Table of Content

05 November 2010, Volume 30 Issue 11

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研究论文

P38MAPK-BCL-xL pathway was involved in HPC-induced reduction of brain ischemic injury in mice

Jing LIANG; Jian-li DU; Yi-jing ZHU; Li ZHAO; Yan-lin LUO; Jun-fa LI

2010, 30(11):  1127-1133. 

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Objective To explore the role of P38 mitogen actived protein kinase (P38MAPK)-BCL-xL antiapoptotic pathway in hypoxic preconditioning (HPC)-induced neuroprotection in ischemic brain. Methods SPF grade male BALB/c mice (18~22g, 8~10w) were randomly divided into four groups: normoxic sham (NS), normoxic ischemia (NI), HPC sham (HS) and HPC-ischemia (HI) groups. Using HPC, middle cerebral artery occlusion (MCAO)-induced focal cerebral ischemia mouse models and P38MAPK inhibitor SB203580 injection, the changes in neural apoptosis were observed by TUNEL staining, the expression of antiapoptotic protein BCL-xL was detected by Western blot. The interaction between BCL-xL and P38MAPK was determined by immunoprecipitation technique. Results HPC could inhibit neural apoptosis and elevated BCL-xL protein level in mitochondria significantly in the penumbra of ischemic cortex. Intracerebroventricular injection of P38MAPK inhibitor SB203580 abolished the HPC-induced neuroprotection. Furthermore, the result of immunoprecipitation showed that there was an interaction between BCL-xL and P38MAPK. Conclusion HPC could protect the brain against MCAO-induced ischemic injuries via P38MAPK-BCL-xL antiapoptotic pathway in mice.

HMGS and HMGR from Streptococcus pneumoniae is Facilitated to Screen Candidate Inhibitors

Ya-li BEN; Gu-zhen CUI; De-li LIU

2010, 30(11):  1134-1137. 

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Objective The 3-hydroxy-3-methylglutaryl-coenzyme A synthase and reductase (HMGS and HMGR) were analyzed by their dynamics and function; Methods The genes of HMGS and HMGR were cloned from S.pneumoniae and expressed. Their inhibition effect was tested by lovastatin and the candidate inhibitors; Results Lovastatin can inhibit HMGS, but not do for HMGR. It is more effective in the virtual screening with the reacting product catalyzed by HMGS instead of 3-hydroxy-3-methylglutaryl-coenzyme A（HMG-CoA）; Conclusions Lovastatin is a kind of competing inhibitor targeted for HMGR. The product can be used to screen preliminarily plentiful candidate inhibitors and develop new inhibitors with more specific and stronger function.

Novel compound FLZ inhibits HIF-1α over-expression in rats vascular dementia

Wen-di GE; Bo MA; Wei LI; Liang GUO; Jian-jun ZHANG

2010, 30(11):  1138-1142. 

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Objective To study the effect of FLZ on the learning and memory ability in vascular dementia rats induced by transient middle cerebral artery occlusion (tMCAO) and its influence on the expression of HIF-1α. Methods tMCAO for 2 hours-induced vascular dementia rats was utilized. The Morris water maze was used to evaluate the learning and memory ability after 30 days of administration. The TTC staining was used to evaluate the infarct volume. The alterations in cortex and hippocampus morphology were assessed by HE staining. In addition, an animal model of tMCAO for 2 hours followed by 24 hours reperfusion was used. The Western blot was used to detect the expression of HIF-1α after 24 hours of reperfusion. Results In the Morris water maze, FLZ administered orally for 30 days reduced remarkably the escape latency time, decreased significantly the infarct volume and also ameliorated the neuropathological alterations in rat cortex and hippocampus. Additionally, FLZ inhibited significantly HIF-1α overexpression induced by tMCAO for 2 hours. Conclusion FLZ could improve significantly memory deficit in vascular dementia rats, its protective effect was related to inhibiting HIF-1α overexpression possibly.

