No abstract available.
Angiotensin II* ; Angiotensins* ; Hydrocortisone* ; Insulin*

No abstract available.
Gastrins*

BACKGROUNDStudies have shown that oxidized low density lipoprotein (ox-LDL) promotes the pathogenesis and development of atherosclerosis (AS), and that the proliferation, migration and phenotype alteration of vascular smooth muscle cells (vSMCs) into foam cells are critical changes in AS. It is proposed that ox-LDL might play a novel role in the pathologic process of vSMCs. The present study was performed ex vivo to investigate the effects of ox-LDL on the growth of cultured human vSMCs.

METHODSUsing NaBr density gradient centrifugation, LDL from human plasma was isolated and purified. ox-LDL was produced from LDL after being incubated with CuSO4. ox-LDL was then added to the culture medium at different concentrations (25 microg/ml, 50 microg/ml, 75 microg/ml, 100 microg/ml, 125 microg/ml, and 150 microg/ml) for 7 days. The influence of ox-LDL on vSMC growth was observed from several aspects as growth curve, mitosis index, lipid staining, and in situ determination of apoptosis. The digital results were analyzed with SPSS 10.0.

RESULTSThe ox-LDL produced ex vivo had a good purity and optimal oxidative degree, which was similar to the intrinsic ox-LDL in atherosclerotic plaque. ox-LDL at a concentration of 25 microg/ml demonstrated the strongest proliferation. At the concentration of 125 microg/ml, ox-LDL suppressed the growth of vSMCs. At concentrations of 25 microg/ml and 50 microg/ml, ox-LDL presented powerful mitotic trigger. When the concentration of ox-LDL increased, the mitotic index of vSMCs decreased gradually. ox-LDL induced more foam cells from vSMCs with rich intracellular lipid accumulation at concentrations of 25 microg/ml and 50 microg/ml. ox-LDL at higher concentrations induced more apoptotic vSMCs.

CONCLUSIONSox-LDL at lower concentrations may trigger proliferation and phenotype alteration into foam cells of vSMCs, and at higher concentrations it may induce apoptosis in vSMCs. ox-LDL plays an important role in the pathogenesis and development of atherosclerosis by its effect on vSMCs proliferation, phenotype alteration and apoptosis.

Apoptosis ; drug effects ; Atherosclerosis ; etiology ; Cell Proliferation ; drug effects ; Cells, Cultured ; Dose-Response Relationship, Drug ; Humans ; Lipoproteins, LDL ; toxicity ; Mitotic Index ; Muscle, Smooth, Vascular ; cytology ; drug effects ; Myocytes, Smooth Muscle ; cytology ; drug effects

OBJECTIVETo assess the effect of long-term high-fat diet on the expressions of insulin receptor substrates in the hippocampus and spatial learning and memory ability of obese rats.

METHODSA total of 100 4-week-old male SD rats were randomly divided into two groups and fed with common diet (CD group, n=40) or high-fat diet (HFD group, n=60) for 16 weeks. At 4, 8, 12, 16 and 20 weeks, 8 rats were randomly selected from each group for testing their spatial learning and memory function using Morris water maze. After the tests, the rats were sacrificed for measurement of the metabolic parameters and detection of the expressions of insulin receptor substrate-1 (IRS-1) and IRS-2 mRNAs in the CA1 region of the hippocampus.

RESULTSCompared with those in CD group, the rats in HFD group showed a prolonged escape latency, longer swimming distance, faster average swimming speed, and shorter stay in the platformat 12 weeks. In HFD group, the serum levels of total cholesterol, triglyceride, low-density lipoprotein cholesterol, and fasting insulin were all significantly increased (P<0.05) and the level of high-density lipoprotein cholesterol decreased (P<0.01) in comparison with those in CD group at each of the time points. No significant difference was found in fast glucose levels between the two groups (P>0.05), but the expressions of IRS-1 and IRS-2 mRNAs were significantly decreased in HFD group at 12 weeks (P<0.05).

CONCLUSIONIn obese rats, long-term feeding with high-fat diet leads to insulin resistance, which interferes with hippocampal expression of insulin receptor substrates and insulin metabolism to cause impairment of the cognitive function and accelerate cognitive deterioration.

