Rutaecarpine_LCMS_25138_MedChemExpress

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西红花提取物调控免疫细胞，提高程序性死亡受体-1抑制剂治疗肺腺癌效果的实验研究

西红花提取物调控免疫细胞，提高程序性死亡受体-1抑制剂治疗肺腺癌效果的实验研究作者：李诗颖李存雅张雪钟薏来源：《上海医药》2024年第01期摘要目的：多项研究提示，西红花提取物能影响肿瘤的发展进程。

本实验探究西红花提取物在肺腺癌小鼠模型中对肿瘤免疫微环境和免疫治疗的影响，为西红花提取物抗肿瘤研究提供更多基础性数据。

方法：构建Lewis肺癌细胞和萤光素酶稳定结合的小鼠皮下瘤模型，观察西红花提取物对小鼠皮下瘤和肿瘤免疫微环境的影响：运用活体成像技术跟踪肿瘤生长情况；运用流式细胞技术检测小鼠CD4+、CD8+ T细胞的数量及占比；运用反转录-聚合酶链式反应技术检测程序性死亡受体配体1、含有T细胞免疫球蛋白和黏蛋白结构域的蛋白3（T cell immunoglobulin and mucin domaincontaining protein 3， TIM3）、淋巴细胞活化基因-3（lymphocyte-activation gene-3， LAG3）、具有免疫球蛋白和ITIM结构域的T细胞免疫受体（T cell immunoreceptor with immunoglobulin and ITIM domain， TIGIT）、胸腺细胞选择相关的高迁移率族蛋白（thymocyte selection-associated high mobility group box， TOX）1、TOX2、TOX3基因的mRNA表达情况。

结果：与对照组相比，给予西红花提取物能一定程度地抑制小鼠皮下瘤的生长（P关键词西红花免疫微环境肺腺癌免疫治疗中图分类号：R965； R282.71 文献标志码：A 文章编号：1006-1533（2024）01-0003-09引用本文李诗颖，李存雅，张雪，等. 西红花提取物调控免疫细胞，提高程序性死亡受体-1抑制剂治疗肺腺癌效果的实验研究[J]. 上海医药， 2024， 45（1）： 3-11； 28.基金项目：上海市2022年度“科技创新行动计划”医学创新研究专项项目（22Y31920104）；上海市虹口区第二轮“国医强优”三年行动计划（2022—2024年）中西医结合重点专科、薄弱专科建设项目（HKGYQYXM-2022-10）；上海市2021年度“科技创新行动计划”扬帆计划项目（21YF444400）；上海市2022年度“科技创新行动计划”启明星培育（扬帆专项）项目（22YF1444900）；山东省乡村振兴基金会张秀兰慈善基金项目Experimental study of saffron extracts to modulate immune cells to improve the efficacy of a programmed death-1 inhibitor in the treatment of lung adenocarcinomaLI Shiying1， LI Cunya1， ZHANG Xue2， ZHONG Yi1（1. Department of Oncology， Shanghai TCM-Integrated Hospital， Shanghai University of Traditional Chinese Medicine， Shanghai 200082， China； 2. Shanghai Traditional Chinese Medicine Co.， Ltd.， Shanghai 200082， China）ABSTRACT Objective： A number of studies have shown that saffron extracts can affect the development of tumor. This study explored the effect of saffron extract on tumor immune microenvironment and immunotherapy in a mouse model of lung adenocarcinoma so as to provide more basic data for the anti-tumor research of saffron extracts. Methods： The transplanted tumor model of Lewis lung carcinoma-luciferase in mice was established to detect the effect of saffron extracts on the transplanted tumor in vivo. At the same time， the tumor growth was tracked by in vivo imaging technique. The number and proportion of CD4+ and CD8+ T cells were determined by flow cytometry. The mRNA levels of programmed death-ligand 1， T cell immunoglobulin and mucin domain-containing protein 3 （TIM3）， lymphocyte-activation gene-3 （LAG3）， T cell immunoreceptor with immunoglobulin and ITIM domain （TIGIT）， thymocyte selection-associated high mobility group box （TOX） 1， TOX2 and TOX3 were detected by reverse transcription-polymerase chain reaction （RT-PCR） and immunohistochemical techniques to verify the effect of saffron extracts on the regulation of tumor immune microenvironment. Results：Compared with the control group， the administration of saffron extracts could inhibit the growth of subcutaneous tumor in mice to a certain extent， and the number and proportion of CD4+ and CD8+ T cells were increased （PKEY WORDS saffron； immune microenvironment； lung adenocarcinoma； immunotherapy肿瘤是一类恶性疾病，2018年全球肿瘤死亡病例数达约960万人，较2008年增加26.3%，其中男性肿瘤死亡病例数增加最多的是肺癌，增加了23.4万人[1-2]。

