Table of Content

25 February 2009, Volume 29 Issue 2

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研究论文

Hypoxic preconditioning attenuated MCAO-induced brain ischemic injuries of mice

Jun JIANG; Wei-wei YANG; Nan ZHANG; Xiang-ning BU; Meng-yu GUO; Xin-yi ZHAO; Jun-fa LI

2009, 29(2):  113-118. 

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Objective To explore the effects of hypoxic preconditioning (HPC) on middle cerebral artery occlusion (MCAO)-induced brain injuries and its possible mechanisms. Methods Using our established HPC and MCAO mouse models, and the techniques of 2,3,5-Triphenyltetrazolium chloride (TTC) staining, neurological evaluation, SDS-PAGE and Western blot, we observed the changes in infarction sizes, edema ratio, behavior score, and nPKC membrane translocation in the ischemic core and penumbra of mice following hypoxic exposure and ischemic injuries. Results MCAO could induce three types of cerebral ischemia: cortical, hippocampal and thalamic ischemia (data not shown due to the rare incidence); In the cortical ischemia, HPC significantly reduced infarction size (P<0.05, n=10), density of infarct area (P<0.05, n=10) and edema ratio (P<0.05, n=6); However, HPC only decreased the density of infarct area significantly (P<0.05, n=7) in the hippocampal ischemia; HPC also partially relieved the MCAO-induced neurological deficits of mice; In addition, HPC could prevent the decreased nPKC membrane translocation induced by MCAO in penumbra of mice brain. Conclusion HPC can attenuate MCAO-induced brain injuries, and nPKC may be involved in the neuroprotection.

Screening of proteins interacting with the cytoplasmic tail of NECL1 by yeast two-hybrid system

Chen LI; Tao CHEN; Bin YIN; Yan-hua GONG

2009, 29(2):  119-123. 

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Objective To screen the proteins interact with the cytoplasmic tail of NECL1. Methods The cytoplasmic tail sequence of human NECL1 gene was inserted into the "bait" vector pGBKT7 in frame. The recombinant pGBKT7-NECL1C was then transformed in to yeast cells and followed by screening of human fetal brain cDNA library. Then the GST pull down assay was used to confirm the interactions between the proteins. Results Nine different sequences by sequencing the positive clones(There are repeated clones) and five alternative proteins were obtained by the amino acid sequence blast. Using the GST pull down analysis, we confirmed that two of them can interact with the cytoplasmic tail of NECL1 in vitro. Conclusion Using yeast two-hybrid system, we got some alternative proteins which may interact with the cytoplasmic tail of NECL1.

Detection of CRP level in rats chronic periodontal and atherosclerosis compound model

Jia NI; Yuan-ming ZHANG; Jun XU; Liang-jun ZHONG; Fang-chuan SHI; Xiao-huan ZHOU

2009, 29(2):  124-128. 

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Objective To detect and analyse CRP level in rats chronic periodontal and atherosclerosis compound model. Methods 60 rats were randomly divided into four groups, each group 15: Group A:control group; Group B:periodontitis group; Group C:atherosclerosis group;Group D:periodontitis and atherosclerosis group. Every group accepts the corresponding treatment. Observe pathological changes in periodontal tissue of experimental teeth and arterial vessels. CRP level in serum were assayed by ELISA. Results Histopathology Observation of periodontal tissue revealed: Obvious inflammation of periodontal tissue were observed in group B,D. Attachment loss level in group B and D were higher than that of A, C groups(P <0.05). Histopathology Observation of arteries revealed: tunica media of artery thickening in group B. Thoracic aorta, abdominal aorta atherosclerotic lesions formationed in group C,D. Serum levels of CRP in group D were higher than other groups (P <0.05). Dependablity analyse revealed: CRP and AL in both group B and D were positive correlation. Conclusion Atherosclerosis and periodontitis could influence each other,the development of two diseases may concerned with serum levels of CRP.

cPKC II and participated in the attenuation of MCAO-induced brain injuries of mice following hypoxic preconditioning

Wei-wei YANG; Jun JIANG; Xiang-ning BU; Nan ZHANG; Pei-lun XIE; Bo-min ZHANG; Jun-fa LI

2009, 29(2):  129-134. 

