首頁 資訊 新型糖尿病治療藥物:糖尿病藥物設(shè)計的希望.pptx

新型糖尿病治療藥物:糖尿病藥物設(shè)計的希望.pptx

來源:泰然健康網(wǎng) 時間:2025年07月10日 09:34

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NovelTherapeuticAgentsforManagementofDiabetesMellitus:AHopeforDrugDesigningagainstDiabetesMellitus新型糖尿病治療藥物:糖尿病藥物設(shè)計的希望Life2025-03-15文獻發(fā)表信息發(fā)表類型:JournalArticle、Review期刊:Life發(fā)表日期:08-1-2024關(guān)鍵詞:糖尿病、治療學、新藥、干細胞、免疫療法和植物療法作者:AhmedM.E.Elkhalifa、AhmedM.E.Elkhalifa、MehakNazar、SofiImtiyazAli、IbraqKhursheed、..、ShowkatUlNabi作者單位:1.DepartmentofPublicHealth,CollegeofHealthSciences,SaudiElectronicUniversity,Riyadh11673,SaudiArabia;a.alkhalifa@.sa2.DepartmentofHaematology,FacultyofMedicalLaboratorySciences,UniversityofElImamElMahdi,Kosti1158,Sudan;lhmelamin@3.PreclinicalResearchLaboratory,DepartmentofClinicalVeterinaryMedicine,Ethics&Jurisprudence,Sher-e-KashmirUniversityofAgriculturalSciencesandTechnology(SKUAST-Kashmir),Srinagar190006,India;mehaknazar2422@(M.N.);imtiyazali@skuastkashmir.ac.in(S.I.A.);syedtaifa786@(S.T.);mahimuzaffar111@(M.A.M.);iqrahussainshah@(I.H.S.);drmasoodmalik16@(M.M.);zahidramzan367@(Z.R.);shubeenaahad786@(S.A.);nusratbashir510@(N.B.)文獻重點信息摘取糖尿病(DM)的特征是胰島素分泌和外周阻力絕對下降,是最常見的代謝和內(nèi)分泌疾病。糖尿病的發(fā)病機制還包括脂肪細胞胰島素抵抗、胰高血糖素分泌增加、腎小球葡萄糖吸收增加和神經(jīng)遞質(zhì)功能障礙。盡管有各種各樣的治療方法可用于血糖控制,但由于確定了糖尿病的各種致病決定因素,糖尿病的管理仍然具有挑戰(zhàn)性和復(fù)雜性。目前針對糖尿病的治療干預(yù)主要集中在血糖控制上,而沒有考慮最終導(dǎo)致治療失敗和糖尿病進展的其他病理決定因素。目前的綜述文章討論了新的治療方案,這些方案特別有希望支持其安全性,并討論了使用這些藥物產(chǎn)生的副作用,以便將這些新的候選藥物有效地制成治療糖尿病的潛在藥物。主要背景關(guān)于胰島素缺乏癥,糖尿病已被分為1型糖尿病(T1DM),也稱為胰島素依賴型糖尿病/青少年發(fā)病型糖尿病,與胰腺β細胞的自身免疫性破壞有關(guān),存在于5-10%的糖尿病患者中。最近,有報道稱,TIDM死亡率和發(fā)病率的增加與低社會人口狀況有關(guān)。2型糖尿病(T2DM)也被認為是胰島素非依賴型糖尿?。∟IDDM)/成熟型糖尿病是各發(fā)達國家死亡的第四大原因,與冠心病和中風等心臟病的可能性并列。妊娠期糖尿?。℅DM)是在懷孕期間觀察到的,由于葡萄糖不耐受而發(fā)生,隨后導(dǎo)致嚴重程度不同的高血糖癥。該疾病的特征包括自身免疫反應(yīng),即身體的免疫系統(tǒng)攻擊并破壞胰腺中產(chǎn)生胰島素的β細胞,成人發(fā)病,逐漸發(fā)病和胰島素依賴。對于無法通過改變生活方式和口服降糖藥物達到血糖目標的患者,胰島素治療已被提倡。主要背景—相關(guān)文獻參考(PMID:26868137)標題:糖尿病作為使用腎素-血管緊張素系統(tǒng)阻滯劑的重要適應(yīng)癥:隨機試驗的系統(tǒng)回顧和薈萃分析。期刊:BMJ(Clinicalresearched.)(影響因子:105.7)發(fā)表日期:2016-02-11第一單位:NewYorkUniversitySchoolofMedicine,NewYork,NY,USAsripalbangalore@.KeyMessages:PubMed、Embase和Cochrane中央對照試驗數(shù)據(jù)庫,用于糖尿病患者中RAS阻斷劑與其他抗高血壓藥物的隨機試驗。與其他抗高血壓藥物相比,RAS阻斷劑與死亡風險相似(相對風險0.99,95%可信區(qū)間0.93-1.05),心血管死亡(1.02,0.83-1.24),心肌梗死(0.87,0.64-1.18),心絞痛(0.80,0.58-1.11),中風(1.04,0.92-1.17),心力衰竭(0.90,0.76至1.07),以及血運重建(0.97,0.77至1.22)。在糖尿病患者中,RAS阻滯劑在降低心血管和腎臟硬終點風險方面并不優(yōu)于其他抗高血壓藥物,如噻嗪類、鈣通道阻滯劑和β受體阻滯劑。主要背景—相關(guān)文獻參考(PMID:23376836)標題:橙皮素對糖尿病大鼠視網(wǎng)膜氧化應(yīng)激、神經(jīng)炎癥和細胞凋亡的保護作用。期刊:Microvascularresearch(影響因子:3.1)發(fā)表日期:2013-05-01第一單位:DepartmentofPharmacology,DelhiInstituteofPharmaceuticalSciences&Research,UniversityofDelhi,NewDelhi,India.binitkumar35@KeyMessages:用熱休克蛋白(100mg/kg體重)處理STZ誘導(dǎo)的糖尿病大鼠24周,觀察抗氧化(超氧化物歧化酶、SOD、過氧化氫酶、CAT和谷胱甘肽、GSH)酶、炎性細胞因子(TNF-α、IL-1β)、caspase-3、膠質(zhì)纖維酸性蛋白(GFAP)和水通道蛋白4(AQP4)的表達。