MSK-1 and CREB were involved in HPC-induced neuroprotection against cerebral ischemic injuries of mice

Jian-li DU; Jing LIANG; Mo-yin LI; Xu ZHANG; Li ZHAO; Yan-lin LUO; Jun-fa LI

2010, 30(11):  1143-1148. 

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Objective To explore the role of mitogen- and stress-activated protein kinase 1 (MSK-1) and cAMP response element binding protein (CREB) in hypoxic preconditioning (HPC)-induced neuroprotection against cerebral ischemic injuries. Methods Healthy adult male BALB/c mice weighing 18～22g were randomly divided into 4 groups as follows: normoxia sham (NS), HPC sham (HS), normoxia ischemia (HI) and HPC ischemia (HI). Using HPC and middle cerebral artery occlusion (MCAO)-induced focal cerebral ischemia mouse models, and the techniques of triphenyltetrazolium chloride (TTC) staining, neurological deficits evaluation and Western blot, we observed the neurological scores, brain infarct volume, the phosphorylation and protein expression levels of MSK-1 and CREB in regions of ischemic cortex. Results HPC attenuated MCAO-induced neurological deficits, and decreased brain infarct volume and edema ratio of mice. The phosphorylation levels of MSK-1 and CREB decreased significantly (p<0.05, n=4) in the ischemic core, while HPC could promote significantly (p<0.05, n=4) both MSK-1 and CREB phosphorylation levels in penumbra of MCAO-induced ischemic cortex. However, there were no significant changes of total MSK-1 and CREB protein expressions in the ischemic regions of MCAO-treated HPC mice. Conclusion The increased MSK-1 and CREB phosphorylations in ischemic penumbra were involved in HPC-induced neuroprotection against cerebral ischemic injuries of mice.

Inhibition of MCF7 cell proliferation in vitro by resveratrol and epirubicin used in combination

Jia-yan ZHOU; Jin-hong DUAN; Zhao SUN; Yan HU; Guang-jin ZHU; Xian-da YANG

2010, 30(11):  1149-1152. 

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Objective To investigate the inhibition of 7 human cancer cell lines by resveratrol and epirubicin treated in combination. Methods: Tumor cell lines were cultured in vitro, treated with resveratrol and epirubicin in combination for 24 hours. The inhibition effect was evaluated with MTS method. The cell morphology and necrosis were evaluated with both regular microscopy and fluorescence microscopy after PI staining. The cell cycle distribution was evaluated with flow cytometry (FCM) after PI staining. Results: The combination of resveratrol and epirubicin generated a synergistic inhibition of MCF7 and MGC803 cell lines, which was greater than the summation of the inhibition produced by either drug alone. The inhibition of the remaining tumor cell lines by the combination treatment was and additive . Obvious necrosis was observed by treated in combination. Cell cycle analysis revealed that the combination treatment tended to arrest the cells in G1 and S phases. Conclusion: A synergistic inhibition of the MCF7 and MGC803 cell line was produced by the combination treatment of resveratrol and epirubicin, which caused the cellular necrosis and cell cycle inhibition. The combination treatment did not generate a synergistic inhibition of the other tumor cell lines evaluated in this study.

Effect of Oncostatin M on Differentiation of the AFP Promoter-Defined Human Hepatic Progenitor Cells in Vitro

Bao-qing LIU; Wei-hong LI; Wei-tao ZHANG; Xin LU; Wei AN; Hai-yan ZHANG

2010, 30(11):  1153-1157. 

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Objective The aim of the present study is to investigate the effect of oncostatin M on differentiation of the AFP promoter-defined human hepatic progenitor cells (APHPs) in vitro. Methods The morphology of APHPs was observed by phase-contrast microscopy including the proliferation condition and OSM inducement. The properties of differentiated APHPs were detected after OSM treatment, which involved the albumin expression with immunofluorescence, the glycogen storage with periodic acid Schiff staining (PAS) and the subcellular structure with electron microcopy. Results Morphology of APHPs was changed after treated with OSM，the APHPs were able to form cluster from day 3 after OSM treatment, the aggregation of tissue-like structure was found from day 7 after inducement, Immunofluorescence results revealed that the tissue-like structure was strong expression of albumin, and PAS results displayed the differentiated APHPs obtained the function of glycogen accumulation. In electron micrographs, cell junction was found localized along the lateral membrane between cells in cultures of OSM. In addition, microvillis were appeared on one side of plasma membrane. Conclusions The APHPs acquired mature function and structure after OSM treatment in vitro.