BACKGROUND: Chronic noise exposure is one environmental hazard that is associated with genetic susceptibility factors that increase Alzheimer's disease (AD) pathogenesis. However, the comprehensive understanding of the link between chronic noise stress and AD is limited. Herein, we investigated the effects of chronic noise exposure on AD-like changes in senescence-accelerated mouse prone 8 (SAMP8). METHODS: A total of 30 male SAMP8 mice were randomly divided into the noise-exposed group, the control group, and aging group (positive controls), and mice in the exposure group were exposed to 98 dB SPL white noise for 30 consecutive days. Transcriptome analysis and AD-like neuropathology of hippocampus were examined by RNA sequencing and immunoblotting. Enzyme-linked immunosorbent assay and real-time PCR were used to further determine the differential gene expression and explore the underlying mechanisms of chronic noise exposure in relation to AD at the genome level. RESULTS: Chronic noise exposure led to amyloid beta accumulation and increased the hyperphosphorylation of tau at the Ser202 and Ser404 sites in young SAMP8 mice; similar observations were noted in aging SAMP8 mice. We identified 21 protein-coding transcripts that were differentially expressed: 6 were downregulated and 15 were upregulated after chronic noise exposure; 8 genes were related to AD. qPCR results indicated that the expression of Arc, Egr1, Egr2, Fos, Nauk1, and Per2 were significantly high in the noise exposure group. These outcomes mirrored the results of the RNA sequencing data. CONCLUSIONS These findings further revealed that chronic noise exposure exacerbated aging-like impairment in the hippocampus of the SAMP8 mice and that the protein-coding transcripts discovered in the study may be key candidate regulators involved in environment-gene interactions.

OBJECTIVE: To observe the clinical efficacy of different treatment frequency of auricular bloodletting combined with auricular point sticking for acne vulgaris. METHODS: A total of 90 patients with acne vulgaris were randomized into a treatment group 1 (30 cases, 2 cases dropped off), a treatment group 2 (30 cases, 4 cases dropped off) and a treatment group 3 (30 cases, 5 cases dropped off). Combination therapy of auricular bloodletting and auricular point sticking at Fei (CO₁₄), Shenmen (TF₄), Neifenmi (CO₁₈) and Shenshangxian (TG₂p) were given once a week, twice a week and 3 times a week in the treatment group 1, the treatment group 2 and the treatment group 3 respectively, 4 weeks were as one course and totally 3 courses were required in the 3 groups. Before treatment and after 1, 2, 3 courses of treatment, the scores of global acne grading system (GAGS), skin lesion and quality of life-acne (QoL-Acne) were observed, the clinical efficacy was evaluated after 3 courses of treatment and the recurrence rate was evaluated in follow-up of 1 month after treatment in the 3 groups. RESULTS: Compared before treatment, the scores of GAGS and skin lesion were decreased at each time point in the 3 groups (P<0.05), the QoL-Acne scores were increased after 1 course of treatment in the treatment group 3 and after 2, 3 courses of treatment in the 3 groups (P<0.05). There were no statistical differences in scores of GAGS, skin lesion and QoL-Acne among the 3 groups (P>0.05). There were no statistical differences in effective rate and recurrence rate among the 3 groups (P>0.05). CONCLUSION Different frequency of auricular bloodletting combined with auricular point sticking have similar efficacy in treating acne vulgaris, all can improve the skin lesion and quality of life in patients with acne vulgaris, and have a cumulative effect and good long-term curative effect.
Acne Vulgaris/therapy* ; Acupuncture Points ; Acupuncture, Ear ; Bloodletting ; Humans ; Quality of Life ; Treatment Outcome

Dihydroflavonol 4-reductase (DFR) plays an essential role in the biosynthesis of anthocyanin and regulation of plant flower color. Based on the transcriptome data of Cistanche tubulosa (Schenk) Wight, a full-length cDNA sequence of CtDFR gene was cloned by reverse transcription-polymerase chain reaction (RT-PCR). CtDFR contains an open reading frame (ORF) of 1 263 bp which encodes 420 amino acids with a predicted molecular weight of 47.5 kDa. The sequence analysis showed that CtDFR contains a nicotinamide adenine dinucleotide phosphate (NADPH) binding domain and a specific substrate binding domain. The expression analysis indicated that CtDFR was highly expressed in red and purple flowers, and the relative expression levels were 4.04 and 19.37 times higher than those of white flowers, respectively. The recombinant CtDFR protein was expressed in E.coli BL21 (DE3) using vector pET-28a-CtDFR and was purified. In vitro enzyme activity analysis, CtDFR could reduce three types of dihydroflavonols including dihydrokaempferol, dihydroquercetin, and dihydromyricetin to leucopelargonidin, leucocyanidin and leucodelphinidin. Subcellular localization analysis showed that CtDFR was mainly localized in the cytoplasm. These results demonstrate that CtDFR plays an important role in regulation of flower color in C. tubulosa and make a valuable contribution for the further investigation on the regulation mechanism of C. tubulosa (Schenk) Wight flower color.