Zengcheng Peoples Hospital

Licheng, China

Zengcheng Peoples Hospital

Licheng, China
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Fang G.,Guangdong Pharmaceutical University | Li G.,ZengCheng Peoples Hospital | Pang C.,Guangdong Pharmaceutical University | Li W.,Guangdong Pharmaceutical University | And 2 more authors.
Biological and Pharmaceutical Bulletin | Year: 2016

This paper describes the ultrasound-assisted extraction (UAE) of pristimerin from Celastrus orbiculatus. Methanol was the most effective for pristimerin extraction, followed by ethanol, ethyl acetate, n-butanol, and water. To optimize the conditions, the Box-Behnken design, a widely used form of response surface methodology, was used to investigate the effects of parameters on UAE. Several variables, such as extraction time, ultrasonic power, extraction temperature, and solvent-to-solid (S/S) ratio were investigated. The highest extraction yield of 1.843 mg/g was obtained using methanol under optimal conditions with an extraction time of 40 min, ultrasonic power of 105 W, an S/S ratio of 40 mL/g, and an extraction temperature of 52°C. The experimental values under optimal conditions agreed well with the predicted values, suggesting that UAE has good potential as an extraction method for pristimerin from C. orbiculatus. © 2016 The Pharmaceutical Society of Japan.


He G.,Zengcheng Peoples Hospital | Guo W.,Peking University | Lou Z.,Peking University | Zhang H.,Peking University
Cell Biochemistry and Biophysics | Year: 2014

Achyranthes bidentata, is a herbal plant commonly used in the treatment of osteoporosis and bone nonunion in the Traditional Chinese Medicine. Saponins are the major compounds extracted from Achyranthes bidentata that have been shown to exert various pharmacological activities such as anti-inflammatory, antipyretic, antirheumatic, diuretic, and anti-osteoporosis. The Achyranthes bidentata saponins (ABS) were found to induce proliferation and differentiation in bone marrow stromal cells (BMSCs) as determined by the cell proliferation and alkaline phosphatase assays. Also, following the osteogenic induction, cells treated with ABS showed increased mRNA levels of rat bone morphogenetic protein-2, runt-related transcription factor 2, and osterix. Furthermore, ABS stimulated the activation of ERK as evidenced by increased phosphorylation of these proteins, which was blocked by an inhibitor of ERK (PD98059). Taken together, these results suggest that ABS stimulated osteogenic differentiation of BMSCs via activation of the ERK signaling pathway. © 2014 Springer Science+Business Media New York.


Li H.-P.,Sun Yat Sen University | Zeng X.-C.,Zengcheng Peoples Hospital | Long J.-T.,Sun Yat Sen University | Zhou B.,Sun Yat Sen University | And 4 more authors.
Carcinogenesis | Year: 2013

It has been demonstrated that nuclear factor-kappa B (NF-κB), which is overactivated in hepatocellular carcinoma (HCC), plays important roles in the development of HCC. Recently, a group of dysregulated micro RNAs were reported to be involved in HCC progression. Further understanding of micro RNA-mediated regulation of NF-κB pathway may provide novel therapeutic targets for HCC. In this study, we found that miR-451 expression was markedly downregulated in HCC cells and tissues compared with immortalized normal liver epithelial cells and adjacent non-cancerous tissues, respectively. Upregulation of miR-451 inhibited, while downregulation of miR-451 promoted, the tumorigenicity of HCC cells both in vitro and in vivo. These changes in the properties of HCC cells were associated with deregulation of two well-known cellular G1/S transitional regulators, cyclin D1 and c-Myc, which are downstream targets of NF-κB pathway. Furthermore, we demonstrated that miR-451 upregulation led to downregulation of cyclin D1 and c-Myc through inhibition of NF-κB pathway initiated by direct targeting of the IKBKB 3′-untranslated region. Therefore, these results suggest that miR-451 downregulation plays an important role in promoting proliferation of HCC cells and may provide the basis for the development of novel anti-HCC therapies. © The Author 2013. Published by Oxford University Press. All rights reserved.


Shi X.,Sun Yat Sen University | Zheng Z.,Sun Yat Sen University | Li J.,Zengcheng Peoples Hospital | Xiao Z.,Sun Yat Sen University | And 4 more authors.
Neuroscience Letters | Year: 2015