Long-Term Calorie Restriction increases SIRT1 expression and Inhibits Vascular Senescence in Mice

Shuang ZHOU; Hou-zao CHEN; Yan-zhen WAN; Ran ZHANG; Qing-jun ZHANG; De-pei LIU

2010, 30(11):  1158-1162. 

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Objective To investigate the effects of calorie restriction on vascular senescence and underlying mechanisms. Methods Comparing ageing-related gene expression in aortas of 2 or 18-month-old C57BL/6 mice by western blotting. Constructing calorie restriction mouse model and analyzing gene expression by western blotting using ageing-related antibodies. Results Ageing decreased the expression of SIRT1, a type III histone deacetylase, in aortas of mice. Whereas long-term calorie restriction increased SIRT1.The ageing-related biomakers P53 and P21 expression were decreased, but MnSOD expression was upregulated in aortas of C57BL/6 mice by long-term calorie restriction. Conclusion Long-term calorie restriction inhibits vascular senescence. SIRT1 is involved in vascular senescence inhibition, leading to decreased oxidative stress.

Transient Potential Vanilloid Receptor 1 participate Chronically Hypoxic Human Pulmonary Arterial Smooth Muscle Cells Proliferation

Yue-xiu WANG; Yan LIU; Cong WANG; Jie LIU; Jun WANG

2010, 30(11):  1163-1166. 

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Objective To investigate the expression and functional change of the transient potential vanilloid receptor 1 (TRPV1) channels in hypoxia-induced proliferation of human pulmonary artery smooth muscle cells (HPASMCs). Method RT-PCR , Real-time PCR and Western blot were used to detect the expression of TRPV1 channels in HPASMCs. Cell number was determined with a hemocytometer. Result Hypoxia upregulated gene and protein expression of TRPV1 in HPASMCs. The capability of HPASMCs proliferation was significantly increased under hypoxic condition. Capsazepine (a TRPV1 channel inhibitor) could inhibit the HPASMCs proliferation in a dose-dependence manner. Conclusion These results suggest that TRPV1 channels may be a critical pathway or mediator in hypoxia-induced the proliferation of HPASMCs.

Decreased expression of TPH2 in median raphe nuclei of perimenopausal depression model rats

Ai-jiao XIAO; Zhi-yu ZHOU; Qing-hua WU; Jian-xin MIN

2010, 30(11):  1167-1171. 

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Objective To explore changes of the concentration of 5-hydroxytryptamine (5-HT) in hippocampus and the expression of tryptophan hydroxylase 2(TPH2) in median raphe nuclei in the perimenopausal depression model rats. Methods The animal model was established by resecting the ovaries of female rats, then giving isolation-housing in combination with chronic unexpected mild stress(CUMS) for 21 days. Behavioral tests were used to evaluate the model. High performance liquid chromatogram-electrochemical detection was employed to measure 5-hydroxytryptamine (5-HT) in hippocampus. Reverse transcription- polymerase chain reaction(RT-PCR) and immunohistochemistry were to detect the relative expression of TPH2 mRNA and TPH2 immunoreactive neurons in median raphe nuclei. Results After 21 days of CUMS, both crossing and rearing in model group were reduced in Open-field test，and percentage of sugar consumption was too. The concentration of 5-HT in hippocampus was lowered in the model one, the relative expression of TPH2 mRNA and the number of TPH2 immunoreactive neurons in raphe nuclei were too. Conclusion Perimenopausal depression model could successfully be induced by ovariectomy, isolation -housing in combination with 21 days of CUMS. The decrease of 5-HT in hippocampus might be through reducing the expression of TPH2 in median raphe nuclei, which leads to lower the synthesis of 5-HT.

