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| 1 | Inhibiting effect of antisense oligonucleotides phosphorthioate on gene expression of TIMP-1 in rat liver fibrosis显示文摘AIM To observe the inhibition of antisenseoligonucleotides (asON) phosphorthioate to thetissue inhibitors metalloproteinase-1 (TIMP-1)gene and protein expression in the liver tissue ofimmunologically induced hepatic fibrosis rats.The possibility of reversing hepatic fibrosisthrough gene therapy was observed.METHODS Human serum albumin (HSA) wasused to attack rats, as hepatic fibrosis model, inwhich asONs were used to block the gene andprotein expressing TIMP-1. According to theanalysis of modulator, structure protein, codingseries of TIMP-1 genome, we designed fourdifferent asONs. These asONs were injected intothe hepatic fibrosis models through coccygealvein. The results was observed by RT-PCR formeasuring TIMP-1 mRNA expression,immunohistochemistry and in situ hybridizationfor collagen Ⅰ, Ⅲ, special staining of collagenfiber, and electron microscopic examination.RESULTS Hepatic fibrosis could last within 363days in our modified model. The expressinglevel of TIMP-1 was high during hepatic fibrosisprocess. It has been proved by theimmunohistochemical and the electronmicroscopic examination that the asONphosphorthioate of TIMP-1 could exactly expressin vivo. The effect of colchicine wasdemonstrated to inhibit the expressing level ofmRNA and the content of collagen Ⅰ, Ⅲ in theliver of experimental hepatic fibrosis rats.However, the electron microscopy research andthe pathologic grading of hepatic fibrosisshowed that there was no significant differencebetween the treatment group and the modelgroup (P>0.05).CONCLUSION The experimental rat model ofhepatic fibrosis is one of the preferable modelsto estimate the curative effect of anti-hepaticfibrosis drugs. The asON phosphorthioate ofTIMP-1 could block the gene and proteinexpression of TIMP-1 in the liver of experimentalhepatic fibrosis rats at the mRNA level. It ispossible to reverse hepatic fibrosis, and it isexpected to study a new drug of anti-hepaticfibrosis on the genetic level. Colchicine has verylimited therapeutic effect on hepatic fibrosis,furthermore, its toxicity and side effects areobvious. | Qing He Nie Yong Qian Cheng Yu Mei Xie Yong Xing Zhou Yi Zhan Cao The Center of Infectious Disease Diagnosis and Treatment of PLA,Tangdu Hospital,Forth Military Medical University,Xi’an 710038,Shaanxi Province,ChinaDr,Qing He Nie graduated from Qinghai Medical College as a doctor in 1983,got master degree at Beijing 302 Army Hospital in 1993,got doctor degree at the Third Military Medical University in 1998,engaged in postdoctoral research at the Fourth Military Medical University from 1998 to 2000,now an associate professor,specialized in clinical and experimental research of infectious diseases,had more than 90 papers published,coauthor of ten books,first author of one book. | 2001 | World Journal of Gastroenterology2001，7，3： | 73 |
| 2 | China land soil moisture EnKF data assimilation based on satellite remote sensing data显示文摘Soil moisture plays an important role in land-atmosphere interactions. It is an important geophysical parameter in research on climate, hydrology, agriculture, and forestry. Soil moisture has important climatic effects by influencing ground evapotranspi ration, runoff, surface reflectivity, surface emissivity, surface sensible heat and latent heat flux. At the global scale, the extent of its influence on the atmosphere is second only to that of sea surface temperature. At the terrestrial scale, its influence is even greater than that of sea surface temperatures. This paper presents a China Land Soil Moisture Data Assimilation System (CLSMDAS) based on EnKF and land process models, and results of the application of this system in the China Land Soil Moisture Data Assimilation tests. CLSMDAS is comprised of the following components: 1) A land