而Hsp治療的視網(wǎng)膜細胞因子水平明顯低于糖尿病視網(wǎng)膜。2.目前的抗糖尿病治療方案Table1:用于治療糖尿病的商業(yè)藥物及其相關(guān)作用機制,具有優(yōu)缺點。治療糖尿病的可用藥物治療包括胰島素和各種口服降糖藥,如磺脲類、二甲雙胍、α-葡萄糖苷酶抑制劑(阿卡波糖和曲格列酮)和吡格列酮/羅格列酮[31](表1和表2)。表1、表3和表4給出了改善和治療糖尿病最常用的常規(guī)治療劑的綜合表,簡要介紹了它們的優(yōu)缺點。AlphaGlucosidaseInhibitorsDrugsTheseAreBuddingTherapeuticsAimedatBlockingα-Glucosidase,Henceforth,PostponingBreakdownofCarbohydratesWhichConsequentlyDiminishesItsIntestinalAssimilation[5]CommercialNameTheseAreBuddingTherapeuticsAimedatBlockingα-Glucosidase,Henceforth,PostponingBreakdownofCarbohydratesWhichConsequentlyDiminishesItsIntestinalAssimilation[5]MechanismofActionTheseAreBuddingTherapeuticsAimedatBlockingα-Glucosidase,Henceforth,PostponingBreakdownofCarbohydratesWhichConsequentlyDiminishesItsIntestinalAssimilation[5]AdvantagesTheseAreBuddingTherapeuticsAimedatBlockingα-Glucosidase,Henceforth,PostponingBreakdownofCarbohydratesWhichConsequentlyDiminishesItsIntestinalAssimilation[5]SideEffectsTheseAreBuddingTherapeuticsAimedatBlockingα-Glucosidase,Henceforth,PostponingBreakdownofCarbohydratesWhichConsequentlyDiminishesItsIntestinalAssimilation[5]References(a)AcarbosePrecoseThereisamendableblockageofglucosidasesesp.glucoamylase,sucrose,maltose,andα-amylaseofbrushborderepitheliumDecreasedpostprandialhyperglycemiainT2DMBorborygmic,abdominalfullness,diarrhea,intestinalflatulence[32](b)MigtitolGlycetWorksbyreducingthedisintegrationandassimilationofsugarinsmallintestineConsiderablehypoglycemiabyachievementofnormoglycemiainpatientsviaenhancementofglucosetoleranceLesserGITafter-effects[5,27,33](c)VogliboseNewlyaddedsignificantsucroseblockerSlowsdowntheglucoseassimilation,accordinglydecreasingthepossibilityofmacrovascularcomplications[5](d)InsulinsensitizersAidtheactivityofinsulininliver,adiposetissue,andmusclesinadditiontodecreasingtheperipheralinsulinresistanceinskeletalmusclesandadipocytesHypoglycemia,weightgain,diarrhea,andgreaterchanceofcardiovasculardiseases[34]2.目前的抗糖尿病治療方案Table2:磺酰脲類藥物用于治療糖尿病及其相關(guān)作用機制,具有優(yōu)缺點。治療糖尿病的可用藥物治療包括胰島素和各種口服降糖藥,如磺脲類、二甲雙胍、α-葡萄糖苷酶抑制劑(阿卡波糖和曲格列酮)和吡格列酮/羅格列酮[31](表1和表2)。SulfonylureasDrugsSulfonylureasAreaClassofOralAntidiabeticDrugsCommonlyUsedintheTreatmentofType2Diabetes.TheyWorkbyStimulatingInsulinReleasefromtheBetaCellsofthePancreasCommercialNameSulfonylureasAreaClassofOralAntidiabeticDrugsCommonlyUsedintheTreatmentofType2Diabetes.TheyWorkbyStimulatingInsulinReleasefromtheBetaCellsofthePancreasMechanismofActionSulfonylureasAreaClassofOralAntidiabeticDrugsCommonlyUsedintheTreatmentofType2Diabetes.TheyWorkbyStimulatingInsulinReleasefromtheBetaCellsofthePancreasAdvantagesSulfonylureasAreaClassofOralAntidiabeticDrugsCommonlyUsedintheTreatmentofType2Diabetes.TheyWorkbyStimulatingInsulinReleasefromtheBetaCellsofthePancreasSideEffectsSulfonylureasAreaClassofOralAntidiabeticDrugsCommonlyUsedintheTreatmentofType2Diabetes.TheyWorkbyStimulatingInsulinReleasefromtheBetaCellsofthePancreasReferencesFirst-generationsulfonylureas(a)Chlorpropamide(b)Tolazamide(c)Tolbutamide(d)Acetohexamide(a)Diabinese(b)Tolinase(c)Orinase(d)DyemelorThesecausestimulationofthesecretionofinsulinfrompancreasConsiderablehypoglycemiaisachievedGITinterferencesandhemolyticanemia[22]2.Second-generationsulfonylureas(a)Glyburide(b)Glimepiride(c)Glipizide(a)Glynase(b)Gleam(c)GlucotrolAllofthesepromotethesecretionofinsulinfromβcellsofpancreasConsiderablehypoglycemiaisachievedGITinterferencesandhemolyticanemia[5,21,35]2.目前的抗糖尿病治療方案Table3:雙胍類藥物用于治療糖尿病及其相關(guān)作用機制,具有優(yōu)缺點。表1、表3和表4給出了改善和治療糖尿病最常用的常規(guī)治療劑的綜合表,簡要介紹了它們的優(yōu)缺點。BiguanidesDrugsTheyPrimarilyWorkbyReducingHepaticGlucoseProductionandImprovingPeripheralInsulinSensitivityMechanismofActionTheyPrimarilyWorkbyReducingHepaticGlucoseProductionandImprovingPeripheralInsulinSensitivityAdvantagesTheyPrimarilyWorkbyReducingHepaticGlucoseProductionandImprovingPeripheralInsulinSensitivitySideEffectsTheyPrimarilyWorkbyReducingHepaticGlucoseProductionandImprovingPeripheralInsulinSensitivityReferencesMetformin(extractedfromplantGalegaofficinalis)WorksbyimprovingtheserumglucoselevelsviahinderingtheliverglucoseproductionalongwithboostingtheuptakeofglucosebymusclefibersDecliningtriglyceridesandlow-densitylipidsandhaslesserfrequencyofhypoglycemiaLacticacidosis,vitB12deficiency,congestiveheartfailure[9]2.目前的抗糖尿病治療方案Table4:噻唑烷二酮類藥物(TZD)用于治療糖尿病及其相關(guān)作用機制的優(yōu)缺點。表1、表3和表4給出了改善和治療糖尿病最常用的常規(guī)治療劑的綜合表,簡要介紹了它們的優(yōu)缺點。Thiazolidinediones(TZD)DrugsTheseDrugsWorkbyTargetingthePeroxisomeProliferator-ActivatedReceptorGamma(PPAR-γ),aNuclearReceptorInvolvedinGlucoseandLipidMetabolismCommercialNameTheseDrugsWorkbyTargetingthePeroxisomeProliferator-ActivatedReceptorGamma(PPAR-γ),aNuclearReceptorInvolvedinGlucoseandLipidMetabolismMechanismofActionTheseDrugsWorkbyTargetingthePeroxisomeProliferator-ActivatedReceptorGamma(PPAR-γ),aNuclearReceptorInvolvedinGlucoseandLipidMetabolismAdvantagesTheseDrugsWorkbyTargetingthePeroxisomeProliferator-ActivatedReceptorGamma(PPAR-γ),aNuclearReceptorInvolvedinGlucoseandLipidMetabolismSideEffectsTheseDrugsWorkbyTargetingthePeroxisomeProliferator-ActivatedReceptorGamma(PPAR-γ),aNuclearReceptorInvolvedinGlucoseandLipidMetabolismReferencesTroglitazoneRosiglitazonePioglitazone(a)Rezulin(b)Avandia(c)ActosEnhancesinsulinsensitivityofalltargettissuesandactsasligandsforPPAR(peroxisomesproliferator-activatedgamma)complexlocatedinsidethenucleusEffectonplasmalow-densitylipids/cholesterol(a)ClassIII–IVheartfailure.