Increase of Radioiodide uptake by co- transfered the human sodium/iodide symporter and the human thyroperoxidase gene into glioma tumor,lung cancer and thyroid cancer cell lines

Wei LI; Jian TAN; Lei LONG

2010, 30(11):  1172-1176. 

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Objective The aim of this study is to investigated the iodide uptake ability of iodide in glioma tumor,lung cancer and thyroid cancer cell lines after co- transfered the human sodium/iodide symporter and the human thyroperoxidase gene. Methods Through cloning, recombination, packaging and amplifying, the recombinant adenosine virus AdTPO was constructed. After purification. After transfected hNIS gene into tumor cell lines through liposome, stably expressing hNIS gene cell lines selected by G418 antibiotics was determined as control group. Using AdTPO, hTPO gene was transducted into control group cell lines, as experimental group. Tumor cell lines without hTPO and hNIS gene was applied as blank control group. Then, we investigated the 125I uptake assay and 125I influx experiments with glioma tumor,lung cancer and thyroid cancer cell lines. Results We were successful in co-transfecting hNIS and hTPO gene into human tumor cell lines, 125I uptakes and effective half life in experimental group was linger than control groups cell lines .After co-transfecting hNIS and hTPO gene, the uptake ability of 125I was 59628 1281,79638 1261,52971 2162and 49638 1281 counts·min-1 in H460, U251, ARO and FRO tumor cell lines. Conclusion The uptake ability of 125I could increase by co-transfection with hNIS and hTPO genes into human tumor cell lines.

Effect of β3 adrenergic receptor agonist and antagonist on expression of MMP-2 and MMP-9 in heart failure rat

Yi-hui KONG; Rong-yuan CAO; Li ZHANG; Yu-bing LIU; Yue LI; Wei-min LI

2010, 30(11):  1177-1183. 

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Objective To investigate the effect of β3 adrenergic receptor (AR)agonist and antagonist on matrix metalloproteinases(MMP)-2 and MMP-9 in heart failure rat model and to study the relations betweenβ3AR and left ventricular remodeling. Methods Ten rats served as control group and 130 rats received isoproterenol to make heart failure model. Heart failure rats were randomly divided into agonist group(n=12), antagonist group(n=10), heart failure group(n=11). Agonist group and antagonist group received BRL37344 1.65μg/kg、SR59230A 50μg/kg through caudal vein for 10 min twice a week dividually. All below were measured at the 4th and 8th week: cardiac function, ratio of LV weight and body weigh(LVW/BW) and collagen volume fraction(CVF), expression of MMP-2 and MMP-9 proteins by the techniques of immuno-histochemistry; the expression levels of MMP-2 and MMP-9 mRNA in myocardium by reverse transcription-polymerase chain reaction (RT-PCR).Results Compared with control group，the cardiac function of heart failure group was aggravated while the cardiac function of agonist group was further aggravated; These change were significantly attenuated in antagonist group; In comparison with the control group, The expressions of MMP-2 and MMP-9 mRNA and proteins increased with time in heart failure models, and SR59230A treatment decreased the expression(all P＜0.01). Conclusions β3AR may play a role in left ventricular remodeling by the effect of MMP-2 and MMP-9.

Role of AMPK in over-expression of collagen IV in rat glomerular mesangial cells induced by high glucose

Zhen-hua JIA; Yi LIU; Ming-feng CAO; Jing XU; Qiang WAN; Rong WANG

2010, 30(11):  1184-1187. 