process mo del—Community Land Model Version 3.0 (CLM3.0)—developed by the US National Center for Atmospheric Research (NCAR); 2) Precipitation of atmospheric forcing data and surface-incident solar radiation data come from hourly outputs of the FY2 geostationary meteorological satellite; 3) EnKF (Ensemble Kalman Filter) land data assimilation method; and 4) Observa tion data including satellite-inverted soil moisture outputs of the AMSR-E satellite and soil moisture observation data. Results of soil moisture assimilation tests from June to September 2006 were analyzed with CLSMDAS. Both simulation and assimila tion results of the land model reflected reasonably the temporal-spatial distribution of soil moisture. The assimilated soil mois ture distribution matches very well with severe summer droughts in Chongqing and Sichuan Province in August 2006, the worst since the foundation of the People’s Republic of China in 1949. It also matches drought regions that occurred in eastern Hubei and southern Guangxi in September. | SHI ChunXiang XIE ZhengHui QIAN Hui LIANG MiaoLing YANG XiaoChun | 2011 | Science China Earth Sciences2011，54，9： | 62 |
| 3 | A Rare Allele of GS2 Enhances Grain Size anc Grain Yield in Rice显示文摘谷物尺寸决定谷物重量并且影响谷物质量。调整谷物尺寸的几主要量的特点 loci (QTL ) 被克隆;然而,我们调整米饭谷物的尺寸的内在的机制的理解仍然保持碎片。这里,我们报导克隆和主导的 QTL 的描述,染色体 2 上的谷物尺寸(GS2 ) 编码调整生长的因素 4,一个 transcriptional 管理者。GS2 本地化到原子核并且可以充当抄写使活跃之物。影响 microRNA 的有约束力的地点的 GS2 的一个稀罕变化, OsmiR396c,原因提高了 GS2/OsGRF4 的表示。GS2 表示的增加导致更大的房间和房间的增加的数字,它因此提高谷物重量和产量。进米饭栽培变种的 GS2/OsGRF4 的这稀罕等位基因的介绍能显著地提高谷物重量和增加谷物产量,用在引起产量很高的米饭变化的可能的应用。 | Jiang Hu Yuexing Wang Yunxia Fang Longjun Zeng Jie Xu Haiping Yu Zhenyuan Shi Jiangjie Pan Dong Zhang Shujing Kang Li Zhu Guojun Dong Longbiao Guo Dali Zeng Guangheng Zhang Lihong Xie Guosheng Xiong Jiayang Li Qian Qian | 2015 | Molecular Plant2015，8，10： | 57 |
| 4 | Plasma exchange-centered artificial liver support system in hepatitis B virus-related acute-onchronic liver failure:a nationwide prospective multicenter study in China显示文摘BACKGROUND:Plasma exchange(PE)-centered artificial liver support system reduced the high mortality rate of hepatitis B virus(HBV)-related acute-on-chronic liver failure(ACLF).But the data were diverse in different medical centers.The present prospective nationwide study was to evaluate the effects of PE on patients with HBV-ACLF at different stages.METHODS:From December 2009 to December 2011,we evaluated 250 patients at different stages of HBV-ACLF from 10 major medical centers in China.All the laboratory parameters were collected at admission,before and after PE.RESULTS:Among the 250 patients who underwent 661 rounds of PE,one-month survival rate was 61.6%; 141(56.4%) showed improvement after PE.Variables such as age(P=0.000),levels of total bilirubin(TB,P=0.000),direct bilirubin(P=0.000),total triglycerides(P=0.000),low-density lipoprotein(P=0.022),Na+(P=0.014),Cl–(P=0.038),creatinine(Cr,P=0.007),fibrinogen(P=0.000),prothrombin time(PT,P=0.000),white blood cell(P=0.000),platelet(P=0.003) and MELD(P=0.000) were significantly related to prognosis.Multivariate logistic regression analysis showed that age,disease stage,TB,Cr and PT levels were independent risk factors of mortality among HBV-ACLF patients.CONCLUSIONS:PE can improve the clinical outcome of patients with HBV-ACLF.Levels of TB,Cr and PT,age and disease stage help to predict prognosis. | Jia-Jia Chen Jian-Rong Huang Qian Yang Xiao-Wei Xu Xiao-Li Liu Shao-Rui Hao Hui-Fen Wang Tao Han Jing Zhang Jian-He Gan Zhi-Liang Gao Yu-Ming Wang Shu-Mei Lin Qing Xie Chen Pan Lan-Juan Li | 2016 | Hepatobiliary & Pancreatic Diseases International2016，15，3： | 48 |