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Objective To explore the protection of hypoxic preconditioning (HPC) on middle cerebral artery occlusion (MCAO)-induced brain injuries of mice and the changes in protein kinase C (PKC) II and membrane translocation in ischemic cortex of MCAO mice. Methods Male BALB/c mice (18-22g, 8-10w) were randomly divided to H0+Sham (n=6), H0+Ischemia (n=6), H4+Sham(n=6) and H4+Ischemia(n=6) group. Using our unique hypoxic preconditioned mouse model and middle cerebral artery occlusion mouse model, combined with TTC staining, SDS-PAGE and Western blot, we observed the changes in infarction sizes, density, edema ratio, and changes in cPKC II and membrane translocation in ischemic cortex of MCAO mice. Results HPC significantly reduced infarction size (P<0.05), density of infarct area (P<0.05) and edema ratio(P<0.05). As compared with H0+sham group, cPKC II and membrane translocation levels in penumbra of ischemic cortex decreased significantly (p<0.05). Whereas cPKC II and membrane translocation levels in penumbra of ischemic cortex in H4+Ischemia group increased significantly compared with that of mice in H0+Ischemia group (p<0.05). Conclusion Hypoxic preconditioning increased levels of cPKC II and membrane translocation in penumbra of middle cerebral artery occluded mice, which may be involved in the protective effect of HPC to severe ischemic injury.

The Up-regulation of the ERK phosphorylation in gastric mucosal cell by the serum derived from the rats treated with electroacupuncture at stomach meridian acupoints

Zong-bao YANG; Jie YAN; Shou-xiang YI; Xiao-rong CHANG; Yan ZHONG

2009, 29(2):  135-138. 

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Objective To study the Extracelluar Regulated protein Kinase(ERK) phosphorylation in gastric mucosal cell by the serum derived from the rats treated with electroacupuncture at stomach meridian acupoints. Methods 72 rats were randomly divided into Normal group, Model group, Stomach group, Gallbladder group, Stomach plus PD153035 group and Gallbladder plus PD153035 group, gastric mucosal cells were separated by using pronase digestion method, and incubated by PD153035, a EGFR inhibitor and 100ml/L serum in sequence, ERK phosphorylation in gastric mucosal cells was tested by Western blot. Results In both Stomach group and Gallbladder group, compared with the Normal group or Model group, the ERK phosphorylation in gastric mucosal cell were more reinforcement（P<0.01）. Furthermore, the effects in Stomach group were more obvious than those in Gallbladder group（P<0.01）. Compared with Stomach group, the reduction of the ERK phosphorylation in Stomach plus PD153035 group was more significant（P<0.01）.Conclusions The serum derived from the rats treated with electroacupuncture at stomach meridian acupoints can activate the ERK phosphorylation in gastric mucosal cells, which also could be one proof for the TCM theory "Relative particularity between Meridian and Viscera".

h-DTD actives the nonselective cation channels in neuroblastoma SH-SY5Y cell line

Jing-xi ZHU; Hong-bo YANG; Xiao-xia YU; Wei HAO; Guang-hong BAO; Ji-min CAO; Yan-hua GONG

2009, 29(2):  139-143. 

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Objective To speculate on the function of the human D-Tyr-tRNATyr deacylase (h-DTD)It's influence on nonselective cation channels permeability of Na+, K+ and Ca2+ in neuroblastoma SH-SY5Y cell line. Methods The enzyme activity of h-DTD was analyzed with capillary electrophoresis; then the h-DTD protein expression level was detected in different tissues and cell lines with western blot. Also, the membrane patch clamp technology was used to test the whole-cell potential change in SH-SY5Y cell line. Results h-DTD has deacylase activity in vitro, and this protein is expressed widely in different tissues. however, it is enriched in brain. As we have found that the L-glutamic acid sensitive channel could be motivated by D-amino acid and L-glutamid acid only in the presence of h-DTD and resulted in the iron permeability enhanced. Conclusion h-DTD could affect the nonselective cation channels through the regulation of dissociative D-form amino acid concentration, which implies it may function as a regulator.