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Objective To observe the expression of collagen IV (COL IV) in cultured rat glomerular mesangial cells (GMCs), and to investigate the role of AMP-activated protein kinase (AMPK) in the process. Methods GMCs were incubated in four groups for 24 hours: control group (glucose 5.6 mmol/L), high glucose group (glucose 22.0mmol/L), low 5-amino-4-imidazolecarboxamide-riboside (AICAR, activator of AMPK) group (0.5mmol/L AICAR＋22.0mmol/L glucose), high AICAR group (1.0mmol/L AICAR＋22.0mmol/L glucose). AMPKα1 mRNA level was measured by RT-PCR, and the protein levels of AMPKα, p-AMPKα and COL4α5 subunit by Western blot analysis. Results Compared with control group, high glucose increased COL4α5 synthesis of GMCs, but reduced AMPKα1 mRNA level and protein levels of AMPKα, p-AMPKα; AICAR suppressed the over-expression of COL4α5, and raised the protein levels of AMPKα, p-AMPKα. Conclusion High glucose can increase COL4α5 synthesis of GMCs, this change maybe correlates with lower expression and activity of AMPK.

Apoptosis induced by Pseudolaricacid B in human melanoma cells

Ai-guo MENG; Chun-yan LIU

2010, 30(11):  1188-1192. 

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Objective To investigate the effect of PLAB-induced apoptosis in human melanoma cells. Methods Apoptotic cells were detected using Hoechst Hoechst 33342/PI staining, and confirmed by DNA fragmentation assay. The expression of genes involved in apoptosis was analysized by RT-PCR. The level of the protein was determined by ELISA kit. Results PLAB clearly induced apoptosis in SK-28 cells; Treatment with PLAB for 12h, the protein expression of p53 was obviously increased; for 24h, caspase-3 activity was enhanced, the protein expression of Fas/APO-1 was increased, and the mRNA expression of Bax was also elevated, but the mRNA expression of Bcl-2 was reduced. Conclusions These results suggest PLAB induced apoptosis in human melanoma cells via a mechanism involving both Bcl-2-associated mitochondrial pathway and Fas-associated death receptor signaling pathway, which are two distinct downstream pathways of p53.

Effects of metabolic enzyme gene polymorphisms and smoking factors on the occurrence of male lung squamous cell carcinoma

Bao SONG; Jie LIU; Hai-yan HUANG; Xing-wu WANG; Yan ZHENG; Jin-xiang HAN; Zhe-hai WANG

2010, 30(11):  1193-1196. 

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Objective To explore the effect of cytochrome P450 enzyme 1A1(CYP1A1), Glutathione-S-transferase M1(GSTM1) genetic polymorphism and smoking factor on the occurrence of male lung squamous carcinoma. Methods CYP1A1、GSTM1 genotypes were detected with oligonucleotidechip technique in 125 male lung squamous carcinoma patients and 125 healthy controls. Results Frequencies of GG genotype at CYP1A1 m2 site and frequencies of GSTM1 null genotypes were significantly increased in lung cancer group compared to control group (P<0.05). When stratified by smoking status, there were elevated risks for smokers in lung cancer cases carrying at least one G allele of CYP1A1 m2 site or GSTM1 null genotype, the odds ratios were 4.50 or 3.18 respectively (P<0.01). Conclusion CYP1A1 and GSTM1 gene polymorphism were associated with the occurrence of male lung squamous cell carcinoma, smoking factors and CYP1A1、GSTM1 polymorphism have a synergistic effect.

Allicin and survivin antisense oligonucleotide on growth of gastric cancer cell SGC7901 cells

Chao-xia LIU; Qing-yan KONG

2010, 30(11):  1197-1201. 

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Objective To investigate the effects of allicin and survivin antisense oligonucleotide(ASODN) on proliferation and apoptosis of gastric cancer cell line SGC7901. Methods The SGC7901 cells were treated by allicin alone or in combination survivin ASODN. After 12, 24, 48h, MTT assay was used to examine the inhibition rate of cell growth. The apoptosis of SGC7901 was examined by flow cytometry(FCM). The expression of Ki67 was detected in gastric cancer cells by immunohistochemical staining. Results Allicin or survivin ASODN effectively inhibited the growth of SGC7901 gastric cancer cells in a concentration- dependent manner at certain range of concentrations. The inhibitory rate of combined treatment with allicin and survivin ASODN was significantly higher than that of allicin or survivin ASODN alone(P<0.05) and the value of combination index(CI) was 0.46. In the allicin and survivin ASODN combined treatment group, the apoptosis rate was 7.30%, 10.44% and 16.44%, respectively, which difference was significantly higher compared with single drug treatment group(P<0.05). The expression of Ki67 protein was down-regulated by allicin plus survivin ASODN compared with single drug treatment and control group (P<0.05). Conclusion Allicin combined with survivin ASODN has synergistic effects in inhibiting the growth and inducing apoptosis of gastric cancer SGC7901 cells.