| 5 | Pathological changes at early stage of multiple organ injury in a rat model of severe acute pancreatitis显示文摘BACKGROUND:Severe acute pancreatitis (SAP) is a commonly seen acute abdominal syndrome characterized by sudden onset,rapid progression and high mortality rate.The damage in peripheral organs may be more severe than that in the pancreas,and can even lead to multiple organ dysfunction.It is critical to recognize early pathological changes in multiple organs.This study aimed to assess the early pathological features of damaged organs in a rat model of SAP.METHODS:Thirty clean grade healthy male Sprague-Dawley rats weighing 250-300 g were randomly divided into a model control group (n=15) and a sham-operated group (n=15).The SAP rat model was induced by sodium taurocholate.Samples of blood and from multiple organs were collected 3 hours after operation.We assessed the levels of IL-6,TNF-α,PLA2,NO,ET-1,MDA,amylases and endotoxin in blood and observed the early pathological changes in multiple damaged organs.RESULTS:Levels of IL-6,TNF-α,PLA2,NO,ET-1 and MDA in serum and of amylase and endotoxin in plasma of the model control group rats were significantly higher than those of the sham-operated group (P<0.01).Different degrees of pathological change were observed in multiple damaged organs.CONCLUSION:Multiple organ injury may occur at the early stage of SAP in rats. | Zhang, Xi-Ping Zhang, Jie Ma, Mei-Li Cai, Yang Xu, Ru-Jun Xie, Qi Jiang, Xin-Ge Ye, Qian | 2010 | Hepatobiliary & Pancreatic Diseases International2010，9，1： | 33 |
| 6 | Caspase-11/4 and gasdermin D-mediated pyroptosis contributes to podocyte injury in mouse diabetic nephropathy显示文摘Diabetic nephropathy(DN)is characterized by sterile inflammation with continuous injury and loss of renal inherent parenchyma cells.Podocyte is an essential early injury target in DN.The injury and loss of podocytes are closely associated with proteinuria,the early symptom of renal injury in DN.However,the exact mechanism for podocyte injury and death in DN remains ambiguous.In this study we investigated whether pyroptosis,a newly discovered cell death pathway was involved in DN.Diabetic mice were generated by high-fat diet/STZ injections.We showed that the expression levels of caspase-11 and cleavage of gasdermin D(GSDMD-N)in podocytes were significantly elevated,accompanied by reduced expression of podocyte makers nephrin and podocin,loss and fusion in podocyte foot processes,increased inflammatory cytokines NF-κB,IL-1β,and IL-18,macrophage infiltration,glomerular matrix expansion and increased urinary albumin to creatinine ratio(UACR).All these changes in diabetic mice were blunted by knockout of caspase-11 or GSDMD.Cultured human and mouse podocytes were treated with high glucose(30 mM),which significantly increased the expression levels of caspase-11 or caspase-4(the homolog of caspase-11 in human),GSDMD-N,NF-κB,IL-1β,and IL-18,and decreased the expression of nephrin and podocin.Either caspase-4 or GSDMD knockdown by siRNA significantly blunted these changes.In summary,our results demonstrate that caspase-11/4 and GSDMD-mediated pyroptosis is activated and involved in podocyte loss under hyperglycemia condition and the development of DN. | Qian Cheng Jing Pan Zhuan-li Zhou Fan Yin Hong-yan Xie Pan-pan Chen Jing-yao Li Pei-qing Zheng Li Zhou Wei Zhang Jun Liu Li-min Lu | 2021 | Acta Pharmacologica Sinica2021，42，6： | 33 |
| 7 | Ketogenic diet poses a significant effect on imbalanced gut microbiota in infants with refractory epilepsy显示文摘AIM To investigate whether patients with refractory epilepsy and healthy infants differ in gut microbiota(GM),and how ketogenic diet(KD) alters GM.METHODS A total of 14 epileptic and 30 healthy infants were recruited and seizure frequencies were recorded. Stool samples were collected for 16 S r DNA sequencing using the Illumina Miseq platform. The composition of GM in each sample was analyzed with MOTHUR,and intergroup comparison was conducted by R software.RESULTS After being on KD treatment for a week,64% of epileptic infants showed an obvious improvement,with a 50% decrease in seizure frequency. GM structure in epileptic infants(P1 group) differed dramatically from that in healthy infants(Health