Elevated glucocorticoid damages gap junction structure and function in rat prefrontal cortex / 药学学报

In this article, we exogenously administered glucocorticoids to rats, observed changes in the structure and function of gap junctions in the prefrontal cortex (PFC) and studied the effects of glucocorticoid receptor (GR) inhibitor mifepristone on these changes. Subcutaneous injection of corticosterone (CORT) was used to increase glucocorticoid levels in rats, intragastric administration of mifepristone antagonist GR. Sucrose preference test was conducted to evaluate anhedonia. Dye transfer assay and electron microscopy were used to analyze the function and ultrastructural changes of gap junctions in astrocytes of PFC. Immunofluorescence was used to detect the expression of connexin 43 (Cx43). Animals exposed to CORT showed behavioral deficits in sucrose preference test, exhibited significant decreases in diffusion of gap junction channel-permeable dye and abnormal gap junctional ultrastructure, as well as reductions in Cx43 puncta density in the PFC. The behavioral and cellular alterations induced by CORT were reversed or blocked by treatment with the GR antagonist mifepristone. The results suggest that mifepristone can improve the gap junction function and structural damage of astrocytes in the PFC of depressive rats induced by CORT. In conclusion, the activation of the GR receptor may contribute to gap junction dysfunction in the PFC.

Protective effects of ginsenoside Rg1 against corticosterone-induced primary astrocytes injury / 药学学报

The study was designed to explore the effects and the underlying mechanism of ginsenoside Rg1 on corticosterone (CORT)-induced astrocytes injury. The primary hippocampal and prefrontal cortical astrocytes from rats were cultured and purified. CORT was used to stimulate stress condition. Western blot was used to detect the effects of ginsenoside Rg1 on the phosphorylation of Cx43. Cell Counting Kit (CCK8) was used to detect the effects of ginsenoside Rg1 on astrocytes viability. The roles of ginsenoside Rg1 was reversed by protein kinase inhibitors in the change of astrocytes morphology. Our results showed that ginsenoside Rg1 reversed the phosphorylation of Cx43 induced by CORT; ginsenoside Rg1 significantly upregulated the cell viability of astrocytes against CORT; the role of ginsenoside Rg1 was obviously inhibited by Src protein kinase inhibitors PP2 and Akt protein kinase inhibitors BAY1125976 in prefrontal cortical astrocytes; in hippocampal astrocytes, Src protein kinase inhibitor PP2, p38 protein kinase inhibitor SB203580, Akt protein kinase inhibitor BAY1125976 significantly inhibited the cell protective effects of ginsenoside Rg1. In conclusion, ginsenoside Rg1 improved the activity of Cx43 gap junctions in astrocytes exposed to CORT; ginsenoside Rg1 protected astrocytes against that CORT activated the Src, p38 and Akt signaling pathways, and the mechanism was different in prefrontal cortical and hippocampal astrocytes.

Significance and Clinical Application of the Establishment of RhD/C/c/E/e Blood Group Base in Chinese Nanyang City / 中国实验血液学杂志

<p><b>OBJECTIVE</b>To understand the regularity of Rh blood typing of valunteary blood donors in Chinese Nanyang city, and to estabbish a Rh DC/c/E/e antigen negative donor base so as to provide the help for clinical emergent blood transfusion to patients and ensure the safety of blood transfusion.</p><p><b>METHODS</b>The Rh D blood group of blood samples from 81462 voluntary blood donors in Chinese Nanyang city in 2014 was identified by serologic method; after first screening and confirmation, the RhE/e/C/c typing of Rh D negative samples was performed; the detailed infornation of donors was registered seriously by using unified creteria; the data base and base in kind of RhE/e/C/c types of valuntary donors were established by means of compater-mamayement system.</p><p><b>RESULTS</b>300 cases (0.37%) were RhD negative blood donors, and the Rh antigen was Ccdee and ccdee in 83%.</p><p><b>CONCLUSION</b>The proportion of RhD negative donors accounts for 4% of Chinese Nanyang peoples, the RhE/e/C/c types of RhD negative donors are ccdee (50.67%)>Ccdee (33.00%)>ccdEe(5.67%)>CCdee (5.33%)>CcdEe(5.33%). The establisment of RhE/e/C/c subbase can show importent significance for clinical blood transfusion.</p>

High insulin level promotes the degradation of high density lipoprotein generation-related functional protein ABCA1 through calpain and proteasome pathway in 3T3-L1 adipocytes / 中华心血管病杂志