26291346_基于UPLC-MS

Abstract: A UPLC-MS/MS method was established to quantitatively determine the content of alliin in animal plasma to study whether alliin and alliin in garlic enteric preparations can react to produce the active ingredient allicin in the in vivo environment. Methods Reversed-phase C18 column (Waters ICQUITY UPLC BEH, 100 × 2.1 mm, 1.7μm), column temperature: 40 ℃, flow rate: 0.15 mL/min, injection volume: 2μl, Mobile phase: 0.1% formic acid (A)-acetonitrile (B), gradient elution; mass spectrometry ionization: ESI+, determination of allicin in rat plasma . Results The results of two parallel experiments of garlic enteric preparation and enzymatic garlic powder showed that in the garlic enteric preparation with allinase, the plasma concentration of alliin in the blood of rats was significantly lower. Conclusion A UPLC-MS/MS method for the quantitative determination of alliin in animal plasma has been established. Alliin and alliin in garlic enteric-coated preparations can react in vivo.Key words: Garlic enteric preparation; garbonine; UPLC-MS-MS基于UPLC-MS/MS大蒜肠溶制剂中蒜氨酸、蒜酶体内反应情况研究杨亮1，胡小霞4 ，宋百灵4，关明3，李新霞2*（1.新疆警察学院新疆乌鲁木齐 8300112.新疆医科大学药学院新疆乌鲁木齐 8300113.新疆师范大学化学化工学院新疆乌鲁木齐 8300544.新疆医科大学中心实验室新疆乌鲁木齐 830011）Study on the Reaction of Garlic and Uterine in the UPLC-MS / MS of Garlic SausolYANG Liang 1，HU Xiaoxia 4 ，SONG Bailing 4，GUAN Ming 3，LI Xinxia 2*(1. Xinjiang Police College, Urumqi 830054, Xinjiang China2.Chemistry and Chemical Engineering of Xinjiang Normal University College, Urumqi 830054, Xinjiang China3.School of Pharmacy, Xinjiang Medical University, Urumqi 830011, Xinjiang China4.Central Laboratory of Xinjiang Medical University, Urumqi 830011, Xinjiang China ）摘要：目的建立定量测定动物血浆中蒜氨酸含量的UPLC-MS/MS 方法，研究大蒜肠溶制剂中蒜氨酸、蒜酶能否在体内环境下反应生成活性成分大蒜辣素。

用于治疗肥胖症的邻苯二酚丁烷的释放的方法和组合物[发明专利]

专利名称：用于治疗肥胖症的邻苯二酚丁烷的释放的方法和组合物
专利类型：发明专利
发明人：乔纳森·赫勒,尼尔·弗雷泽,张智川,伊莱恩·林,茹智·C·黄
申请号：CN200480021054.0
申请日：20040520
公开号：CN1852705A
公开日：
20061025
专利内容由知识产权出版社提供
摘要：本发明提供了用于治疗肥胖症的试剂盒、方法和组合物。

此处的该组合物含有一种基本上纯的至少一种邻苯二酚丁烷，包括，例如在一种制药学上可接受的载体或赋形剂中的NDGA化合物的制剂。

该邻苯二酚丁烷诸如NDGA或其衍生物被给药至一名或多名需要治疗的受试者。

申请人：埃里莫斯医药品有限公司,约翰霍普金斯大学
地址：美国德克萨斯州
国籍：US
代理机构：北京邦信阳专利商标代理有限公司
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碱基切除修复抑制剂甲氧胺联合β-榄香烯治疗恶性脑胶质瘤的实验研究

序言β-榄香烯属国家二类非细胞毒性抗肿瘤新药，临床研究证实其对包括脑胶质瘤在内的多种肿瘤疗效确切，且无其他传统化疗药常有的骨髓抑制、肝肾功能损害等毒副作用。

但目前临床应用的榄香烯乳注射液因其存在静脉炎发生率很高、剂型性质不稳定等缺点，其进一步的应用受到了较大的限制。

碱基切除修复抑制剂甲氧胺（Methoxyamine），可通过裂解核酸内切酶破坏DNA碱基切除修复过程，从而抑制肿瘤细胞对损伤作用的修复反应。

据此，可认为抑制DNA 碱基切除修复可能是增强肿瘤细胞化疗敏感性的潜在靶点，目前多项实验报道也已证实了甲氧胺可增强烷化剂和放疗的抗肿瘤效果。

近年来，通过纳米技术构建的纳米脂质体在提高药物溶解度、增加药物稳定性、降低药物副作用、缓控释给药等方面较普通的脂质体有了显著的提高。

研究表明，纳米脂质体对正常细胞和组织无损伤作用，并可长时间吸附于靶细胞周围，因此使药物能充分向靶组织渗透，也可以通过静电吸附效应与细胞膜接触而融合而进入细胞内。

因此将药物包封于纳米脂质体被认为可以改变被包封药物的体内分布，提高药物治疗指数，降低药物毒性。

基于增强β-榄香烯的疗效，减少毒副作用的目的，本课题研究内容分两部分：（一）联合碱基切除修复抑制剂甲氧胺，探讨是否在体内外抗瘤活性上具有协同作用，以期减少榄香烯用量，降低毒副反应，为其在临床的应用提供实验和理论依据。