Increased expression of high-mobility group box chromosomal protein 1 in patients with acute pancreatitis

Gan-zhen LU; Chuan-xin WU; Qi LIU; Jian-ping GONG; Hang SUN

2010, 30(11):  1202-1205. 

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Objective To investigate the expression of high-mobility group box chromosomal protein 1(HMGB1) in patients with acute pancreatitis (AP) and its clinical value. Methods We measured blood HMGB1 mRNA levels by RT-PCR and serum HMGB1,TNF-α and IL-6 concentrations by an enzyme-linked immunosorbent assay in 20 patients with mild AP (MAP), 10 patients of severe acute pancreatitis without organ dysfunction (SAP-1), 10 patients of SAP with organ dysfunction (SAP-2). Furthermore, relationship between their serum HMGB1 levels and severity of AP was analyzed. Results The mean value of serum HMGB1 concentrations in patients with MAP, SAP-1 and SAP-2 were 3.5 ± 0.8 , 5.7 ± 1.6 and 8.3 ± 1.7 ng/mL respectively and were significantly higher than that in healthy subjects 1.6 ± 0.4 ng/mL. Blood HMGB1 mRNA levels in patients with MAP, SAP-1 and SAP-2 were 0.56±0.11，0.71±0.07，0.89±0.09 respectively and were significantly higher than that in healthy subjects 0.25±0.04. Serum HMGB1 levels and HMGB1 mRNA were significantly increased in patients with AP and were correlated with disease severity. Conclusion These results suggest that HMGB1 may act as a key mediator for inflammation and organ failure in AP.

Lipopolysaccharides regulated the expression of toll-like receptors in astrocytes through NF-κB signal pathway

Hong ZHANG; Xue-zhong LI; Long-mei BAI; Ya-ping YANG; Yuan ZHOU; Chun-feng LIU

2010, 30(11):  1206-1209. 

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Objective To investigate the expression of toll-like receptors in astrocytes administrated with lipopolysaccharide (LPS). Methods LPS was administrated to rat astrocytes for 24h, and the expression of toll-like receptors and NF-κB p65 in astrocytes was detected by immunofluorescence and western blotting. At the same time, the effect of inhibitor of NF-κB signal pathway was investigated. Results Astrocytes expressed both cell surface and intracellular TLR3, low-level TLR4 in normal circumstance. LPS up-regulated the expression of TLR4 and NF-κB p65 in astrocytes in a concentration-dependent manner, while the expression of TLR3 kept constant. Pretreatment with SN90 (inhibitor of NF-κB) could block the increase of the expression of TLR4. Conclusion The expression of toll-like receptors in astrocytes was not homogeneous but rather tailored environmental signal. The molecular mechanism of the changes may be related to the expression of NF-κB p65.

临床园地

Giant hypertrophy gastritis responsive to glucocorticoid: a case report

Yan XU; Gui-jun FEI; Feng ZHU; Ai-ming YANG; Xing-hua LU

2010, 30(11):  1210-1213. 

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Objective To investigate the clinical feature, diagnosis and therapy of giant hypertrophy gastritis. Methods We reported a case of giant hypertrophy gastritis with hypoproteinemia secondary to a loss of albumin into the gastric lumen. The diagnosis of giant hypertrophy gastritis was made by using a combination of radiologic examination, endoscopic imaging, and histologic analysis. Glucocorticoid treatment was given to the patient. Through literature review, the clinical and pathological features, diagnosis, therapy of giant hypertrophy gastritis were overviewed. Results Endoscopic and radiologic examination revealed enlarged gastric folds on the body of stomach. Endoscopic sonography revealed marked thickening of mucosal layer on the body of stomach and gastric fundus. Pathologic findings are consistent with giant hypertrophy gastritis. After glucocorticoid treatment, hypoproteinemia resolved. Conclusion　Giant hypertrophy gastritis may be responsive to glucocorticoid. Understanding of this disease should be improved to avert misdiagnosing.