Amyloid β (Aβ) plays an important role in Alzheimer's disease (AD) by inducing microglia activation. Once activated, microglial cells promote the release of reactive species and cytokines that are known to enhance immune responses in AD brain. Thus, negative regulators of microglia activation are considered as potential therapeutic candidates for AD. Curcumin, the major yellow pigment in turmeric (Curcuma longa), is proposed for its anti-inflammatory properties. Several studies have indicated the suppressive effects of curcumin on LPS-induced microglia activation and MAPK activities. However, the effects of curcumin on Aβ-treated microglia and the possible mechanisms are still not fully understood. In the present study, we found that curcumin improved microglial viability against Aβ42 in a time- and dose-dependent manner and remarkably suppressed Aβ42-induced CD68 expression. Moreover, curcumin concentration-dependently abolished Aβ42-induced interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) production in mRNA and protein levels in microglia. Besides, curcumin exerted an inhibitory effect on phosphorylation of ERK1/2 and p38 in Aβ42-activated microglia. Further experiments indicated that blockage of ERK1/2 and p38 pathways reduced inflammatory cytokines production from microglia. These results show that curcumin suppresses ERK1/2 and p38 signaling, thus, attenuating inflammatory responses of brain microglia. © 2015 Elsevier Ireland Ltd.


Liu S.,Sun Yat Sen University | Li W.,Sun Yat Sen University | Xu M.,Sun Yat Sen University | Huang H.,Sun Yat Sen University | And 3 more authors.
Canadian Journal of Cardiology | Year: 2014

Background: Micro-RNA 21 (miR-21) has been shown to contribute to cardiac fibrosis in many diseases. In this study we investigated the roleof miR-21 in excessive production of collagen in diabetic cardiomyopathy. Methods: The proliferation rate of cardiac fibroblasts was analyzed by Western blot, Cell Counting Kit-8 kit (Dojindo Molecular Technologies, Kumamoto, Japan), and Cell-Light EdU Apollo 488 In Vitro Imaging Kit (RiboBio, Guangzhou, China). Real-time polymerase chain reaction and Western blotting were conducted to determine gene expression levels. A luciferase reporter assay was used to verify the interaction between miR-21 and the 3' untranslated region (3'UTR) of dual specific phosphatase 8 (DUSP8). Results: Our results show that high glucose promoted the proliferation and collagen synthesis of rat cardiac fibroblasts, which was accompanied by an increase of miR-21. Gain-of-function and loss-of-function assays confirmed that miR-21 mediated this effect, suggesting the crucial role of miR-21 in diabetic cardiomyopathy. Our study also identified a direct target of miR-21, DUSP8, which regulates cell proliferation and collagen synthesis in cardiac fibroblasts through p38 and c-Jun N-terminal kinase (JNK)/stress-activated kinase (SAPK) signalling. Our results show that miR-21 bound to the 3'UTR of DUSP8 post-transcriptionally repressed its expression. In addition, enforced expression of miR-21 activated the JNK/SAPK and p38 signalling pathways. Conclusions: Our study shows that miR-21 promotes high glucose-induced cardiac fibrosis through the JNK/SAPK and p38 signalling pathways by suppressing DUSP8 expression. © 2014 Canadian Cardiovascular Society.


PubMed | Wannan Medical College, Xi'an Jiaotong University, Sun Yat Sen University and Zengcheng Peoples Hospital
Type: | Journal: Molecular neurobiology | Year: 2016

Activated microglia are classified into two specific states: classically activated (M1) and alternatively activated (M2) subtypes. It is believed that the polarization of M1/M2 phenotype plays an important role in Alzheimers disease (AD). However, the mechanisms regulating this process remain unclear. Thus, we addressed this question focusing on milk fat globule epidermal growth factor 8 (MFG-E8). MFG-E8 is a unique protein which can bind to microglia and regulate its inflammatory responses. It is speculated that it might play a role in the balance of microglial polarization. In the current study, we used fibril A42 in vitro to stimulate mouse primary microglial cultures and found subsequent M1 marker expression, along with retained M2 marker production. Then, we discovered that MFG-E8 pretreatment reversed the increased trend of M1 markers and the decreased expression of M2 markers, which were induced by A42. Moreover, MFG-E8 effects could be effectively blocked by an MFG-E8 antibody. Further analysis on the signaling pathways showed that NF-B upregulation and Akt downregulation in microglial cultures were observed after A42 incubation. And the alteration of these pathways could also be reversed by MFG-E8. We then assessed the effects of NF-B and PI3K-Akt on M1/M2 alteration using their specific inhibitors. Pyrrolidine dithiocarbamate, a NF-B inhibitor, inhibited M1 marker expression; moreover, LY294002, an Akt inhibitor, enhanced M1 marker expression. Our study indicated the regulatory role of MFG-E8 on microglia M1/M2 alteration for the first time, providing a basis for understanding the potential role of microglia activation in AD.