（二）、利用纳米脂质体技术构建新型的β-榄香烯-纳米脂质体药物传递系统，初步探讨其体外抗瘤活性。

II碱基切除修复抑制剂甲氧胺联合β-榄香烯治疗恶性脑胶质瘤的实验研究中文摘要胶质瘤是成人神经系统最常见的原发性肿瘤，手术全切除率很低，复发率高，当前多种治疗效果仍不理想。

榄香烯属国家二类非细胞毒性抗肿瘤新药，临床研究发现其对多种肿瘤疗效确切，而且还具有提高和改善机体免疫功能，与放化疗协同作用等独特效果。

但是肿瘤细胞具有强大的DNA损伤修复机制，会对化疗药物产生抗性。

因此抑制这种内在的DNA修复过程，如碱基切除修复抑制剂甲氧胺的联合应用有利于提高化疗药物的抗瘤效果。

含萘三氮唑甲烷骨架的硫代乙酸类尿酸转运体1(URAT1)抑制剂的合成及其构效关系

含萘三氮唑甲烷骨架的硫代乙酸类尿酸转运体1(URAT1)抑制剂的合成及其构效关系辛晓;刘巍;谢亚非;刘长鹰;汤立达;徐为人;赵桂龙【摘要】分别以1-溴萘和酮或1-萘甲醛及有机金属试剂为原料,经12步反应合成了8个含萘三氮唑甲烷骨架的硫代乙酸类尿酸转运体1(URAT1)抑制剂(1h～1o),其结构经1H NMR,13C NMR和MS (ESI)表征.体外活性测试结果显示:对URAT1的抑制活性最强的是1k,是阳性对照药lesinurad的133倍[IC50=0.054 μmol·L-1(1k),7.18 μmol·L-1(lesinurad)].%Eight naphthyltriazolylmethane-based thioacetic acids(1h ～ 1o) were synthesized as uric acid transporter 1 (URAT1) inhibitors by 12 steps using 1-bromonaphthalene and ketones or 1-naphth-aldehyde and alkyl organometallic reagents as starting materials.The structures were characterized by 1H NMR,13C NMR and MS(ESI).In vitro URAT1 inhibitory assay showed that 1k was the most potent URAT1 inhibitor among target compounds,which was 133-fold more potent than positive contr ol lesinurad(IC5o =0.054 μmol · L-1 for 1k against human URAT1 vs 7.18 μmol · L-1 for lesinurad).【期刊名称】《合成化学》【年(卷),期】2017(025)006【总页数】14页(P461-474)【关键词】1-溴萘;1-萘甲醛;痛风;高尿酸血症;尿酸转运体1 (URAT1);合成;lesinurad;构效关系【作者】辛晓;刘巍;谢亚非;刘长鹰;汤立达;徐为人;赵桂龙【作者单位】天津中医药大学研究生院,天津300193;天津药物研究院天津市新药设计与发现重点实验室,天津300193;天津药物研究院天津市新药设计与发现重点实验室,天津300193;天津药物研究院天津市新药设计与发现重点实验室,天津300193;天津药物研究院天津市新药设计与发现重点实验室,天津300193;天津药物研究院天津市新药设计与发现重点实验室,天津300193;天津中医药大学研究生院,天津300193;天津药物研究院天津市新药设计与发现重点实验室,天津300193;天津药物研究院天津市新药设计与发现重点实验室,天津300193【正文语种】中文【中图分类】O623.626;O621.3痛风是困扰人类最古老的疾病之一[1]，是由于尿酸单钠盐(MSU)在关节和关节周围的组织等部位沉积引起的，是最常见的类风性关节炎。

依达拉奉右莰醇通过铁死亡-脂质过氧化通路对脑出血大鼠神经保护的作用机制

实验研究依达拉奉右莰醇通过铁死亡-脂质过氧化通路对脑出血大鼠神经保护的作用机制毛权西，李作孝△摘要：目的探讨依达拉奉右莰醇对脑出血大鼠的神经保护作用及血肿周围脑组织脂质过氧化的影响。

