ⅰ,Ⅲ,Ⅳ,Ⅴ).Immunohistochemistry,in situ hybridization labeled with Dig-oligonucleotide probe and the image analyzing system were used to observe the expressions of NSE and BMP4 in rat hippocampus.Results In PTZ kindled epilepsy rats,the number of cells positive for NSE and BMP4 was increased in many regions of hippocampal formation.Compared with control group,the expressions of NSE and BMP4 in CA3 and DG was elevated obviously in the grade Ⅲ group and grade Ⅳ group(P

Objective To investigate the expression levels of the CD14 mRNA and TLR4 mRNA in peripheral blood mononuclear cells from patients with Parkinson disease and to explore the clinical signicance. Methods For?ty-four patients with Parkinson disease and 37 healthy controls were recruited. We recorded age of onset, duration of ill?ness and sex of all recruited patients. PD patients were evaulated using the Hoehn-Yahr stages, Unified Parkinson Dis?ease Rating Scale (UPDRS) Ⅱand UPDRS Ⅲ,non-motor symptoms scale (NMSS) on“off”time. Reverse transcrip?tion-polymerase chain reaction was performed to determine the expression levels of CD14 mRNA and toll-like receptor 4 (TLR4) mRNA. Results The expression levels of CD14 mRNA(1.459±0.658)2-△△CT and TLR4 mRNA (1.408±0.698)2-△△CT was significantly up-regulated (P<0.05) in Parkinson disease compared with controls((1.162 ± 0.631)2-△△CT、(1.122 ± 0.557)2-△△CT). In addition, there was positive correlation between the expression levels of CD14 mRNA in Parkinson dis?ease patients with the Hoehn-Yahr stages. Meanwhile, there was no significant correlation between the expression levels of CD14 mRNA and TLR4 mRNA with other clinical scores. Conclusions There is positive correlation between the ex?pression levels of CD14 mRNA in Parkinson disease patients with the Hoehn-Yahr stages,indicating that CD14/TLR4 positive monocyte may be involved in the pathogenesis of the Parkinson disease.

Objective To study the effect of exosomes ( EXs) released from high expression of miR-132-3p mesenchymal stem cells (MSCs) on hypoxia/reoxygenation (H/R) injured endothelial cell function. Methods MSCs extracted from bone marrow of C57BL/6 mice were cultured primarily. MSCmiR-132-3p was obtained from MSCs infected with lentivirus loaded with miR-132-3p vector. At the same time,MSCNC was obtained by infecting MSCs with control lentivirus loaded with scramble sequence. EXs released from MSCNCand MSCmiR-132-3pwas isolated,and MSC-EXs and MSC-EXsmiR-132-3pwere obtained respectively. The obtained EXs and H/R damaged mouse brain microvascular endothelial cells (bend3) were co-cultured. According to culture conditions,the cells were divided into normal culture group (normal cell culture),H/R group (making a H/R model),MSC-EXs group (MSC-EXs co-culture),MSC-EXsmiR-132-3p group (MSC-EXsmiR-132-3pco-culture), and MSC-EXsmiR-132-3p+ LY294002 group ( before the cells and MSC-EXsmiR-132-3pwere co-cultured,treated by adding phosphatidyl alcohol 3 kinase [ PI3K] signaling pathway blocker LY294002 [20 μmol/L]). Quantitative real-time quantitative polymerase chain reaction was used to detect the expression of miR-132-3p in MSCs,MSC-EXs,and bend3 cells. Angiogenesis kit was used to detect angiogenic ability of bend3 cells,and 3-(4,5-dimethylthiazole-2)-2,5-diphenyltetrazolium bromide (MTT) assay was used to detect the proliferative capacity of bend3 cells. Scratch test was used to detect the migration ability of bend3 cells. hochest33258 staining showed cell apoptosis. Western blot was used to detect the phosphorylation level of protein kinase B ( Akt) . Results Compared with the H/R group, the MSC-EXs treatment group significantly improved the angiogenesis,proliferation,migration abilities, and Akt phosphorylation level of bend 3 cell damage induced by H/R (The H/R group were 3 ± 1,0. 275 ± 0. 020,147 ± 8 μm,and 0. 89 ± 0. 12,respectively;the MSC-EXs treatment group were 8 ± 3,0. 358 ± 0. 030,218 ± 10 μm, and 1. 37 ± 0. 25 μm,respectively;all P<0. 01). Apoptosis was significantly reduced (47 ± 2% vs. 63 ± 2%,all P<0. 01). Compared with the MSC-EXs treatment group,the angiogenesis,proliferation,migration abilities,and Akt phosphorylation level of bend 3 cells in the MSC-EXsmiR-132-3ptreatment group were increased (14 ±3,0. 444 ± 0.050,357±10μm,and1.67±0.23,respectively,all P<0.01).Apoptosis was significantly reduced (34±1%,all P<0. 01) . Compared with the MSC-EXsmiR-132-3ptreatment group, cell proliferation, migration, angiogenesis abilities,and Akt phosphorylation level in the MSC-EXsmiR-132-3p+LY294002 group were significantly reduced (5 ± 2,0. 304 ± 0. 050,175 ± 8 μm and 0. 95 ± 0. 11,respectively,all P<0. 01). Conclusion MSC-EXs with high expression of miR-132-3p may improve many physiological functions of H/R-induced damaged cerebrovascular endothelial cells by activating PI3K/Akt signaling pathway.

OBJECTIVETo investigate the inhibitory effect of salinomycin on human breast cancer cells in vitro, and to explore the related molecular mechanism.

METHODSHuman breast cancer MDA-MB-231 cells were treated with salinomycin at different concentrations and at various time points. The effect of salinomycin on MDA-MB-231 cells proliferation was studied by CCK-8 method. The cell cycle status was examined by flow cytometry. RT-PCR and Western blot were used to detect the expression of Shh, Smo and Gli1 in the Hedgehog pathway at mRNA and protein levels.

RESULTSProliferation of MDA-MB-231 cells treated with salinomycin was markedly inhibited in a concentration and time dependent manner. Salinomycin at concentrations of 0, 0.4, 0.8 and 1.6 µmol/L inhibited the growth at the rates of 11.18%, 25.88%, 50.03%, 92.65%, respectively. Salinomycin prevented MDA-MB-231 cells from G1 into S phase. Salinomycin at concentrations of 0, 0.8 and 1.6 µmol/L resulted in S-phase percentage of 25.03%, 11.85% and 35.21%, respectively (P < 0.05). RT-PCR and Western blot showed that the expression of key elements Shh, Smo and Gli1 in the Hedgehog pathway was inhibited by salinomycin in a concentration dependent manner (P < 0.05).

CONCLUSIONSalinomycin prevents breast cancer cell transition from G1 to S phase through downregulation of the target genes of Hedgehog signaling pathway, leading to an effective inhibition of MDA-MB-231 cells.

Rab27a gene can participate in the secretion, transportation and exocytosis of T lymphocytes, mast cells, neutrophils, pancreatic β cells and hematopoietic cells through its encoded proteins, and participate in the development of diseases such as albinism, cancer, diabetes, inflammation and thrombosis. In addition, the secretion regulation of Rab27a to exosomes has also received much attention. The current research status of the secretion of exosome and the genetically modified exosomes of Rab27a gene in the treatment of diseases such as inflammatory injury, thrombosis and tumor were reviewed.