group). Proteobacteria,which had accumulated significantly in the P1 group,decreased dramatically after KD treatment(P2 group). Cronobacter predominated in the P1 group and remained at a low level both in the Health and P2 groups. Bacteroides increased significantly in the P2 group,in which Prevotella and Bifidobacterium also grew in numbers and kept increasing.CONCLUSION GM pattern in healthy infants differed dramatically from that of the epileptic group. KD could significantly modify symptoms of epilepsy and reshape the GM of epileptic infants. | Gan Xie Qian Zhou Chuang-Zhao Qiu Wen-Kui Dai He-Ping Wang Yin-Hu Li Jian-Xiang Liao Xin-Guo Lu Su-Fang Lin Jing-Hua Ye Zhuo-Ya Ma Wen-Jian Wang | 2017 | World Journal of Gastroenterology2017，23，33： | 25 |
| 8 | SF/HGF-c-Met autocrine and paracrine promote metastasis of hepatocellular carcinoma显示文摘AIM: To explore the role of SF/HGF-Met autocrine and parscrine in metastasis of hepatocellular carcinoma (HCC).METHODS: SF/HGF and c-met transcription and protein expression in HCC were examined by RT-PCR and Western Blot in 4 HCC cell lines, including HepG2, Hep3B,SMMC7721 and MHCC-1, the last cell line had a higher potential of metastasis. Sf/hgf cDNA was transfected by the method of Lipofectin into SMMC7721. SF/HGF and c-met antibody were used to stimulate and block SF/HGF-c-met signal transduction. Cell morphology, mobility, and proliferation were respectively compared by microscopic observation, wound healing assay and cell growth curve.RESULTS: HCC malignancy appeared to be relative to its met-SF/HGF expression. In MHCC-1, c-met expression was much stronger than that in other cell lines with lower potential of metastasis and only SF/HGF autocrine existed in MHCC-1. After sf/hgf cDNA transfection or conditioned medium of MHCC-1 stimulation, SMMC7721 changed into elongated morphology, and the abilities of proliferation ( P < 0.05) and mobility increased. Such bio-activity could he blocked by c-met antibody ( P< 0.05).CONCLUSION: The system of SF/HGF-c-met autocrine and paracrine played an important role in development and metastasis potential of HCC. Inhibition of SF/HGF-c-met signal transduction system may reduce the growth and metastasis of HCC. | Qian Xie Kang-Da Liu Mei-Yu Hu Kang Zhou Experimental Research Center of Zhongshan Hospital,Fudan University,Shanghai,200032,China | 2001 | World Journal of Gastroenterology2001，7，6： | 24 |
| 9 | Effect of Lichong decoction on expression of Bcl-2 and Bcl-2-associated X protein mRNAs in hysteromyoma model rat显示文摘OBJECTIVE:To study on effects of Lichong decoction on expression of apoptosis-controlling genes,Bcl-2 and Bcl-2-associated X protein(Bax) mRNAs in hysteromyoma tissue of the hysteromyoma model rat.METHODS:Fifty Wistar female rats were randomly divided into a normal group,a model group,a Lichong decoction group,a Guizifuling capsule group and a Mifepristone group.The hysteromyoma rat model was established by intraperitoneal injection of exogenous estrin and progestogens.Pathological examination of uterine tissue,uterine coefficient and uterine transverse diameter were made under optic microscope and expressions of Bcl-2 and Bax mRNAs in uterine tissue in the groups were detected with real-time fluorescent quantitative polymerase chain reaction(PCR) technique.RESULTS:After treatment,under microscope it was found that in the Lichong decoction group myometrium thinned,muscle fiber slightly overgrowth or long and thin,regular arrangement,inserting phenomenon of inner circular muscle and external longitudinal muscle was occasionally or not seen in the Lichong decoction group.The uterine coefficient and the uterine transverse diameter significantly decreased(P<0.01),and Bcl-2 mRNA expression significantly decreased(P<0.01) and Bax mRNA expression significantly increased in hysteromyoma tissue(P<0.01) in the Lichong decoction group as compared with the model group.CONCLUSION:Therapeutic effects of Lichong decoction on hysteromyoma is related with decrease of Bcl-2 mRNA expression and increase of Bax mRNA expression. | Donghua Li Xin Xu Ruiya Qian Jianguo Geng Yan Zhang Xiaolei Xie Yasong Wang Xiaoli Zou | 2013 | Journal of Traditional Chinese Medicine2013，33，2： | 24 |