方法将128只SD大鼠随机分为假手术组、脑出血组、依达拉奉组和依达拉奉右莰醇组，每组32只。

除假手术组外，其余组大鼠构建急性脑出血模型，依达拉奉组、依达拉奉右莰醇组于造模后分别腹腔注射依达拉奉6mg/kg、依达拉奉右莰醇7.5mg/kg，每12h注射1次，假手术组和脑出血组腹腔注射等量生理盐水。

术后1d、3d、7d和14d按Garcia评分标准进行神经功能评分，HE染色观察血肿周围脑组织病理变化，化学荧光法检测血肿周围脑组织活性氧（ROS）含量，微量酶标法检测血肿周围脑组织还原型谷胱甘肽（GSH）含量，蛋白免疫印迹法检测血肿周围脑组织谷胱甘肽过氧化物酶4（GPX4）、长链脂酰辅酶A合成酶4（ACSL4）和磷脂胆碱酰基转移酶3（LPCAT3）表达。

结果与假手术组比较，脑出血组大鼠神经功能评分降低，血肿周围脑组织出现大量炎性细胞浸润及神经细胞变性，ROS含量、ACSL4和LPCAT3蛋白表达水平升高，GSH含量、GPX4蛋白表达水平降低（P＜0.05）；与脑出血组比较，依达拉奉组和依达拉奉右莰醇组大鼠神经功能评分升高，血肿周围脑组织病理损伤明显减轻，ROS含量、ACSL4和LPCAT3蛋白表达水平降低，GSH含量、GPX4蛋白表达水平增加（P＜0.05）；依达拉奉右莰醇组干预效果优于依达拉奉组（P＜0.05）；除假手术组外，其余各组均在术后3d时变化最明显，术后7d、14d逐渐恢复（P＜0.05）。

结论依达拉奉右莰醇可能通过调节脑出血大鼠神经细胞铁死亡相关蛋白的表达，减少脑组织脂质过氧化，抑制神经细胞铁死亡，从而发挥脑保护作用。

关键词：依达拉奉右莰醇；依达拉奉；脑出血；铁死亡；脂质过氧化中图分类号：R743.34文献标志码：A DOI：10.11958/20221777Neuroprotective mechanism of edaravone dexborneol in rats with cerebral hemorrhage throughferroptosis-lipid peroxidation pathwayMAO Quanxi,LI Zuoxiao△Department of Neurology,the Affiliated Hospital of Southwest Medical University,Luzhou646000,China△Corresponding Author E-mail:Abstract:Objective To investigate the neuroprotective effect of edaravone dexborneol on cerebral hemorrhage in rats and the effect of lipid peroxidation on perihematomal brain tissue.Methods A total of128SD rats were randomly divided into the sham-operated group,the cerebral hemorrhage group,the edaravone group and the edaravone dexborneol group, with32rats in each group.The acute cerebral hemorrhage model was constructed in all groups except for the sham-operated group.The edaravone group and edaravone dexamphene group were injected intraperitoneally with6mg/kg of edaravone and edaravone dexamphene7.5mg/kg,one injection every12hours.The sham-operated group and the cerebral hemorrhage group were injected intraperitoneally with equal amounts of saline.The neurological function was scored according to Garcia score at1d,3d,7d,and14d after surgery.Brain tissue around hematoma was stained with HE staining.Chemo fluorescence assay was used to observe pathological changes and reactive oxygen species(ROS)content of brain tissue around hematoma.Micro enzyme labeling assay was used to detect glutathione(GSH)content of brain tissue around hematoma.The expression levels of glutathione peroxidase4(GPX4),long-chain lipid acyl-coenzyme A synthase4(ACSL4) and phospholipid choline acyltransferase3(LPCAT3)in brain tissue around hematoma were detected by protein immunoblotting.Results Compared with the sham-operated group,neurological function scores were decreased in the cerebral hemorrhage group.Massive inflammatory cell infiltration and neuronal degeneration in brain tissue around hematoma were found,and ROS content,ACSL4and LPCAT3protein expression level increased.GSH content and GPX4 protein expression level decreased in the cerebral hemorrhage group(P＜0.05).Compared with the cerebral hemorrhage group,neurological function scores were increased,histopathological damage around the hematoma was significantly基金项目：泸州市人民政府-西南医科大学科技战略合作基金项目（2018LZXNYD-ZK17）作者单位：西南医科大学附属医院神经内科（邮编646000）作者简介：毛权西（1990），男，硕士在读，主要从事神经免疫方向研究。