<p><b>OBJECTIVE</b>To explore effects and potential mechanisms of high insulin environment on high density lipoprotein (HDL) generation-related functional protein ABCA1.</p><p><b>METHODS</b>[(3)H] labeled cholesterol efflux from mature 3T3-L1 adipocytes was detected by liquid scintillation counting. ABCA1 mRNA and protein expression in mature 3T3-L1 adipocytes post stimulation with various concentrations of insulin was detected by real-time fluorescence-based quantitative techniques and Western blot, respectively, in the absence and presence of CHX (cycloheximide, CHX), calpeptin (calpain pathway inhibitor) or MG-132 (proteasome pathway inhibitor).</p><p><b>RESULTS</b>Cholesterol efflux rates were reduced post insulin stimulation in a dose-dependent manner ((7.06 ± 0.27)%, (6.59 ± 0.30)%, (6.34 ± 0.24)%, (5.07 ± 0.40)%, and (4.71 ± 0.40)% at 0, 1, 10, 10², and 10³ nmol/L of insulin, P < 0.05). Cholesterol efflux rates decreased in a time-dependent manner post 10³ nmol/L insulin stimulation (6.52 ± 0.30)%, (5.59 ± 0.71)%, (5.44 ± 0.37)%, (4.52 ± 0.32)%, and (4.38 ± 0.33)% at 0, 2, 4, 6, 12 h, respectively). ABCA1mRNA levels were not affected by insulin (P > 0.05). ABCA1 protein level was significantly downregulated in 10³ nmol/L insulin group compared to 0 nmol/L insulin group (P < 0.01). Compared with the 0 h group, ABCA1 protein level was significantly reduced in 6 h group (P < 0.05) and further reduced in 12 h group (P < 0.01). Both calpeptin and MG-132 could partly reduce insulin-induced degradation of ABCA1. Compared with the negative control group, ABCA1 protein levels were significantly upregulated by cotreatment with calpeptin and MG-132, respectively (both P < 0.01).</p><p><b>CONCLUSION</b>Our data suggest that high insulin level could promote the ABCA1 protein degradation and reduce cholesterol efflux from mature 3T3-L1 adipocytes through calpain and proteasome pathway, thus, produce a circumference not suitable for nascent HDL formation in 3T3-L1 adipocytes.</p>

Leptin and clustering of the components of risk factors for metabolic syndrome / 中华预防医学杂志

<p><b>OBJECTIVES</b>To evaluate relationship between serum level of leptin and the components of risk factors for metabolic syndrome and to analyze the characteristics and laws of clustering of the risk factors.</p><p><b>METHODS</b>Totally, 795 non-diabetic adult Chinese subjects (691 men and 104 women, aged 40 - 75 years) from a diabetes prevalence survey in 2000 were involved in this study. Measurements included serum levels of true insulin (TI), leptin, fasting lipids, fasting glucose (FBG) and 2 h postchallenge glucose, as well as seated blood pressure (BP), body mass index (BMI), ratio of waist circumference to hip circumference (WHR), calculated quantitative insulin sensitivity check index (QUICKI), etc. Relationship between serum level of leptin and all the variables mentioned above was studied by statistical methods such as factor analysis, etc.</p><p><b>RESULTS</b>Serum level of leptin in the study subjects increased with the number of components of abnormal metabolism they had. Detection rates of obesity, hypertension, dyslipidemia and metabolic syndrome were significantly higher in those with the upper tertile of serum leptin level than in those with the lower tertile. Factor analysis revealed that variation of the 11 variables including serum level of leptin was affected by the three factors, i.e., the central factor associated with BMI, WHR, FTI, QUICKI and higher serum level of triglyceride (TG) and lower serum level of high-density lipoprotein-cholesterol (HDL-C), the glucose intolerance factor loaded with blood glucose level, FTI, QUICKI and higher serum level of TG (in women only) and the hypertension factor loaded with blood pressure and BMI (in men only), which could explain 62.0% and 66.7% of total variance in men and women, respectively, and higher serum level of TI and insulin resistance also loaded with both the central factor and glucose tolerance factor.</p><p><b>CONCLUSIONS</b>Serum level of leptin was significantly associated with the key markers of metabolic syndrome. Hyperleptinaemia could be a new component of metabolic syndrome. Clustering of the risk factors for metabolic syndrome could be affected by many factors, and although insulin resistance played an important role in it, insulin resistance alone could not explain its etiology.</p>

STUDIES ON THE LIPOTROPIC EFFECT OF THE PANCREAS Ⅲ. THE EXPERIMENTAL FATTY LIVER OF RATS AND THE CHANGES OF PANCREAS / 营养学报

When albino rats were fed with high cholesterol diet or injected With a large dose of carbon tetrachloride or chloroform, severe fatty liver developed but without any morphological changes in the pancreas. However, when fatty liver was produced with a protein free diet, the atrophic change in the acinar cells was observed prior to fatty infiltration in the liver. No change was found in the islets of Langerhans.The presence of lipocaic factor as an internal secretion of the pancreas cannot be verified by these studies or by our previous works.