Fever, valvular vegetation, blood-culture negtive: Q fever

Jun-yi ZHANG; Dong WU; Wei-gang FANG; Hong-wei FAN

2010, 30(11):  1214-1215. 

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研究短文

Changes of Cerebral Water Content, Plasma NE level and Cardiac Function after Photochemically-induced Cerebral Thrombosis in Tree Shrews

Chun BI; Qiang MENG; Guang-jian LIU; Xian KUANG; Shu-qing LI

2010, 30(11):  1216-1217. 

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短篇综述

Programmed death receptor 1 and viral hepatitis C

Jun-ying ZHOU; Feng WEI; Jun-qing LI

2010, 30(11):  1218-1221. 

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Programmed death 1 (PD-1) can exhaust the function of virus-specific CD8+ T cells PD-1 increased in the chronic progress of HCV infection. Blockage of PD-1 signal pathway may restore the immunological function of CD8+ T cell, which benefit for virus clearance.

The treatment of mesenchymal stem cells in hepatic disease

Qian ZHANG; Cun-liang DENG

2010, 30(11):  1222-1225. 

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Mesenchymal stem cells are multipotent stem cells,they have specific immune characteristics,for example,they could suppress activation of T cells and modulate immune tolerance of allogeneic transplants. Liver transplantation is the primary treatment for various end-stage hepatic diseases but is hindered by the lack of donor organs and by complications associated with rejection and immunosuppression. Studys have shown that bone marrow is one of transplantable source of hepatic progenitors. Multipotent bone marrow-derived mesenchymal stem cells can differentiate into functional hepatocyts,secrete related cytokines promoting regeneration of the hepatocytes under defined conditions, it provides a new way for treating kinds of liver injury.The function of mesenchymal stem cells for hepatic disease is discussed in this review.

Adipose Tissue-Derived Cells in Ischemic Heart Disease

Hua YANG; Zhu-jun SHEN

2010, 30(11):  1226-1229. 

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Ischemic heart disease leading to heart failure seriously affects the quality of patients'life. Stem cell transplantation has been proposed to be a promising therapy for ischemic heart disease. Adipose-tissue derived stem cells (ADSC)and Dedifferentiated FAT (DFAT) cells are able to differentiate into multiple cell lineages including cardiac myocytes. Transplantation of adipose-derived cells after myocardial infarction significantly improves heart function, reduces ventricular remolding. Hence, adipose-derived cells are emerging as a new sourse of adult stem cells for cardiovascular repair.

Self-renewal signaling pathway of haemopoietic stem cells

Xing CUI; Rui-rong XU; Wen-jing ZHANG; Yan WANG; Jing-yi WANG

2010, 30(11):  1230-1233. 

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The self-renewal of HSCs is co-regulated by the micro-environment and its own genes including HOX、MYC、BMI-1. At the same time, some signaling pathways such as WNT，NOTCH/JAGGED，FGF，JAK-STAT also play crucial roles in the self-renewal of HSCs.

Peripheral Signals in the Control of Food Intake

Yan-mei LI; Shu-kun YAO

2010, 30(11):  1234-1237. 

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The regulation of food intake is complex and involves many peripheral peptides. The short-term signals include satiety signals and hunger signals generated by gastrointestinal tract. The long-term signals mainly include adiposity signals produced by adipose tissue. In this paper, we review the effects of cholecystokinin, Glucagon-like peptide 1, peptide YY, pancreatic polypeptide, oxyntomodulin，ghrelin, leptin and insulin on appetite and body weight control, and their roles in obese treatment.