益生菌对阿尔茨海默病作用的研究进展

益生菌对阿尔茨海默病作用的研究进展发布时间：2021-12-14T06:08:15.523Z 来源：《中国结合医学杂志》2021年12期作者：宋鑫萍1,2，李盛钰2，金清1[导读] 阿尔茨海默病已成为威胁全球老年人生命健康的主要疾病之一，患者数量逐年攀升，其护理的经济成本高，给全球经济造成重大挑战。

近年来研究显示，益生菌在适量使用时作为有益于宿主健康的微生物，在防治阿尔茨海默病方面具有积极影响，其作用机制可能通过调节肠道菌群，影响神经免疫系统，调控神经活性物质以及代谢产物，通过肠-脑轴影响该病发生和发展。

宋鑫萍1,2，李盛钰2，金清11.延边大学农学院，吉林延吉 1330022.吉林省农业科学院农产品加工研究所，吉林长春 130033摘要：阿尔茨海默病已成为威胁全球老年人生命健康的主要疾病之一，患者数量逐年攀升，其护理的经济成本高，给全球经济造成重大挑战。

本文综述了近几年来国内外益生菌对阿尔茨海默病的作用进展，以及其预防和治疗阿尔茨海默病的潜在作用机制。

关键词：益生菌；阿尔茨海默病；肠道菌群；机制Recent Progress in Research on Probiotics Effect on Alzheimer’s DiseaseSONG Xinping1,2，LI Shengyu2，JI Qing1*(1.College of Agricultural, Yanbian University, Yanji 133002，China)(2.Institute of Agro-food Technology, Jilin Academy of Agricultural Sciences, Chanchun 130033, China)Abstract：Alzheimer’s disease has become one of the major diseases threatening the life and health of the global elderly. The number of patients is increasing year by year, and the economic cost of nursing is high, which poses a major challenge to the global economy. In recent years, studies have shown that probiotics, as microorganisms beneficial to the health of the host, have a positive impact on the prevention and treatment of Alzheimer’s disease. Its mechanism may be through regulating intestinal flora, affecting the nervous immune system, regulating the neuroactive substances and metabolites, and affecting the occurrence and development of the disease through thegut- brain axis. This paper reviews the progress of probiotics on Alzheimer’s disease at home and abroad in recent years, as well as its potential mechanism of prevention and treatment.Key words：probiotics; Alzheimer’s disease; gut microbiota; mechanism阿尔茨海默病（Alzheimer’s disease, AD），系中枢神经系统退行性疾病，属于老年期痴呆常见类型，临床特征主要包括：记忆力减退、认知功能障碍、行为改变、焦虑和抑郁等。

