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Liu B.,Xian Central Hospital | Yuan B.,Xian Central Hospital | Zhang L.,Second Affiliated Hospital Of Xian Jiaotong University | Mu W.,Xian Central Hospital | Wang C.,Xian Central Hospital
International Journal of Clinical and Experimental Medicine | Year: 2015

Aim: Emodin was found effective in suppressing proliferation of cancer cells including colorectal cancer (CRC), but the mechanisms were still unclear. This study was aimed to investigate the possible mechanism of emodin’s anti-CRC effects. Methods: Two most frequently used CRC cell lines, SW480 and SW620, were investigated in this study. Serially diluted emodin solutions were used to incubate CRC cells. siRNAs were used to silence the expressions of p38 and Puma respectively. Intracellular ROS production was detected by DCFH-DA staining; proliferation and apoptosis of CRC cells were assessed by MTT assay and Hoechst staining respectively. Western blotting was applied to evaluate the activation of p38/p53/Puma signaling. Results: Both in SW480 and SW620 cells, emodin inhibited proliferation by inducing ROS-mediated apoptosis in a concentration-dependent manner. The p38/p53/Puma signaling was also activated after emodin incubation in a concentration-dependent manner. The ROS scavenger NAC, p38 silencing and Puma silencing impaired the anti-proliferation and apoptosis- inducing effects of emodin. Conclusions: emodin inhibited proliferation of human CRC cells by inducing cell apoptosis by activating ROS/p38/p53/Puma signaling. © 2015, E-Century Publishing Corporation. All rights reserved. Source


Yang D.,First Affiliated Hospital Of Xian Jiaotong University | Wang T.,First Affiliated Hospital Of Xian Jiaotong University | Wang T.,Shaanxi Key Laboratory Of Molecular Cardiology Xian Jiaotong University | Wang T.,Key Laboratory Of Environment And Genes Related To Diseases Xian Jiaotong University | And 9 more authors.
Journal of Membrane Biology | Year: 2015

Recent studies have shown that the sensitivity of apamin-sensitive K+ current (IKAS, mediated by apamin-sensitive small conductance calcium-activated potassium channels subunits) to intracellular Ca2+ is increased in heart failure (HF), leading to IKAS upregulation, action potential duration shortening, early after depolarization, and recurrent spontaneous ventricular fibrillation. We hypothesized that casein kinase 2 (CK2) interacted with small conductance calcium-activated potassium channels (SK) is decreased in HF, and protein phosphatase 2A (PP2A) is increased on the opposite, upregulating the sensitivity of IKAS to intracellular Ca2+ in HF. Rat model of volume-overload HF was established by an abdominal arteriovenous fistula procedure. The expression of SK channels, PP2A and CK2 was detected by Western blot analysis. Interaction and colocalization of CK2 with SK channel were detected by co-immunoprecipitation analysis and double immunofluorescence staining. In HF rat left ventricle, SK3 was increased by 100 % (P < 0.05), and SK2 was not significantly changed. PP2A protein was increased by 94.7 % in HF rats (P < 0.05), whereas the level of CK2 was almost unchanged. We found that CK2 colocalized with SK2 and SK3 in rat left ventricle. With anti-CK2α antibody, SK2 and SK3 were immunoprecipitated, the level of precipitated SK2 decreased by half, whereas precipitated SK3 was almost unchanged. In conclusion, the increased expression of total PP2A and decreased interaction of CK2 with SK2 may underlie enhanced sensitivity of IKAS to intracellular Ca2+ in volume-overload HF rat. © 2015, Springer Science+Business Media New York. Source


Ma D.L.,National University of Singapore | Qu J.Q.,Second Affiliated Hospital Of Xian Jiaotong University | Goh E.L.K.,National University of Singapore | Goh E.L.K.,Research Center | Tang F.R.,National University of Singapore
Frontiers in Neuroanatomy | Year: 2016