| 10 | Effect of ulinastatin on paraquat-induced-oxidative stress in human type Ⅱ alveolar epithelial cells显示文摘BACKGROUND:Ulinastatin(UTI) is a urinary trypsin inhibitor extracted and purified from urine of males.This study aimed to explore the effects of UTI on paraquat-induced-oxidative stress in human type Ⅱ alveolar epithelial cells.METHODS:The human type II alveolar epithelial cells,A549 cells,were cultured in vitro.The A549 cells were treated with different concentrations of paraquat(200,400,600,800,1 000,1 200 umol/L) and ulinastatin(0,2 000,4 000,6 000,8 000 U/mL) for 24 hours,the cell viability was measured by cell counting kit-8 and the median lethal concentration was selected.In order to establish an in vitro model of paraquat intoxication and to determine the safe dose of ulinastatin,we calculated LD50 using cell counting kit-8 to determine the survival rate of the cells.A549 cells were divided into normal control group,paraquat group and paraquat+ulinastatin group.The levels of malondialdehyde(MDA) and myeloperoxidase(MPO) were detected by biochemistry colorimetry,while the level of reactive oxygen spies(ROS) was detected by DCFH-DA assay.RESULTS:The survival rate of A549 cells treated with different concentrations of paraquat decreased in a concentration-dependent manner.Whereas there was no decrease in the survival rate of cells treated with 0-4 000 U/mL ulinastatin.The levels of MDA,MPO,and ROS were significantly higher in the paraquat group than in the normal control group after 24-hour-exposure.And the survival rate of the paraquat+ulinastatin group was higher than that of the paraquat group,but lower than that of the normal control group.The levels of MDA,MPO,and ROS were lower than those of the paraquat group.CONCLUSION:Ulinastatin can alleviate the paraquat-induced A549 cell damage by reducing oxidative stress. | Xiao-xiao Meng Rui-lan Wang Shan Gao Hui Xie Jiu-ting Tan Yong-bin Qian | 2013 | World Journal of Emergency Medicine2013，4，2： | 24 |
| 11 | Exogenous NADPH ameliorates myocardial ischemia–reperfusion injury in rats through activating AMPK/mTOR pathway显示文摘Our previous study shows that nicotinamide adenine dinucleotide phosphate(NADPH)plays an important role in protecting against cerebral ischemia injury.In this study we investigated whether NADPH exerted cardioprotection against myocardial ischemia/reperfusion(I/R)injury.To induce myocardial I/R injury,rats were subjected to ligation of the left anterior descending branch of coronary artery for 30 min followed by reperfusion for 2 h.At the onset of reperfusion,NADPH(4,8,16 mg·kg?1·d?1,iv)was administered to the rats.We found that NADPH concentrations in plasma and heart were signi?cantly increased at 4 h after intravenous administration.Exogenous NADPH(8?16 mg/kg)signi?cantly decreased myocardial infarct size and reduced serum levels of lactate dehydrogenase(LDH)and cardiac troponin I(cTn-I).Exogenous NADPH signi?cantly decreased the apoptotic rate of cardiomyocytes,and reduced the cleavage of PARP and caspase-3.In addition,exogenous NADPH reduced mitochondrial vacuolation and increased mitochondrial membrane protein COXIV and TOM20,decreased BNIP3L and increased Bcl-2 to protect mitochondrial function.We conducted in vitro experiments in neonatal rat cardiomyocytes(NRCM)subjected to oxygen–glucose deprivation/restoration(OGD/R).Pretreatment with NADPH(60,500 nM)signi?cantly rescued the cell viability and inhibited OGD/R-induced apoptosis.Pretreatment with NADPH signi?cantly increased the phosphorylation of AMPK and downregulated the phosphorylation of mTOR in OGD/R-treated NRCM.Compound C,an AMPK inhibitor,abolished NADPH-induced AMPK phosphorylation and cardioprotection in OGD/R-treated NRCM.In conclusion,exogenous NADPH exerts cardioprotection against myocardial I/R injury through the activation of AMPK/mTOR pathway and inhibiting mitochondrial damage and cardiomyocyte apoptosis.NADPH may be a potential candidate for the prevention and treatment of myocardial ischemic diseases. | Jiang Zhu Yi-fei Wang Xiao-ming Chai Ke Qian Ling-wei Zhang Peng Peng Pei-min Chen Jian-fang Cao Zheng-hong Qin Rui Sheng Hong Xie | 2020 | Acta Pharmacologica Sinica2020，41，4： | 19 |