Firategrast-SDS-MedChemExpress

Inhibitors, Agonists, Screening LibrariesSafety Data Sheet Revision Date:Oct.-11-2018Print Date:Oct.-11-20181. PRODUCT AND COMPANY IDENTIFICATION1.1 Product identifierProduct name :FirategrastCatalog No. :HY-14951CAS No. :402567-16-21.2 Relevant identified uses of the substance or mixture and uses advised againstIdentified uses :Laboratory chemicals, manufacture of substances.1.3 Details of the supplier of the safety data sheetCompany:MedChemExpress USATel:609-228-6898Fax:609-228-5909E-mail:sales@1.4 Emergency telephone numberEmergency Phone #:609-228-68982. HAZARDS IDENTIFICATION2.1 Classification of the substance or mixtureNot a hazardous substance or mixture.2.2 GHS Label elements, including precautionary statementsNot a hazardous substance or mixture.2.3 Other hazardsNone.3. COMPOSITION/INFORMATION ON INGREDIENTS3.1 SubstancesSynonyms:SB 683699;SB683699;SB-683699Formula:C27H27F2NO6Molecular Weight:499.50CAS No. :402567-16-24. FIRST AID MEASURES4.1 Description of first aid measuresEye contactRemove any contact lenses, locate eye-wash station, and flush eyes immediately with large amounts of water. Separate eyelids with fingers to ensure adequate flushing. Promptly call a physician.Skin contactRinse skin thoroughly with large amounts of water. Remove contaminated clothing and shoes and call a physician.InhalationImmediately relocate self or casualty to fresh air. If breathing is difficult, give cardiopulmonary resuscitation (CPR). Avoid mouth-to-mouth resuscitation.IngestionWash out mouth with water; Do NOT induce vomiting; call a physician.4.2 Most important symptoms and effects, both acute and delayedThe most important known symptoms and effects are described in the labelling (see section 2.2).4.3 Indication of any immediate medical attention and special treatment neededTreat symptomatically.5. FIRE FIGHTING MEASURES5.1 Extinguishing mediaSuitable extinguishing mediaUse water spray, dry chemical, foam, and carbon dioxide fire extinguisher.5.2 Special hazards arising from the substance or mixtureDuring combustion, may emit irritant fumes.5.3 Advice for firefightersWear self-contained breathing apparatus and protective clothing.6. ACCIDENTAL RELEASE MEASURES6.1 Personal precautions, protective equipment and emergency proceduresUse full personal protective equipment. Avoid breathing vapors, mist, dust or gas. Ensure adequate ventilation. Evacuate personnel to safe areas.Refer to protective measures listed in sections 8.6.2 Environmental precautionsTry to prevent further leakage or spillage. Keep the product away from drains or water courses.6.3 Methods and materials for containment and cleaning upAbsorb solutions with finely-powdered liquid-binding material (diatomite, universal binders); Decontaminate surfaces and equipment by scrubbing with alcohol; Dispose of contaminated material according to Section 13.7. HANDLING AND STORAGE7.1 Precautions for safe handlingAvoid inhalation, contact with eyes and skin. Avoid dust and aerosol formation. Use only in areas with appropriate exhaust ventilation.7.2 Conditions for safe storage, including any incompatibilitiesKeep container tightly sealed in cool, well-ventilated area. Keep away from direct sunlight and sources of ignition.Recommended storage temperature:Powder-20°C 3 years4°C 2 yearsIn solvent-80°C 6 months-20°C 1 monthShipping at room temperature if less than 2 weeks.7.3 Specific end use(s)No data available.8. 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PHYSICAL AND CHEMICAL PROPERTIES9.1 Information on basic physical and chemical propertiesAppearance White to off-white (Solid)Odor No data availableOdor threshold No data availablepH No data availableMelting/freezing point No data availableBoiling point/range No data availableFlash point No data availableEvaporation rate No data availableFlammability (solid, gas)No data availableUpper/lower flammability or explosive limits No data availableVapor pressure No data availableVapor density No data availableRelative density No data availableWater Solubility No data availablePartition coefficient No data availableAuto-ignition temperature No data availableDecomposition temperature No data availableViscosity No data availableExplosive properties No data availableOxidizing properties No data available9.2 Other safety informationNo data available.10. 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For more details, see section 2Aspiration hazardClassified based on available data. For more details, see section 212. ECOLOGICAL INFORMATION12.1 ToxicityNo data available.12.2 Persistence and degradabilityNo data available.12.3 Bioaccumlative potentialNo data available.12.4 Mobility in soilNo data available.12.5 Results of PBT and vPvB assessmentPBT/vPvB assessment unavailable as chemical safety assessment not required or not conducted.12.6 Other adverse effectsNo data available.13. DISPOSAL CONSIDERATIONS13.1 Waste treatment methodsProductDispose substance in accordance with prevailing country, federal, state and local regulations.Contaminated packagingConduct recycling or disposal in accordance with prevailing country, federal, state and local regulations.14. 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Expression, Purification and Crystallization of