PubMed | Zengcheng Peoples Hospital and Sun Yat Sen University
Type: Journal Article | Journal: Neural regeneration research | Year: 2015

This study examined a 24-year-old patient with delayed encephalopathy, who was admitted to hospital with complaints of headache and visual impairment 1 week after acute carbon monoxide poisoning. The results of a visual field assessment, electroencephalography and head magnetic resonance imaging indicated damage to the cerebral cortex. After a 2-week treatment period, the patient had recovered from the visual impairment, but exhibited digit- and letter-reading difficulty. The Chinese aphasia battery and the number and letter battery supplement were conducted. The results revealed that the patient exhibited digit and letter alexia, while the ability to read Chinese characters was preserved. In contrast, the patient exhibited a deficit in Chinese character writing, while number and letter writing remained intact. Following treatment, reading and writing ability was improved and electroencephalographic abnormalities were ameliorated. Overall, our experimental findings demonstrated that delayed encephalopathy following acute carbon monoxide poisoning was characterized by digit and letter alexia.


PubMed | Zengcheng Peoples Hospital and Sun Yat Sen University
Type: | Journal: Neuroscience letters | Year: 2015

Amyloid (A) plays an important role in Alzheimers disease (AD) by inducing microglia activation. Once activated, microglial cells promote the release of reactive species and cytokines that are known to enhance immune responses in AD brain. Thus, negative regulators of microglia activation are considered as potential therapeutic candidates for AD. Curcumin, the major yellow pigment in turmeric (Curcuma longa), is proposed for its anti-inflammatory properties. Several studies have indicated the suppressive effects of curcumin on LPS-induced microglia activation and MAPK activities. However, the effects of curcumin on A-treated microglia and the possible mechanisms are still not fully understood. In the present study, we found that curcumin improved microglial viability against A42 in a time- and dose-dependent manner and remarkably suppressed A42-induced CD68 expression. Moreover, curcumin concentration-dependently abolished A42-induced interleukin-1 (IL-1), interleukin-6 (IL-6) and tumor necrosis factor- (TNF-) production in mRNA and protein levels in microglia. Besides, curcumin exerted an inhibitory effect on phosphorylation of ERK1/2 and p38 in A42-activated microglia. Further experiments indicated that blockage of ERK1/2 and p38 pathways reduced inflammatory cytokines production from microglia. These results show that curcumin suppresses ERK1/2 and p38 signaling, thus, attenuating inflammatory responses of brain microglia.


Wu G.,Zengcheng Peoples Hospital | Zhao H.,Zengcheng Peoples Hospital | He N.,Zengcheng Peoples Hospital | Han H.,Zengcheng Peoples Hospital
Nan fang yi ke da xue xue bao = Journal of Southern Medical University | Year: 2015

OBJECTIVE: To detect miR-200a expression in human colorectal carcinnoma (CRC) cell lines and explore the role of miR-200a in regulating the biological behavior of CRC cells.METHODS: Real-time quantitative RT-PCR (qRT-PCR) was used to detect miR-200a expression levels in 6 CRC cell lines (HCT116, HT29, LS174T, SW480, SW620 and LoVo). miR-200a mimics were transiently transfected into LoVo, and the changes in cell proliferation, apoptosis, migration, and cell-cell adhesion were assessed using CCK-8 assay, TUNEL assay, transwell migration assay, and homogenous adhesion experiment, respectively.RESULTS: The expression of miR-200a was down-regulated in the 6 CRC cell lines, among which the highly metastatic LoVo cell line showed the lowest expression and the tumorigenic but non-metastatic CRC cell line HCT116 had the highest expression. Overexpression of miR-200a depressed cell proliferation and migration but promoted cell apoptosis and cell-cell adhesion in LoVo cells.CONCLUSION: miR-200a plays a role in regulating the invasiveness and metastasis of CRC, and overexpression of miR-200a causes a significant reduction of cell proliferation and migration and promotes apoptosis and cell-cell adhesion in LoVo cells.


PubMed | Zengcheng Peoples Hospital
Type: Journal Article | Journal: Nan fang yi ke da xue xue bao = Journal of Southern Medical University | Year: 2015

To detect miR-200a expression in human colorectal carcinnoma (CRC) cell lines and explore the role of miR-200a in regulating the biological behavior of CRC cells.Real-time quantitative RT-PCR (qRT-PCR) was used to detect miR-200a expression levels in 6 CRC cell lines (HCT116, HT29, LS174T, SW480, SW620 and LoVo). miR-200a mimics were transiently transfected into LoVo, and the changes in cell proliferation, apoptosis, migration, and cell-cell adhesion were assessed using CCK-8 assay, TUNEL assay, transwell migration assay, and homogenous adhesion experiment, respectively.The expression of miR-200a was down-regulated in the 6 CRC cell lines, among which the highly metastatic LoVo cell line showed the lowest expression and the tumorigenic but non-metastatic CRC cell line HCT116 had the highest expression. Overexpression of miR-200a depressed cell proliferation and migration but promoted cell apoptosis and cell-cell adhesion in LoVo cells.miR-200a plays a role in regulating the invasiveness and metastasis of CRC, and overexpression of miR-200a causes a significant reduction of cell proliferation and migration and promotes apoptosis and cell-cell adhesion in LoVo cells.

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