| 12 | Sophocarpine attenuates liver fibrosis by inhibiting the TLR4 signaling pathway in rats显示文摘AIM:To explore the effect of sophocarpine on experimental liver fibrosis and the potential mechanism involved.METHODS:Sophocarpine was injected intraperitoneally in two distinct rat hepatic fibrosis models induced either by dimethylnitrosamine or bile duct ligation.Masson’s trichrome staining,Sirius red staining and hepatic hydroxyproline level were used for collagen determination.Primary hepatic stellate cells(HSCs)were isolated and treated with different concentrations of sophocarpine.Real-time reverse transcription-polymerase chain reaction was used to detect the mRNA levels of fibrotic markers and cytokines.The expression of pathway proteins was measured by Western blot.The Cell Counting Kit-8 test was used to detect the proliferation rate of activated HSCs treated with a gradient concentration of sophocarpine.RESULTS:Sophocarpine decreased serum levels of aminotransferases and total bilirubin in rats under chronic insult.Moreover,administration of sophocarpine suppressed extracellular matrix deposition and prevented the development of hepatic fibrosis.Furthermore,sophocarpine inhibited the expression ofα-smooth muscle actin(SMA),interleukin(IL)-6,transforming growth factor-β1(TGF-β1),Toll-like receptor 4(TLR4),and extracellular-related kinase(ERK)in rats.Sophocarpine also down-regulated the mRNA expression ofα-SMA,collagenⅠ,collagenⅢ,TGF-β1,IL-6,tumor necrosis factor-αand monocyte chemoattractant protein-1,and decreased protein levels of TLR4,p-ERK,p-JNK,p-P38 and p-IKK in vitro after Lipopolysaccharide induction.In addition,sophocarpine inhibited the proliferation of HSCs accompanied by a decrease in the expression of Cyclin D1.The protein level of proliferating cell nuclear antigen was decreased in activated HSCs following a gradient concentration of sophocarpine.CONCLUSION:Sophocarpine can alleviate liver fibrosis mainly by inhibiting the TLR4 pathway.Sophocarpine may be a potential chemotherapeutic agent for chronic liver diseases. | Hui Qian Jian Shi Ting-Ting Fan Jiao Lv Si-Wen Chen Chun-Yan Song Zhi-Wu Zheng Wei-Fen Xie Yue-Xiang Chen | 2014 | World Journal of Gastroenterology2014，20，7： | 19 |
| 13 | Inhibition of SIRT6 in prostate cancer reduces cell viability and increases sensitivity to chemotherapeutics显示文摘SI RT6 is an important histone modifying protein that regulates DNA repair,telomere maintenance,energy me-tabolism,and target gene expression.Recently SIRT6 has been identifi ed as a tumor suppressor and is down-regulated in certain cancer types,but not in other can-cers.From deposited gene profi ling studies we found that SIRT6 was overexpressed in prostate tumors,compared with normal or paratumor prostate tissues.Tissue micro-array studies confi rmed the higher levels of SIRT6 in both prostate tumor tissues and prostate cancer cells than in their normal counterparts.Knockdown of SIRT6 in human prostate cancer cells led to sub-G1 phase arrest of cell cy-cle,increased apoptosis,elevated DNA damage level and decrease in BCL2 gene expression.Moreover,SIRT6-de-fi ciency reduced cell viability and enhanced chemothera-peutics sensitivity.Taken together,this study provides the fi rst evidence of SIRT6 overexpression in human prostate cancer,and SIRT6 regulation could be exploited for pros-tate cancer therapy. | Yewei Liu Qian Reuben Xie Boshi Wang Jiaxiang Shao Tingting Zhang Tengyuan Liu Gang Huang Weiliang Xia | 2013 | Protein & Cell2013，4，9： | 17 |
