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1.
Article in English | WPRIM | ID: wpr-903977

ABSTRACT

Although the contributions of sitagliptin to endothelial dysfunction in diabetes mellitus were previously reported, the mechanisms still undefined. Autophagy plays an important role in the development of diabetes mellitus, but its role in diabetic macrovascular complications is unclear. This study aims to observe the effect of sitagliptin on macrovascular endothelium in diabetes and explore the role of autophagy in this process. Diabetic rats were induced through administration of high-fat diet and intraperitoneal injection of streptozotocin. Then diabetic rats were treated with or without sitagliptin for 12 weeks. Endothelial damage and autophagy were measured. Human umbilical vein endothelial cells were cultured either in normal glucose or in high glucose medium and intervened with different concentrations of sitagliptin. Rapamycin was used to induce autophagy. Cell viability, apoptosis and autophagy were detected. The expressions of proteins in c-Jun N-terminal kinase (JNK)-Bcl-2-Beclin-1 pathway were measured. Sitagliptin attenuated injuries of endothelium in vivo and in vitro. The expression of microtubuleassociated protein 1 light chain 3 II (LC3II) and beclin-1 were increased in aortas of diabetic rats and cells cultured with high-glucose, while sitagliptin inhibited the over-expression of LC3II and beclin-1. In vitro pre-treatment with sitagliptin decreased rapamycin-induced autophagy. However, after pretreatment with rapamycin, the protective effect of sitagliptin on endothelial cells was abolished. Further studies revealed sitagliptin increased the expression of Bcl-2, while inhibited the expression of JNK in vivo . Sitagliptin attenuates injuries of vascular endothelial cells caused by high glucose through inhibiting over-activated autophagy. JNK-Bcl-2-Beclin-1 pathway may be involved in this process.

2.
Article in English | WPRIM | ID: wpr-896273

ABSTRACT

Although the contributions of sitagliptin to endothelial dysfunction in diabetes mellitus were previously reported, the mechanisms still undefined. Autophagy plays an important role in the development of diabetes mellitus, but its role in diabetic macrovascular complications is unclear. This study aims to observe the effect of sitagliptin on macrovascular endothelium in diabetes and explore the role of autophagy in this process. Diabetic rats were induced through administration of high-fat diet and intraperitoneal injection of streptozotocin. Then diabetic rats were treated with or without sitagliptin for 12 weeks. Endothelial damage and autophagy were measured. Human umbilical vein endothelial cells were cultured either in normal glucose or in high glucose medium and intervened with different concentrations of sitagliptin. Rapamycin was used to induce autophagy. Cell viability, apoptosis and autophagy were detected. The expressions of proteins in c-Jun N-terminal kinase (JNK)-Bcl-2-Beclin-1 pathway were measured. Sitagliptin attenuated injuries of endothelium in vivo and in vitro. The expression of microtubuleassociated protein 1 light chain 3 II (LC3II) and beclin-1 were increased in aortas of diabetic rats and cells cultured with high-glucose, while sitagliptin inhibited the over-expression of LC3II and beclin-1. In vitro pre-treatment with sitagliptin decreased rapamycin-induced autophagy. However, after pretreatment with rapamycin, the protective effect of sitagliptin on endothelial cells was abolished. Further studies revealed sitagliptin increased the expression of Bcl-2, while inhibited the expression of JNK in vivo . Sitagliptin attenuates injuries of vascular endothelial cells caused by high glucose through inhibiting over-activated autophagy. JNK-Bcl-2-Beclin-1 pathway may be involved in this process.

3.
Neuroscience Bulletin ; (6): 735-742, 2019.
Article in English | WPRIM | ID: wpr-776487

ABSTRACT

ZNF804A rs1344706 has been identified as one of the risk genes for schizophrenia. However, the neural mechanisms underlying this association are unknown. Given that ZNF804A upregulates the expression of COMT, we hypothesized that ZNF804A may influence brain activity by interacting with COMT. Here, we genotyped ZNF804A rs1344706 and COMT rs4680 in 218 healthy Chinese participants. Amplitudes of low-frequency fluctuations (ALFFs) were applied to analyze the main and interaction effects of ZNF804A rs1344706 and COMT rs4680. The ALFFs of the bilateral dorsolateral prefrontal cortex showed a significant ZNF804A rs1344706 × COMT rs4680 interaction, manifesting as a U-shaped modulation, presumably by dopamine signaling. Significant main effects were also found. These findings suggest that ZNF804A affects the resting-state functional activation by interacting with COMT, and may improve our understanding of the neurobiological effects of ZNF804A and its association with schizophrenia.