(b)Fluidretention,peripheraledema(c)CHF(congestiveheartfailure)[5,38,39]2.目前的抗糖尿病治療方案Table5:用于治療糖尿病的新型肽類似物類藥物及其相關(guān)作用機制,具有優(yōu)缺點。本綜述的結(jié)果將推動確定最新的糖尿病治療方案,并闡明其在細胞水平和亞細胞水平上的作用機制(表5)。在本手稿的后續(xù)部分,我們討論了未來可用于有效管理糖尿病的新型糖尿病治療劑,其中一些治療劑處于臨床試驗的第3階段,一些處于臨床前開發(fā)階段(表5和表6)。PeptideAnaloguesDrugsTheseAnaloguesAreSyntheticCompoundsDesignedtoMimictheActionsofEndogenousPeptidesInvolvedinGlucoseHomeostasisMechanismofActionTheseAnaloguesAreSyntheticCompoundsDesignedtoMimictheActionsofEndogenousPeptidesInvolvedinGlucoseHomeostasisAdvantagesTheseAnaloguesAreSyntheticCompoundsDesignedtoMimictheActionsofEndogenousPeptidesInvolvedinGlucoseHomeostasisSideEffectsTheseAnaloguesAreSyntheticCompoundsDesignedtoMimictheActionsofEndogenousPeptidesInvolvedinGlucoseHomeostasisReferencesIncretinmimeticsLiberatedinripostetotheingestionoffood,elicitingtheglucose-inducedinsulinresponseAppetencedecreasingpositiveimpactoftheseagentsoncardiovascular,inflammation,andthecentralnervoussystemDoesnothindertheglucagonemission[43,44]Glucagon-likepeptideanalogsandagonists(GLP-1)Retardingthegastricclearing,boostingtheinsulinsecretionalongsidehamperingtheglucagonsecretionfrompancreasPreventsgastricacidsecretioninadditiontopromotinginsulinsecretionNotreported[35,45,46]Glucose-dependentinsulinotropicpolypeptideanalogs(GIP)TheseanalogsaresyntheticcompoundsdesignedtomimictheactionsofendogenouspeptidesinvolvedinglucosehomeostasisReducingthepostprandialglucoselevelsandglycosylatedhemoglobinLesserdangerofhypoglycemiawiththeuseofthisagent[20,47]DPP-4inhibitorsGIPproducedoutofthekcellsoftheuppersmallintestineworksbyaffectingthemetabolismoflipidsFastingplasmaglucoselevelsreducedalongwiththechangesinglycosylatedhemoglobinEffectslikevomitingandanorexia[8,12]LiraglutideActionviaenzymaticincretindisintegrationAgonistforreceptor(GLP-1)Appetencedecreasingpositiveimpactoftheseagentsoncardiovascular,inflammation,andthecentralnervoussystemComparedtotheshort-actingforms,long-actingoneshavelesschanceofcausinghypoglycemia[9,48,49,50]3.新型治療藥物Table6:用于治療糖尿病的新型抗糖尿病藥物及其相關(guān)作用機制,具有優(yōu)缺點。在本手稿的后續(xù)部分,我們討論了未來可用于有效管理糖尿病的新型糖尿病治療劑,其中一些治療劑處于臨床試驗的第3階段,一些處于臨床前開發(fā)階段(表5和表6)。NovelAnti-DiabeticAgentsDrugsTheLatestDevelopmentsinPharmacotherapy,FocusingonInnovativeApproachesThatAddresstheComplexChallengesofDiabetesMechanismofActionTheLatestDevelopmentsinPharmacotherapy,FocusingonInnovativeApproachesThatAddresstheComplexChallengesofDiabetesAdvantagesTheLatestDevelopmentsinPharmacotherapy,FocusingonInnovativeApproachesThatAddresstheComplexChallengesofDiabetesSideEffectsTheLatestDevelopmentsinPharmacotherapy,FocusingonInnovativeApproachesThatAddresstheComplexChallengesofDiabetesReferencesAmylinanalogs(isletamyloidpolypeptideSignificantdeclineinthelevelsofglucoseinT1DMandT2DMDecreasesthebloodglucoselevelbyreducingtheglucagonsecretionUsedassolotherapyorsometimesincombinationwithorallyactiveanti-diabeticagents.