Expression, Purification and Crystallization of the Mycobacterium Tuberculosis HSP16.3 Molecular Chaperone Background of Mycobacterium Tuberculosis HSP16.3HSP16.3, a 16.3 kDa protein from Mycobacterium Tuberculosis, was originally identified as a prominent antigen (Kingston et al., 1987). During the stationary phase, HSP16.3 is maximally expressed and becomes a main protein of the latent phase (Yuan et al., 1996). Previous studies showed that HSP16.3 can make the cell structure stable and prevent stationary Mycobacterium Tuberculosis from autolysing (Cunningham et al., 1998). In previous studies, HSP16.3 was found as one of theα-crystallin-related small heat shock proteins (sHSP) with molecular chaperone activity. Experiments in vitro revealed that HSP16.3 can suppress the thermal aggregation of citrate synthase at 39.5˚C, without consumption of A TP (Chang et al., 1996).Now the Mycobacterium Tuberculosis HSP16.3 gene was cloned to the plasmid pSTE-HSP16.3, and transformed to E.Coli. BL21(DE3) strain.Material and MethodExpressionThings to have ready before Starting.-Plate or glycerol culture-Sterile LB 25ml in a 50mL shaker flasker, 250ml in a 500mL shaker flasker, all together autoclaved, antibiotic added afterword.- antibiotic and sterile water- TipsPrepare the LB and autoclave:Fomula of the LB medium for 1 Liter:Bacto Tryptone (BT) 10 gBacto Y east Extract (BYE) 10 gNaCl 10gThe LB medium, dd H2O and the tips all together autoclaved at 121 ˚C for 20 minutes.Method:1 Innoculate 25 ml LB Medium ( containing 100 ug) and grow culture overnight(37˚C, 200rpm).2 Next morning inoculate 250 ml prewarmed LB Medium ( containing 100 ug) with the 25 ml overnight culture and grow at 37 ˚C, 200rpm, HSP16.3 was overexpressed in soluble form intracellularly without IPTG induction.3 Incubate the Culture for 10 hours before havesting the cell at 4000 g for 20 minutes.4 Resuspend the cell pellet in 30 ml Butter A and freeze the Sample in -80˚C refigerator.PurificationDE52 Ion-Exchange columnThings to have ready before Starting.-Butter A: 50 mM Imidazole pH 6.5 (1 liter)-Butter B: 50 mM Imidazole pH 6.5 , 300mM NaClall together Fitrate with 0.2 um membrane.- DE52 medium , column ,Gradient maker, UV-monitor and Fractioner- TipsMethod:1 Thaw the cell pellet and vortex .2 Add 0.4ml 100 mM PMSF and sonicate (400kw, 4s-6s 50 cycle* 5 )3 Centrifuge 15000 rpm, 30 minutes to pellet debris4 Transfer supernatant to a 50 ml conicale tube and discard the pellet.5 The supernatant dilute to 50 ml with Buffer A and then load to DE52 ion-exchange columns (20ml), which was pre-equibrated with 100ml Buffer A. And then wash the unbound proteins with 100 ml Buffer A.6 Elute the protein with a linear gradient : 200ml buffer A plus 200ml buffer B, 2ml/min, 6ml each fraction.7 Run 15% SDS-PAGE to determine the HSP16.3 peak.Desalting by dialysis1 Preparation of the dialysis tubeCut the tube in a suitable length (20-30 cm)Boil the tube in solution containing 10 mM NaHCO3 for a few minutes.Boil the tube in solution containing 10 mM EDTA for a few minutes.Rasin the tube with de-ion water2 Pool the HSP16.3 peak and dialysis the Sample against 1000ml Buffer A for more than 6hours.Q-Separose (HP) Ion-Exchange Column1 load the sample to Q-Separose (HP) Ion-Exchange column (20ml), which was pre-equibrated with 100ml Buffer A. And then wash the unbound proteins with 100 ml Buffer A.2 Elute the protein with a linear gradient : 200ml buffer A plus 200ml buffer B, 2ml/min, 6ml each fraction.3 Run 15% SDS-PAGE to determine the purity of the HSP16.3 peak.Gel filtration ColumnThe HSP peak was a final volumn 0.3ml and then run though a Superdex75 (HR, 10/30mm) gel filtration column in 150mM NaCl and 5mM Imdazole, pH6.5. Crystallization1 The purified HSP16.3 was solvent-exchanged to water and concentrated to 20mg/ml before crystallization trails (Bradford). All the crystallization trials were carried out using the hanging-drop vapor-diffusion method at 291K: drops consisted of2 microlitres of HSP16.3 protein solution plus 2 microlitres of the precipitant. The drops were equilibrated against 0.2 ml precipitant at room temperature. The crystallization conditions were investigated with a PEG4000 Kit.Result and discussionThe purity of the final HSP16.3 was over 95% by SDS-PAGE. The crystallization trials of HSP16.3 yielded Cubic crystals with a size of 0.8*0.8*0.6mm in a few days.20040060080010001200mAUBuffer Tris-HCL pH 8.5 Precipitant PEG 4000 MethodV apor Diffusion Temperature 293 K Size0.8*0.8*0.6mmReferencesChang Z., Primm, T.P., Jakana J., Lee H. I., Serysheva I., Chiu W., Gilber H. F., Quiocho F. A., (1996) J Biol Chem 271:7218-7223Cunningham A. F., Spreadbury C. L., (1998) J. Bacteriol. 184:801-808Kingston A. E., Salgame P. R., Mitchison N.A., Colston M. J. (1987) Infect. Immun 55,3149-3154Yuan Y., Crane D. D., Barry C. E. III (1996) J Bacteriol178: 4484-4492。

瑞舒伐他汀合成路线和分析

课程论文课程名称 __________________姓名_____________________学号________________________________院____________________专业______________班______年 ___月 ___日现代药物合成毛梧宇药学药物化学硕 124 2013 1 5瑞舒伐他汀结构式：通用名：Rosuvastatin calcium瑞舒伐他汀钙化学名：(+)-(3R,5S)-双{7-[4-(4-氟苯基)-6-异丙基-2-(N-甲基-N-甲磺酰胺基)嘧啶-5-基]-3，5-二羟基-6-(E)-庚烯酸}半钙盐商品名：可定 (Crestor)开发商：日本盐野义制药株式会社在上世纪80年代末研制开发、筛选，之后，英国AstraZeneca公司在除日本等东亚国家之外的世界范围内再次开发得到的。