4.
Chinese Journal of Radiology ; (12): 64-67, 2013.
Article in Chinese | WPRIM | ID: wpr-432963

ABSTRACT

Objective To analyze the CT imaging features of Castleman disease and enhance our knowledge of Castleman disease.Methods Twenty two patients with lymph node biopsy-proved or surgeryproved Castleman disease were retrospectively reviewed in this study.Of the 22 patients,18 had localized lesion and 4 patients had multicentric lesions.Correlation was made between CT and pathologic findings.Results Eighteen patients with localized Castleman disease had the hyaline-vascular type and showed well-circumscribed masses with soft-tissue density [mean CT value,(45 ± 16) HU],punctate or bifurcate calcification and linear low-density areas on non-enhanced CT images.All localized masses showed significant enhancementwith an increase of(56 ± 22)HU on arterial phase and showed residual enhancement and some low-density areas on delayed phase.Enhancing patterns were variable,including homogeneous enhancement,gradual enhancement from the edge to the center of mass and heterogeneous enhancement.Four patients with localized lesion demonstrated enhancing vessels around masses.Four patients with muhicentric CD belonged to the plasma cell type and had multiple enlarged lymph nodes.Plasma cell type masses with homogeneous density also showed enhancement after injection of contrast media but appeared to reveal a less increase of (32 ± 10) HU than the hyaline vascular type.Conclusions The localized Castleman disease showed certain characteristics on CT imaging includingcalcification and contrast enhancing patterns,which could help in the differential diagnosis of this disease.The muhicentric Castleman disease did not reveal any useful imaging features.

5.
Chinese Medical Journal ; (24): 511-516, 2012.
Article in English | WPRIM | ID: wpr-262581

ABSTRACT

<p><b>BACKGROUND</b>Despite recent reports on the molecular epidemiology of cryptococcal infections in China, clinical isolates have been mostly reported from human immunodeficiency virus (HIV)-negative patients, and environmental isolates from China have rarely been included. The aim of this study was to investigate the ecological profile of Cryptococcus (C.) neoformans and C. gattii in China.</p><p><b>METHODS</b>A survey was performed in 10 cities from 20°N (North latitude) to 50°N and in a Eucalyptus (E.) camaldulensis forestry farm at the Guixi forestry center, China.</p><p><b>RESULTS</b>Six hundred and twenty samples of pigeon droppings from 10 cities and 819 E. camaldulensis tree samples were collected and inoculated on caffeic acid cornmeal agar (CACA). The brown-colored colonies were recultured to observe their morphology, growth on canavanine-glycine-bromothymol-blue (CGB) medium, phenol oxidase and urease activities, serotype and mating type. There were obvious differences in the positive sample rates of C. neoformans in pigeon droppings collected from the different cities, ranging from 50% in the cities located at latitudes from 30°N - 40°N, 29% at 20°N - 30°N and 13% at 40°N - 50°N.</p><p><b>CONCLUSIONS</b>There were no differences in positive bevy rates (approximately 80%) among the three grouped cities. Mycological tests of 101 isolates purified from pigeon droppings revealed that they were C. neoformans var. grubii. We also observed variable capsular size around the C. neoformans cells in colonies with variable melanin production and the bio-adhesion of the natural C. neoformans cells with other microorganisms. One urease-negative C. neoformans isolate was isolated from pigeon droppings in Jinan city. No C. gattii was isolated in this study.</p>


Subject(s)
Animals , China , Columbidae , Microbiology , Cryptococcosis , Microbiology , Cryptococcus , Cryptococcus gattii , Cryptococcus neoformans , Eucalyptus , Microbiology , Feces , Microbiology
6.
Chinese Journal of Pathology ; (12): 99-103, 2011.
Article in Chinese | WPRIM | ID: wpr-295101

ABSTRACT

<p><b>OBJECTIVE</b>To investigate HIF-1α gene expression in human breast cancer cells and the role of HIF-1 in tumor metastasis and invasion.</p><p><b>METHODS</b>Human breast cancer cell lines were cultured under normoxic or hypoxic conditions. Western blot was used to evaluate the protein expression of HIF-1α, p-vimentin and α-tubulin. Small interfering RNA targeting HIF-1α was used to block the expression of HIF-1α in MDA-MB-231 and SK-BR-3 cell lines. Matrigel transwell and cell wound healing assays were used to detect the capability of cellular invasion and migration, respectively.</p><p><b>RESULTS</b>Under normoxic condition, all the cell lines tested showed a base-level of HIF-1α expression. The highest expression level of HIF-1α protein was obtained in the MDA-MB-231 cell line, which is also noticed to be highly invasive and migratory in behavior. HIF-1α siRNA was capable of blocking the protein expression of both HIF-1α and p-vimentin and in addition, the attenuated ability of invasion and migration.</p><p><b>CONCLUSION</b>Since HIF-1 is able to promote invasion and metastasis of tumor cells, which may be considered as a target in anti-cancer therapy.</p>


Subject(s)
Breast Neoplasms , Genetics , Metabolism , Pathology , Cell Line, Tumor , Cell Movement , Down-Regulation , Female , Gene Expression Regulation, Neoplastic , Humans , Hypoxia , Hypoxia-Inducible Factor 1, alpha Subunit , Genetics , Metabolism , Neoplasm Invasiveness , Neoplasm Metastasis , Phosphorylation , RNA, Small Interfering , Genetics , Vimentin , Metabolism
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