[23,52,53,54]2.PramlintideSecretedandstoredincombinationwithinsulinandhinderingtheglucagonsecretioninadditiontoslowingdowntheunloadingofgastriccontentsIfthereissomebetacellfunctionremaining,thenatthattime,replacementcurativeaidedwithbasalinsulincanprovetobeusefulIncreasedarterialpressure,inducingkidneydysfunction,onsetofhypertension,boostingtheoccurrenceofdiabetesandhypothyroidism[23,52,53,54]3.Nitrate/NitriteMoleculesproducedfromL-arginineviatheenzymesnitricoxidesynthase(NOS)namelyinducible,neuronal,endothelial,andmitochondrialhavebeenobservedtoabatethelevelsoftriglyceridesinserumRegulationofTGlevelsinbloodPromotionoffatdepositioninliver[23,52,53,54]4.Antioxidanttherapy:vitaminE,vitaminC,andβcaroteneFastingplasmainsulinandHbA1clevelsaredeclinedbyadministrationofvitaminC.Moreover,thereisseentoberefinementofinsulinaction.Likewise,withtheadministrationofβcarotene,reductionofoxidativelow-densitylipidshasbeennotedNeweffectivetherapyforthecureofT2DMpatientsisantioxidanttherapy,whichmightreflectasignificantroleindiminishingthechancesofdiabetichyperglycemiaandthereafteritsassociateddrawbacks[23,52,53,54]5.FBPase(fructose1,6-bisphosphatase)inhibitorsModeofactionviainhibitingtheFBPaseenzyme(rate-limitingenzymeingluconeogenesispathway)Liverhyperplasia,liverhypertrophy,andlivercarcinogenesis[23,52,53,54]6.BromocriptineRecently,Swift-liberatedbromocriptineevolvedinfavorofT2DMameliorationbutthemodeofactionisnotclearyetTheliteraturehasprovedthatafter24weeksoftherapy,theaverageglycatedhemoglobinlevelsdeclinedby0.0%to0.2%[23,52,53,54]7.Imeglimin(yettopasstheclinicaltrial)Quiteeffectiveinthesensethatitstimulatesglucoseuptakeinmuscles,livergluconeogenesisisdepressedalongwithboostinthesugar-dependentinsulinreleaseHamperingoxidativephosphorylation[23,52,53,54]8.Peroxisomeproliferator-activatedreceptors(PPARs)Mostlyparticipatingincontrollingtheenergyhomeostasissupplementarytoreductionoftriglycerides[23,52,53,54]3.6.民族醫(yī)學Table7:用于治療糖尿病的植物藥物制劑,植物部分應(yīng)具有高水平的藥理活性成分——為其治療作用確定的活性成分,以及可能的作用機制。(1)不同植物化學物質(zhì)及其作用方式的綜合表如(表7)所示,它們被加工成潛在的藥物(圖3)。