Repairing on Rabbit Facial Nerve by the Transplanted of NSCs－ HA－NT-3 Complex

Han ZHANG; Yue-teng WEI; Chong-ran SUN; Jin LI; Hua HUANG; Fu-zhai CUI; Yi-hua AN

2009, 29(2):  144-147. 

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Objective This experiment explored the possibility of repairing injured facial nerve with tissue engineering technology and neural stem cells（NSCs）. The complex consisted of NSCs, scaffold and NT-3. NSCs were immature cells with the potential of self-renewal and multiple differentiation to neurons and glial cells. The scaffold with porous surface was made of hyaluronic acid and collagen (HA-Col gel) which degenerate in vivo after transplantation. NT-3 is the signal proved effective in promoting neurons survival in vitro. Methods NSCs of S-D rat were co-cultured with scaffold and NT-3 in vitro. The two stumps of disconnected facial nerve of rabbit were re-connected with the complex. Electrophysiology and morphology tests were used to examine the functional and morphological changes.Results NSCs adhered to the HA-Col gel and survived. Injured facial nerve fixed by NSCs-HA-Col gel-NT-3 complex showed significant improvement in function and anatomical structure. Conclusion The result demonstrated that combinative implant of NSCs, HA-Col gel and NT-3 could promote the regeneration of injured facial nerve.

Effects of FKN on PKC-ERK1/2 activation and TNF-α expression in human peripheral blood monocytes

Ming-ming LEI; Jian SUN; Zhe WU; Chun-yan YANG; Yu-hua CHEN

2009, 29(2):  148-151. 

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Objective To explore one of the possible signal transduction pathways of FKN/CX3CR1 in human peripheral blood monocytes (PBMC) and the mechanism of FKN in promoting atherosclerosis,the function of protein kinase C is also studied.Methods （1）Human peripheral blood monocytes were isolated from fresh blood of healthy volunteers by Ficoll-Paque gradient centrifugation.（2）Divided the PBMC into four groups:control,FKN,Ro31-8220 and PD98059 groups.（3）Measured the ERK 1/2 expression of monocytes from each group by Western blot.（4）Collected the supernatant of monocytes from each group ,determined the expression of TNF-α by enzyme-linked immunosorbent assay(ELISA).Results （1）The expression of ERK1/2 and TNF－α from FKN group was significantly higher compared with the control and TNF－α from FKN group was significantly higher compared with the control group（P<0.05）.（2）The expression of ERK1/2 and TNF－α from Ro31-8220 group was decreased compared with the FKN group（P<0.05）.Conclusions FKN－CX3CR1 induces the expression of TNF－α via PKC/ERK signal pathway which contributines to the development and progression of atherosclerosis.

Expression of OBR and NPY in mouse hypothalamus

Chun YANG; Hui-xian CUI; Ping FAN

2009, 29(2):  152-155. 

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Obective To observe the expression of OBR and NPY in mouse hypothalamus. Methods In mouse hypothalamus, the location and coexpression of OBR and NPY were observed with immunohistochemistry and double immunohistochemistry. Results OBR positive cells distributed as clump in hypothalamus ME, ARC and VMN, having obscure boundary. OBR positive cells were also present in choroid plexus, brain ependymal layer cell and vascular endothelial cell. In hypothalamus ARC, NPY positive neurons were present with bright red color in cell plasma. The NPY positive neurons were found as round or ellipse, having many neurites. NPY positive fibers were present in ME. In double immunohistochemitry result, the coexpression of OBR and NPY showed black color, because that OBR positive cells showed brown purple or dark purple granula near the NPY positive neurons. Conclusions OBR distributed in ME, ARC, VMN of mouse hypothalamus, choroid plexus, brain ependymal layer cells and vascular endothelial cells. Meanwhile NPY also distributed in ME, ARC, cerebral cortex and hippocampus and so on. Moreover the coexpression of OBR and NPY was present in mouse hypothalamus ARC.