上市时间：2003年2月，2006年中国上市上市国家与地区：英国美国加拿大中国等六十余个国家与地区适应症：1、高脂血症和高胆固醇血症。

2、用于无心脏病临床表现但潜在心血管疾病风险的患者，以减少心肌梗塞、中风和进行冠状动脉血管再造的风险。

3.也适用于纯合子家族性高胆固醇血症的患者，作为饮食控制和其它降脂措施（如LDL去除疗法）的辅助治疗，或在这些方法不适用时使用。

作用机制：是一种选择性HMG-CoA还原酶抑制剂。

HMG-CoA还原酶抑制剂是转变3-羟基-3-甲基戊二酰辅酶A为甲戊酸盐—胆固醇的前体—的限速酶。

瑞舒伐他汀的主要作用部位是肝—降低胆固醇的靶向器官。

瑞舒伐他汀增加了肝LDL细胞表面受体数目，促进LDL的吸收和分解代谢，抑制了VLDL的肝合成，由此降低VLDL和LDL微粒的总数。

对于纯合子与杂合子家族性高胆固醇血症患者、非家族性高胆固醇血症患者、混合型血脂异常患者、瑞舒伐他汀能降低总胆固醇、LDL-C、ApoB、非HDL-C水平。

瑞舒伐他汀也能降低TG、升高HDL-C水平。

德谷门冬双胰岛素注射液治疗2_型糖尿病的疗效及安全性研究

DOI：10.16658/ki.1672-4062.2023.19.084德谷门冬双胰岛素注射液治疗2型糖尿病的疗效及安全性研究戴卉，张开凤，朱凤丽江苏省镇江市丹徒区人民医院内分泌科，江苏镇江212000[摘要]目的探讨德谷门冬双胰岛素注射液在2型糖尿病中的效果以及安全性。

方法选取2022年1月—2023年7月江苏省镇江市丹徒区人民医院收治的62例2型糖尿病患者为研究对象，按随机数表法分为对照组（n=31）和观察组（n=31）。

对照组患者接受门冬胰岛素30注射液治疗，观察组患者接受德谷门冬双胰岛素注射治疗。

对比两组患者临床疗效、血糖变化和不良反应发生率。

结果观察组治疗有效为96.77%，高于对照组的77.42%，差异有统计学意义（χ2=5.167，P=0.023）。

治疗前，两组患者血糖水平比较，差异无统计学意义（P>0.05）；治疗后，两组患者血糖水平均改善，且观察组血糖指标低于对照组，差异有统计学意义（P< 0.05）。

观察组不良反应发生率低与对照组，差异有统计学意义（P<0.05）。

结论德谷门冬双胰岛素的应用可以明显改善2型糖尿病患者血糖水平，疗效更为确切，且安全性更高，不会增加用药后不良反应。

[关键词] 2型糖尿病；德谷门冬双胰岛素；门冬胰岛素30注射液；安全性[中图分类号] R587 [文献标识码] A [文章编号] 1672-4062（2023）10（a）-0084-04Study on the Efficacy and Safety of Insulin Degludec and Insulin Aspart Injection in the Treatment of Type 2 Diabetes MellitusDAI Hui, ZHANG Kaifeng, ZHU FengliDepartment of Endocrinology, Zhenjiang Dantu District People's Hospital, Zhenjiang, Jiangsu Province, 212000 China [Abstract] Objective To explore the effect and safety of insulin degludec and insulin aspart injection in type 2 diabe⁃tes mellitus.Methods 62 patients of type 2 diabetes mellitus patients admitted to Zhenjiang Dantu District People's Hospital, Jiangsu Province from January 2022 to July 2023 were selected as study objects and divided into the control group (n=31) and the observation group (n=31) by taking the random number table method. The patients in the control group were treated with insulin aspart 30 injection and the patients in the observation group were treated with insulin degludec and insulin aspart injection. Compared the clinical efficacy, the changes in blood glucose and the incidence of adverse reactions between the two groups of patients.Results The treatment effectiveness of the observation group was 96.77%, which was higher than that of the control group, which was 77.42%, and the difference was statistically significant (χ2=5.167, P=0.023). There was no statistically significant difference in blood glucose levels between the two groups before treatment (P>0.05). After treatment, blood glucose levels improved in both groups, and the level of blood glucose in the observation group were lower than those in the control group, and the difference was statistically significant (P<0.05). The incidence of adverse reactions in the observation group was lower than that in the control group, and the difference was statistically significant (P<0.05).Conclusion The application of insulin degludec and in⁃sulin aspart can significantly improve the blood glucose level of patients with type 2 diabetes mellitus, the efficacy is more accurate, and the safety is higher, and it will not increase the occurrence of adverse reactions after the use of medication.[作者简介]戴卉（1985-），女，本科，主治医师，研究方向为内分泌科。