| 14 | Role of Tenascin-X in regulating TGF-β/Smad signaling pathway in pathogenesis of slow transit constipation显示文摘BACKGROUND Chronic constipation is a gastrointestinal functional disease that seriously harms physical and mental health and impacts the quality of life of patients.Its incidence rate is 2%-27%.Slow transit constipation(STC)is a common type of chronic functional constipation,accounting for 10.3%-45.5%of such cases.Scholars have performed many studies on the pathogenesis of STC.These studies have indicated that the occurrence of STC may be related to multiple factors,such as dysfunction of the enteric nervous system,interstitial cells of Cajal(ICC)damage,and changes in neurotransmitters regulating intestinal peristalsis.AIM To investigate the role of Tenascin-X(TNX)in regulating the TGF-β/Smad signaling pathway in the pathogenesis of STC.METHODS This study included an experimental group and a control group.The experimental group included 28 patients with severe colonic STC,and the control group included 18 patients with normal colon tissues.Immunohistochemistry(IHC)was used to detect c-Kit,a specific marker of the ICC.Western blot,immunofluorescence,and IHC were used to detect the localization and expression of TNX and TGF-β/Smad.RESULTS IHC showed that the number of ICC with positive c-Kit expression was significantly reduced in the colon of STC patients(22.17±3.28 vs 28.69±3.53,P<0.05)and that the distribution was abnormal.Western blot results showed that c-Kit and Smad7 levels were significantly decreased in the colon of STC patients(c-kit:0.462±0.099 vs 0.783±0.178,P<0.01;Smad7:0.626±0.058 vs 0.799±0.03,P<0.01)and that TNX and Smad2/3 levels were higher in the STC group(TNX:0.868±0.028 vs 0.482±0.032,P<0.01).There was no significant difference in TGF-βbetween the two groups(0.476±0.028 vs 0.511±0.044,P=0.272).Pearson correlation analysis showed that the TNX protein exhibited a strong correlation with Smad2/3 and Smad7(P<0.05,|R|>0.8)and TGF-β(P<0.05,|R|=0.7).CONCLUSION The extracellular matrix protein TNX may activate the TGF-β/Smad signaling pathway by upregulating the Smad 2/3 signaling protein and thereby induce slight or complete epithelial stromal cell transformation,leading to an abnormal distribution and dysfunction of ICC in the diseased colon,which promotes the occurrence and development of STC. | Yi-Chao Zhang Bao-Xiang Chen Xiao-Yu Xie Yan Zhou Qun Qian Cong-Qing Jiang | 2020 | World Journal of Gastroenterology2020，26，7： | 16 |
| 15 | An HNF 1α-regulated feedback circuit modulates hepatic fibrogenesis via the crosstalk between hepatocytes and hepatic stellate cells显示文摘 | Hui Qian Xing Deng Zhao-Wei Huang Ji Wei Chen-Hong Ding Ren-Xin Feng Xin Zeng Yue-Xiang Chen Jin Ding Lei Qiu Zhen-Lin Hu Xin Zhang Hong-Yang Wang Jun-Ping Zhang Wei-Fen Xie | 2015 | Cell Research2015，25，8： | 15 |
| 16 | Shanghai Score: A Prognostic and Adjuvant Treatment-evaluating System Constructed for Chinese Patients with Hepatocellular Carcinoma after Curative Resection显示文摘 | Hui-Chuan Sun Lu Xie Xin-Rong Yang Wei Li Jian Yu Xiao-Dong Zhu Yong Xia Ti Zhang Yang Xu Bo Hu Li-Ping Du Ling-Yao Zeng Jian Ouyang Wei Zhang Tian-Qiang Song Qiang Li Ying-Hong Shi Jian Zhou Shuang-Jian Qiu Qian Liu Yi-Xue Li Zhao-You Tang Yu Shyr Feng Shen Jia Fan | 2017 | Chinese Medical Journal2017，，22： | 15 |
| 17 | Associations of ABCB1, NFKB1, CYP3A, and NR112 polymorphisms with cyclosporine trough concentrations in Chinese renal transplant recipients显示文摘 | Yu ZHANG Jia-li LI Qian FU Xue-ding WANG Long-shan LIU Chang-xi WANG Wen XIE Zhuo-jia CHEN Wen-ying SHU Min HUANG | 2013 | Acta Pharmacologica Sinica2013，34，4： | 15 |