Mechanism on STZ induced pancreatic islets apoptosis effect of Fructose-1,6-Disphosphate

Qian ZHENG; Hong LIU; Di-yong CAO; Hai-tao LAN; Hua LIU; Hai-li FANG; Neng ZHANG

2009, 29(2):  156-160. 

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Object To investigate the protective role of FDP in STZ induced islest apoptosis and to explore the mechanisms of the protective effect of FDP. Methods:The pancreases of the rats were removed to collect islets cells.The cells were incubated with STZ with/or FDP. Cell ,insulin secretion ,HO-1 activity ,CO content ,SOD activity ,GSH-px activity, iNOS activity, No conetent and apoptotic percentage were detected. Results: HO-1 activity and CO content of the normal control group were low. STZ induced a significant decrease of cell activity and insulin release, flow cytometry analysis showed that apoptotic percentage of islet cells remarkably increased following the addition of STZ, FDP obviously improved the the islets cellular activity damaged by STZ,and basic amount of insulin secretion and stimulated by high glucose were improved（P＜0.01）. Content of CO , activity of HO-1, SOD activity ,GSH-PX activity were lower in the STZ group than the normal control group（P＜0.01）,and there were significant differences between conetent were higher in the STZ group than in the FDP group.FDP decreased cell the FDP groups and STZ group （P＜0.01 or P＜0.05）. iNOS activity and No apoptotic percentage（P＜0.01 or P＜0.05）. Activities of HO-1 and content of CO were higher than in the STZ group （P＜0.01 or P＜0.05）. Conclusion: FDP can attenuate the STZ induced apoptosis of culturedβcells.the mechanisms may be improved HO-1 activity and CO content, also improved SOD activity ,GSH-px activity and decreased iNOS activity and NO content.

Arsenic trioxide induces endoplasmic reticulum stress-related apoptosis in drug-resistant K562/ADM cells

Yan-yun MA; Jing CHEN; Juan YI; Lin-jing LI; Hui-lai WEI

2009, 29(2):  161-165. 

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Objective To explore whether arsenic trioxide(As2O3)-induced apopotosis in drug-resistant leukemia K562/ADM cells is involved in endoplasmic reticulum stress-related apopotosis. Methods The apoptosis of K562/ADM cells was identified by double staining of FITC-Annexin V and propidium iodide (PI), and the morphological ultrastructure of the cells, endoplasmic reticulum and mitochondria was observed using transmission electron microscopy. Flow cytometry (FCM) techenique was employed to assess mitochondrial inner membrane potential(Δψm), intracellular calcium concentration, cytochrome c (Cyt c) release and caspase-3 activity. The expression of GRP78 protein was analyzed by Western blot. Result During the apoptotic process of K562/ADM cells induced with 2 mol/L and 5 mol/L As2O3, the endoplasmic reticulum exhibited obvious expansion and degranulation, and the mitochondria illustrated inner and outer membranes fusion, reduced and confused cristae, swelling and vacuolization. The mitochondrial Δψm decreased, the intracellular calcium concentration and releasing of cytochrome c from mitochondria increased, and caspase-3 was activated. Western blot result indicated upregulation of GRP78 protein at endoplasmic reticulum in apopototic K562/ADM cells. Conclusion As2O3 can initiate the endoplasmic reticulum stress in K562/ADM cells, and induces the drug-resistant cell to apoptosis via endoplasmic reticulum-mitochondrial pathway.

