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| 1 | Surface modification of small intestine submucosa in tissue engineering显示文摘With the development of tissue engineering,the required biomaterials need to have the ability to promote cell adhesion and proliferation in vitro and in vivo.Especially,surface modification of the scaffold material has a great influence on biocompatibility and functionality of materials.The small intestine submucosa(SIS)is an extracellular matrix isolated from the submucosal layer of porcine jejunum,which has good tissue mechanical properties and regenerative activity,and is suitable for cell adhesion,proliferation and differentiation.In recent years,SIS is widely used in different areas of tissue reconstruction,such as blood vessels,bone,cartilage,bladder and ureter,etc.This paper discusses the main methods for surface modification of SIS to improve and optimize the performance of SIS bioscaffolds,including functional group bonding,protein adsorption,mineral coating,topography and formatting modification and drug combination.In addition,the reasonable combination of these methods also offers great improvement on SIS surface modification.This article makes a shallow review of the surface modification of SIS and its application in tissue engineering. | Pan Zhao Xiang Li Qin Fang Fanglin Wang Qiang Ao Xiaohong Wang Xiaohong Tian Hao Tong Shuling Bai Jun Fan | 2020 | Regenerative Biomaterials2020，7，4： | 9 |
| 2 | Nanoscale control of silks for regular hydroxyapatite formation | Xingliang He Xiaowei Huang Qiang Lu Shuling Bai Hesun Zhu | 2012 | Progress in Natural Science:Materials International2012，22，2： | 4 |
| 3 | Autologous transplantation of adipose-derived mesenchymal stem cellsameliorates streptozotocin-induced diabetic nephropathy in rats by inhibitingoxidative stress, pro-inflammatory cytokines and the p38 MAPK signaling pathway显示文摘 | Yan Fang Xiaohong Tian Shuling Bai Jun Fan Weijian Hou Hao Tong Dehua Li | 2012 | International Journal of Molecular Medicine2012，，1： | 1 |
| 4 | Autologous transplantation of adipose-derived mesenchymal stem cellsameliorates streptozotocin-induced diabetic nephropathy in rats by inhibitingoxidative stress, pro-inflammatory cytokines and the p38 MAPK signaling pathway显示文摘 | Yan Fang Xiaohong Tian Shuling Bai Jun Fan Weijian Hou Hao Tong Dehua Li | 2012 | International Journal of Molecular Medicine2012，，1： | 1 |
| 5 | SKL promotes patency and endothelialization of small-caliber vascular grafts in rabbit carotid artery model显示文摘The Klotho.(KL)gene is related to aging.In this study,SKL(secreted KL)and heparin were cross:linked to the acellular small intestinal submucosa(SIS).Based on this,small-diameter tissue engineered blood vessels(TEVs)were constructed.The role of SKL on improving the patency of TEVs through promoting cell adherence was investigated.The SIS membrane was cross linked with heparin and SKL,respectively,to prepare heparin group and SKL group artificial blood vessels.The CCK8 assay showed that SKL treatment promoted endothelial cells proliferation.Western blot showed that SKL upregulated the levels of FAK and RHOA. | Fan Jun Bai Shuling Zhao Pan Fang Qin Gao Dongsheng | 2021 | 解剖学杂志2021，44，S01： | 0 |
| 6 | Effect of growth hormone-releasing peptide on cardiac cholinergic nerve fiber density distribution in a rat model of heart failure显示文摘BACKGROUND:Changes in the cardiac autonomic nerve are considered to be important factors in the mechanisms of heart failure.It is possible to reduce or slow down nerve degeneration and necrosis,provided that patients take effective neuroprotectants during the early stages of heart failure.Moreover,it is possible to relieve the pathological process and reduce the risk of death. OBJECTIVE:To study the effect of growth hormone releasing peptide(GHRP) on cardiac cholinergic nerve fiber density distribution in a rat model of heart failure,and verify whether GHRP can ameliorate denervation. DESIGN,TIME AND SETTING:A randomized controlled study was performed at the Key Laboratory of Anatomy,Harbin Medical University,between June and October 2009. MATERIALS:Fifty adult,healthy,female,Wistar rats,weighing(200±20) g,were randomly divided into GHRP(n = 30),model(n = 10),and sham operation(n = 10) groups.GHRP-2 was made in Shanghai,China(batch No.z071212-03). METHODS:Acute myocardial infarction was established by ligating the left anterior descending coronary artery in the GHRP and model groups.Five weeks later,myocardial function was detected using color ultrasound electrocardiograph.Ejection fraction<60%was considered to be a successful marker of chronic heart failure models.However,the left anterior descending coronary artery was not ligated in the sham operation group.The GHRP group was injected with 100μg/kg GHRP-2,and the other two groups were injected with the same volume of physiological saline,once per day. MAIN OUTCOME MEASURES:After 4 weeks,pathological changes in cardiac cholinergic nerve fibers were detected under optic microscopy following hematoxylin/eosin staining.In addition, density distribution was measured using a multi-function color pathological image system. RESULTS:In the sham operation group,myocardial cells were regular,uniformly stained,and no inflammatory cells were present.In the model group,myocardial cells were unevenly stained, exhibited nuclear atrophy,degeneration,dissolution,or disappearance.In the GHRP group, myocardial damage was less than in the model group;cardiac muscle fibers exhibited slight degeneration.The myocardium in the sham operation group was serried,spreading the cholinergic innervations along the cardiac fiber.In the model group,there was a decreased number of cholinergic nerve fibers decreased,which also became shorter and smaller,compared with the sham operation group(P<0.01).In the GHRP group,cholinergic positive nerve fibers were significantly increased compared with the model group(P<0.01),but still less than the sham surgery group(P<0.05). CONCLUSION:GHRP delayed denervation and reduced nerve reconstitution following heart failure in rats. | Guozhong Tian Xiuqin Ni Yong Zhao Jia Feng Yanjun Li Zhenya Zhong Shuling Bai | 2009 | Neural Regeneration Research2009，4，4： | 0 |
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