| 18 | Magnolol additive as a replacer of antibiotic enhances the growth performance of Linwu ducks显示文摘Magnolol rich in Magnolia officinalis is a bioactive polyphenolic compound. The aim of this study was to examine the effects of magnolol additive(MA) on growth performance, expression levels of antioxidantrelated genes, and intestinal mucosal morphology of Linwu ducks aged from 49 to 70 days, comparing with that of an antibiotic additive(colistin sulfate [CS]). A total of 275,49-day-old ducks were assigned to5 groups with 5 cages of 11 ducks each and fed diets supplemented with 0,100, 200 and 300 mg of MA/kg and 300 mg of CS/kg for 3 weeks, respectively. The results showed that the average daily body weight gain(ADG) was increased significantly in MA-fed groups(200 and 300 mg/kg), compared with the basal diet(BD) group(P < 0.05). The mRNA levels of superoxide dismutase-1(SOD1), manganese superoxide dismutase-2(MnSOD2) and catalase(CAT) were also increased significantly in MA groups(P < 0.05). In addition, hematoxylin and eosin staining revealed that Linwu ducks fed the diets with MA had more intact intestinal mucosa than those fed the BD and CS diets. In addition, ileal villus height, ileal villus height/crypt depth ratio(V/C) and duodenal V/C were also improved significantly(P < 0.05). Taken together, these data demonstrated that MA is an effective feed additive to enhance the growth performance of the Linwu ducks by improving the antioxidant and intestinal mucosal status, suggesting that MA will be a potential additive to replace antibiotic(CS). | Qian Lin Jianfei Zhao Kun Xie Yushi Wang Guili Hu Guitao Jiang Qiuzhong Dai Zhiyong Fan Jianhua He Xi He De-Xing Hou | 2017 | Animal Nutrition2017，，2： | 14 |
| 19 | Rice Ferredoxin-Dependent Glutamate Synthase Regulates Nitrogen-Carbon Metabolomes and Is Genetically Differentiated between japonica and indica Subspecies显示文摘当通过夫酸安 synthetase/glutamine:2-oxoglutarate amidotransferase (GS/GOGAT ) 的 Gln 和 Glu 骑车,植物吸收从土壤吸收进器官的形式的无机的氮。而 GS 从 Glu 和氨催化 Gln 的形成, GOGAT 从 Gln 催化一个酰胺组的转移到 2-oxoglutarate 生产 Glu 的二个分子。然而,处于碳氮平衡的 GS/GOGAT 周期的规章的角色很好没被理解。这里,我们报导米饭的功能的描述反常细胞激动素反应 1 (ABC1 ) 编码一个铁氧化还原蛋白依赖者(Fd ) 的基因 -GOGAT。弱变异的等位基因 abc1-1 异种显示出典型氮缺乏的症候群,而 T-DNA insertional 异种 abc1-2 是幼苗致命。Metabolomics 分析在 abc1-1 在 tricarboxylic 酸周期与高 N/C 比率(Gln 和 Asn ) 和几中介揭示了氨基酸的过多的数量的累积,建议 ABC1 起在氮吸收和碳氮平衡的一个关键作用。五非同义的单个核苷酸的多型性在编码区域的 ABC1 被识别并且作为三不同 haplotypes 描绘了,它高度并且明确地在装饰用的梨树和 indica 亚种之间被区分了。一起,这些结果建议 ABC1/OsFd-GOGAT 由 modulating 氮吸收和碳氮平衡为植物生长和开发是必要的。 | Xiaolu Yang Jinqiang Nian Qincliun xie Jian Feng Fengxia Zhang Hongwei Jing Jian Zhang Guojun Dong Yan Liang Juli Peng GuodongWang Qian Qian Jianru Zuo | 2016 | Molecular Plant2016，9，11： | 14 |
| 20 | Role of gut microbiota via the gut-liver-brain axis in digestive diseases显示文摘The gut-brain axis is a bidirectional information interaction system between the central nervous system(CNS) and the gastrointestinal tract, in which gut microbiota plays a key role. The gut microbiota forms a complex network with the enteric nervous system, the autonomic nervous system, and the neuroendocrine and neuroimmunity of the CNS, which is called the microbiota-gut-brain axis. Due to the close anatomical and functional interaction of the gut-liver axis, the microbiota-gut-liver-brain axis has attracted increased attention in recent years. The microbiota-gut-liver-brain axis mediates the occurrence and development of many diseases, and it offers a direction for the research of disease treatment. In this review, we mainly discuss the role of the gut microbiota in the irritable bowel syndrome, inflammatory bowel disease, functional dyspepsia, non-alcoholic fatty liver disease, alcoholic liver disease, cirrhosis and hepatic encephalopathy via the gut-liver-brain axis, and the focus is to clarify the potential mechanisms and treatment of digestive diseases based on the further understanding of the microbiota-gut-liver-brain axis. | Jian-Hong Ding Zhe Jin Xiao-Xu Yang Jun Lou Wei-Xi Shan Yan-Xia Hu Qian Du Qiu-Shi Liao Rui Xie Jing-Yu Xu | 2020 | World Journal of Gastroenterology2020，26，40： | 13 |
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