Relation between the role of promoting disequilibrium of cell proliferation and apoptosis of BID and the pathogenetic condition of IgAN

Lin MA; Shu-xia FU; Lin YANG; Jian-rong WANG

2009, 29(2):  166-169. 

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Objective:To explore the expression of BID and the relation between cell proliferation and apoptosis at various stages of IgAN. Method:The expression of BID、PCNA and FN in renal tissue were detected by immunohistochemistry, TUNEL and light microscope were used to detect apoptotic cells. Result:With the progress of IgAN, the expression of BID、PCNA、the number of apoptotic cells and FN increased gradually (P< 0.05),especially in IV group(PCNA：Ⅳ is in the same rank as Ⅲgroup), The expression of BID in glomcrulus had positive correlation with the rate of apoptotic cells、the express of PCNA and FN、the rate of glomerular sclerosis and urine protein，and had negative correlation with glomerular filtration rate(P<0.01).Conclusion: BID can accelerate the progression of IgAN through promoting disequilibrium of cell proliferation and apoptosis，and it may serve as a marker for judging prognosis.

Increase of p-p38 and uPA expression in human breast cancer

Yan-chun HAN; Lu-ying LIU; Dong-xia YANG; Gui-hua WANG

2009, 29(2):  170-173. 

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Objective To study the expression and significance of phosphorylated p38 (p-p38) and uPA in breast cancer tissues and cells. Methods Immunohistochemistry (S-P) was used to test the protein expression of p-p38 and uPA in 60 specimens excised during operation from 50 patients with breast cancer. Western blotting was adopted to detect the protein expression of p-p38 and uPA in breast cancer cells and uPA protein expression after SB203580, an specific inhibitor of p38 MAPK blocked p38MAPK signaling pathway. Results The positive rate of p-p38 protein and uPA protein in breast cancer tissues was 56.7%and 60.0%,respectively. The protein expression levels of p-p38 and uPA in breast cancer tissues were significantly higher than those in the adjacent normal tissues(P<0.05) The protein expression of p-p38 was linearly correlated with uPA expression(r=0.316, P<0.05). The expression of p-p38 and uPA was related to lymph node metastasis and TNM stage (P<0.05), and it was not related to patients'age and tumor size. The protein expression levels of p-p38 and uPA in breast cancer cells MDA-MB-231 were higher than that in MCF-7. SB203580 nhibited p38MAPK pathway and down-regulated uPA protein expression. Conclusion Overexpression of p-p38 and uPA may play a critical role in breast cancer malignant progression. These results provide instructive clues to breast cancer invasion and metastasis research.

Expression of Calcitoningene related peptide in pathological tissue of congenital pseudarthrosis of tibia

Shi-wei QI; Ke-lai WANG; Yan ZHUANG; Hong-yi QU; Guo-xin SONG

2009, 29(2):  174-177. 

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Objective To determine the expression of CGRP in congenital pseudarthrosis of tibia(CPT),in order to study the cause and pathogenesis of CPT.Method periosteum and bones taken from CPT patients were as experimental group,and those taken from normal persons were as control group.Immunohistochemistry stain were applied to determine the differences of the expression of CGRP in two groups.Results CGRP was located at vessel wall in periosteum and intracytoplasm of osteoblasts and osteoclasts in bones,its expressions were less both in periosteum and bones of CPT than that in control group,and the differences were significant(P<0.05).Conclusion anormaly expression of CGRP in CPT may be one of the causes of CPT.

The effect of estrogen and progesterone on expression of LPA3 in uterine endometrium during the period of periimplantation

Yan-hong GUO; Lei ZHANG; Su-xia SHAO; Qing YIN; Miao GONG; Jin-ping ZHANG; Jing ZHAO

2009, 29(2):  178-182. 