In this study, we investigated the reorganized basolateral amygdala (BLA)-subiculum pathway in a status epilepticus (SE) mouse model with epileptic episodes induced by pilocarpine. We have previously observed a dramatic loss of neurons in the CA1-3 fields of the hippocampus in epileptic mice. Herein, we observed a 43-57% reduction in the number of neurons in the BLA of epileptic mice. However, injection of an anterograde tracer, Phaseolus vulgaris leucoagglutinin (PHA-L) into the BLA indicated 25.63% increase in the number of PHA-L-immunopositive terminal-like structures in the ventral subiculum (v-Sub) of epileptic mice as compared to control mice. These data suggest that the projections from the basal nucleus at BLA to the vSub in epileptic mice are resistant to epilepsy-induced damage. Consequently, these epileptic mice exhibit partially impairment but not total loss of context-dependent fear memory. Epileptic mice also show increased c-Fos expression in the BLA and vSub when subjected to contextual memory test, suggesting the participation of these two brain areas in foot shock-dependent fear conditioning. These results indicate the presence of functional neural connections between the BLA-vSub regions that participate in learning and memory in epileptic mice. © 2016 Ma, Qu, Goh and Tang. Source


Gu Q.-Y.,Second Affiliated Hospital Of Xian Jiaotong University | Gu Q.-Y.,Affiliated Hospital Of Yanan University | Zhang J.,Second Affiliated Hospital Of Xian Jiaotong University | Feng Y.-C.,Affiliated Hospital Of Yanan University | And 2 more authors.
International Journal of Clinical and Experimental Medicine | Year: 2015

Objective: The present study aims to investigate the relationship between genetic polymorphisms in HTR3A and HTR3E and diarrhea predominant irritable bowel syndrome (D-IBS) in a Chinese population. Methods: We enrolled 500 D-IBS patients and 500 age- and sex-matched healthy control subjects to detect the genotypes in HTR3A and HTR3B gene by using of PCR-RFLP method. Results: There were significant difference between the D-IBS patients and the health control subjects in the distribution of genotype and allele of rs1062613 in HTR3A gene. As regarding rs62625044 in HTR3E gene, we found there was a significant different between the case and the control group in the distribution of GA genotype and A allele in female but not in male. Conclusion: The present study suggested that there are associations of D-IBS risk with genetic polymorphisms in HTR3A and HTR3E. © 2015, Int J Clin Exp Med. All rights reserved. Source


Yongtao Z.,Second Affiliated Hospital Of Xian Jiaotong University | Kunzheng W.,Second Affiliated Hospital Of Xian Jiaotong University | Jianqiang K.,Qingdao University | Ruiyu L.,Second Affiliated Hospital Of Xian Jiaotong University | Chunsheng W.,Second Affiliated Hospital Of Xian Jiaotong University
Endocrine | Year: 2014

Bone metabolism disorder has been identified to play a vital role in the pathogenesis of glucocorticoid-induced osteoporosis (GIOP). The local renin–angiotensin system (RAS) in bone is newly defined to be closely related to the bone metabolism. However, it is unknown whether the local RAS is involved in GIOP. Adult male New Zealand white rabbits were treated with saline, dexamethasone (DXM) alone, or DXM combined with perindopril. The expression of main RAS components in trabecular bone was examined at mRNA and/or protein levels. Bone metabolism was analyzed using dual-energy X-ray absorptiometry, histomorphometry, biomechanics, biochemical techniques, and quantitative RT-PCR. The expressions of local bone angiotensin II, angiotensin types 1 and 2 receptors, and angiotensin-converting enzyme at mRNA and/or protein levels increased when DXM-induced osteoporosis was present. Whereas, perindopril significantly blocked the activation of the local RAS and partially reversed GIOP. Mineralizing surface, mineral apposition rate, and bone formation rate were decreased by DXM, along with serum osteocalcin being downregulated. These changes were then reversed by the use of perindopril. Osteoclast number, osteoclast surface, and eroded surface increased after the administration of DXM, and urinary deoxypyridinoline was upregulated. These were also inhibited when perindopril was given. Quantitative RT-PCR using RNA isolated from the lumbar vertebrae revealed an increase in the SOST expression and a decrease in the Runx2 expression, whereas the receptor activator of nuclear factor-κB ligand/osteoprotegerin ratio and the expression of tartrate resistant acid phosphatase were increased, which were all inhibited by perindopril. The results of this study provide evidence for the role of local RAS is involved in GIOP, and GIOP may be ameliorated by blocking the activation of local RAS in the bone. © 2014, Springer Science+Business Media New York. Source

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