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Objective To investigate the expression and distribution of lysophosphatidic acid receptor 3 (LPA3) during the period of mouse embryo implantation and the effect of estrogen and progesterone and RU486 on murine endometrial LPA3 expression. Methods Immunohistochemistry was employed to observe and analyze the expression and distribution of LPA3 protein in the uterine endometrium during the 1~6th pregnancy day (d1~6). Ovariectomized mice were randomly divided into control and treatment groups,estrogen, progesterone and RU486 was given to ovariectomized mice.The expression of LPA3 mRNA and protein were detected by RT-PCR and Western blotting. Results LPA3 protein was expressed in the endometrium of 1~6th pregnancy day . The LPA3 protein level in the uteri increased on d3 , peaking around d4., then returned to the basal levels on d5 and d6 . LPA3 mRNA and protein expression remained at a low level in ovariectomized mice. Progesterone up-regulated LPA3 mRNA and protein. Estrogen counteracted the effect of progesterone. RU486 inhibited the effect of progestin. Conclusions LPA3 may participate in the period of mouse embryo implantation. Progesterone and estrogen cooperatively regulate LPA3 expression, thereby contributing to the receptivity of uteri during early pregnancy.

Implantation of autologous bone marrow mononuclear cells in treatment of ischemia hindlimb in rats

Hai-tao WANG; Wei-liang JIANG; Zhan-feng SUN; Ying-nan ZHANG; Jun MA; Qing-feng SUN

2009, 29(2):  183-187. 

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Objective To investigate the ability of bone marrow mononuclear cells (BM-MNCs) to induce vasculogenesis in ischemic hindlimb, and develop an easier and safer therapy method in treatment of ischemic arterial disease of the lower extremity. Methods Build ischemia hindlimb models in rats. BM-MNCs isolated from rat bone marrow were autonomously transplanted into the ischemic area in rat. The animals were killed at 2 days, 30 days after taking the angiography, respectively. Differentiation of the endothelial progenitor cells (EPCs), capillaries density and vascular endothelial growth factor (VEGF) expression of the local tissue was analyzed by immunohistochemical staining. Results EPCs were found in muscles of the control group, however its number increased in ischemic muscle（P<0.01）. The density of capillaries was much higher in the BM-MNC implantation group than the others after 30 days （P<0.01）. In angiography, collateral arteries were significantly increased in ischemic hindlimbs （P<0.01）. The expression of VEGF was significantly higher in the transplanted muscles after 2 days （P<0.01）. Conclusion BM-MNCs can induce vasculogenesis in the ischemic muscle. Implantation of autologous BM-MNCs could be a simple and efficient therapy for the ischemic hindlimbs.

技术与方法

Plasmid Construction of Dominant Negative Survivin Mutant

Wen-jie CAI Ming-jie WANG Yu-ling ZHANG Li-hua JU Yi-chun ZHU

2009, 29(2):  188-192. 

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Objective To construct dominant negative mutant plasmid of survivin. Methods Total RNA was extracted from rat cardiac microvascular endothelial cells and reverse transcripted into cDNA. Survivin gene was amplified and the restriction enzyme cutting sites were added using nested PCR, followed by site-specific mutagenesis of survivin by overlap PCR. The product was reconstructed into eukaryotic expression plasmid pEGFP-N3 and sequence analysis was used to examine the recombinant. Cells were transfected with the recombinant and cell apoptosis was then estimated. Results PCR-amplified 496 bp fragment coding for survivin and 452 bp fragment containing restriction enzyme cutting sites were obtained using nested PCR. Site-specific mutagenesis of 452 bp survivin fragment was gained after three PCR reactions by overlap extention. The recombinant was identified by sequence analysis. Transfected cells emitted bright green fluorescence and underwent severe apopotosis compare with control cells. Conclusion The dominant negative plasmid pEGFP-DN-survivin was successfully constructed.

Histocompatibility of Canine VSMLCs and PGA\Collagen Scaffold

Zhen-zong DU; Hua REN; Chao-ji ZHANG; Jian-fei SONG; Yue-pei LIANG; An-gui LI

2009, 29(2):  193-197. 

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Objective To study the histocompatibility of canine vascular smooth muscular-like cells(VSMLCs) and polyglycolic acid (PGA) coated with cross-linked collagen(PGA\collagen) scaffold by morphology observation ,cell proliferation and so on. Methods Rat's tail collagen and PGA\collagen scaffold were produced and constructed firstly. VSMLCs derived from bone marrow mesenchymal stem cells were cultured on the PGA\collagen scaffold. Morphological characteristics were observed by HE staining, toluidine blue staining and scanning electron microscope. Cells adhesion and proliferation were detected with MTT assay. Results The PGA\collagen scaffold had elasticity and tenacity. Histological and ultrastructural observation showed that there were lots of micropores in the scaffold. HE staining, toluidine blue staining ,scanning electron microscope and growth curve from MTT assay showed that VSMLCs seeded on the PGA\collagen scaffold grew well. Conclusion The PGA\collagen scaffold had a good histocompatibility with VSMLCs.

研究短文

Inhibiting effects of rosiglitazone on expression of TGF-β1 and FIBRONECTIN in rat hepatocytes cultured with CsA

Gen-yang CHENG; Jian-sheng LI; Zhang-suo LIU

2009, 29(2):  198-200. 

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Up-Regulation of Midkine Protein Expression in Non-Small Cell Lung Cancer Tissue

Shi-hua ZHANG; Kai-hua LU; Qing-ling WANG; Ya-yi HOU

2009, 29(2):  201-203. 

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Role of expression of connective tissue growth factor in lung fibrosis of pulmonary hypertensive rats

Bin LIU; Xian-min WANG; Xiao-qin WANG; Li WEI; Tong-fu ZHOU; Yi-min HUA; Han-min LIU

2009, 29(2):  204-206. 

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Regulation of human macrophage cholesterol efflux by Nicotine

Mo-ye CHEN; Zong-jie QIAN

2009, 29(2):  207-209. 

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Alpha-lipoic acid mitigates beta-cell damage induced by streptozotocin in rats

Huai-qing WANG; Ming-li SU; Yin-xue LEI; Jun-jie ZOU; Xiu-lan ZOU; Ying ZHAO; Yong-quan SHI; Zhi-min LIU

2009, 29(2):  210-211. 

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短篇综述

BNP and Cardiovascular Events

Xiao-yan ZHOU; Jin-xiang HAN; Xue-qin GAO; Bo ZHU

2009, 29(2):  212-215. 

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B-type natriuretic peptide,a heart-derived hormone, was found in 1988, which belongs to natriuretic peptides.Like other natriuretic peptides, it can also inhibit the renin-angiotensin-aldosterone system and sympathetic system，and conclusively, play a crucial role in cardiovascular homeostasis. The relationship between BNP and cardiovascular events has always been an issue. So far, clinically, BNP testing has been useful in the evaluation of heart failure as a cause of acute dyspnea in the emergency department. The role of BNP in cardiovascular events diagnosis, therapy and prognosis still calls for further investigation. In this narrative review, we will summarize the progressive investigation of BNP molecular biology and its role in cardiovascular events

Research and application of microRNA in the liver diseases

Ya-dong WANG; Cai-yan ZHAO

2009, 29(2):  216-219. 

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MicroRNAs (miRNAs, miR) are a class of 21~22 nt small non-protein-coding single strand RNA molecules. In the liver, the phenotypic alternation or expressed abnormality of many miRNAs can influence the hepatitis virus replication on the gene level, which would provocate the development from hepatitis to hepatic fibrosis, cirrhosis, and even primary hepatic carcinoma on target. And so, several miRNAs are confirmed to be a new class of related gene to carcinoma. Furthermore, the dysfunction or abnormal quantity of miRNAs will promote the formation of fatty liver disease by interfering with signal transduction of insulin, inducing insulin resistance and then influencing normal metabolism of endosomatic lipid, Therefore, the specific medicine or methods, which might retrieve the expression or function of miRNAs in the hepatocytes, will provide a new valuable method to oppose human liver disease.