PhytomedicinewithFamilyPortionActiveChemicalConstituentsMechanismofActionReferencesAlliumcepa(Onion)AlliaceaeCormS-methylcysteinesulphoxideandallylpropyldisulfideArousetheactionofenzymeshexokinaseandreductaseinadditiontotheproductionofinsulin[66]CaricapapayaCaricaceaeSeedandextractofleaves------Alleviatewoundsinalloxan-induceddiabeticratsinadditiontoreducingtheserumglucoselevel[37]Catharantusroseus(Vincaroses)ApocynaceaeLeavesandtwigs-------Boostingthebiosynthesisofinsulinfromthepancreaticislets[91]AcaciaArabicaFabaceaeBarkandseedPolyphenolsandtanninsCommencementofinsulinsecretionfrompancreaticβcells[92]Alliumsativum(Garlic)AlliaceaeCormAllicinandallylpropyldisulfideModifiestheactionofenzymesglucose-6-phosphate,HMGCoAreductase,andhexokinase,inadditiontomanagingglucoselevelsinserumandtissues[51]Aloebarbadensis(Aloevera/Ghikanwar)LiliaceaeLeafBarbaloinandalloinRevitalizingtheprocessofhepatogluconeogenesis/glycogenolysisalongsidetheliberationofinsulinfromthepancreas.Inaddition,theglutathionelevelsindiabeticratswereelevatedbyafactorof4[4,63]Betavulgaris(Beetroot)RootBetacyaninsandphenolicsNon-enzymaticglycosylationofserumglucoseandskinproteinsdeclined[92]Azadirachtaindica(Neem)MeliaceaeSeedandleafNimbinandazadirachtinβcellsofthepancreasarerevived/revitalizedAlso,ithasbeennotedtoamendbloodcirculationviadilatingbloodvessels(Mishraetal.,2011)[93,94]Brassicanigra(Mustard)BrassicaceaeWholeplantSinignin,isorhamnetin,diglucoside,andisothiocynateTheconductofglycogensynthetaseisboostedunliketheactionofglycogenphosphorylaseandgluconeogenicenzymes,whichisreducedtherebydepressingglycogenolysisandgluconeogenesis[51]3.6.民族醫(yī)學Table7:用于治療糖尿病的植物藥物制劑,植物部分應(yīng)具有高水平的藥理活性成分——為其治療作用確定的活性成分,以及可能的作用機制。(2)不同植物化學物質(zhì)及其作用方式的綜合表如(表7)所示,它們被加工成潛在的藥物(圖3)。PhytomedicinewithFamilyPortionActiveChemicalConstituentsMechanismofActionReferencesCassiaauriculata(Senna)LeguminaceaeFlowerSennosideAandSennosedeBTheactivityofhepatichexokinaseandphosphofructokinaseenzymesisamplifiedwhiletheactivityofglucose-6-phosphateandfructose-1,6-biphosphataseenzymesissuppressed.Further,thereisanincreaseintheno.ofisletsandbetacellsinpancreas[51]AndrographisPaniculata(Kalmegh)AcanthaceaeWholeplantAndrographolide,kalmeghin,andditerpenoidlactoneGlucoseassimilationfromtheintestinalwalliscountered[51,62]Gymnemasylvestre(Gudmar)AsclepiadaceaeLeafGymnemasaponinsandgymnemicacidBoostingthenumberofβcellsalongwithinsulinsecretion[63]Ficusbenglenesis(Banyan)MoraceaeBarkandleafTannin,taraxasterol,quercetin-3-galactoside,andrutinBloodinsulinlevelsintype2diabetesmellitusweretriggeredviatheactionofhypoglycemiccomponentsseparated[63]Capsicumfrutescens(Mirch)SolanaceaeEntireplantorFruitCapsaicin,proteinThereisthedevaluationofinsulinbindingoninsulinreceptorsalongwithboostinginsulinvoiding[51]Coriandrumsativum(Corianderfruits)UmbelliferaeSeedBloodglucoseleveldeclinedincludingtheactivityofbetacellsescalatedthereafteraugmentinginsulinrelease[62]Cuminumcyminum(Jira)UmbelliferaceaeSeedGeraniol,coriandrol,pinene,coriendrlyacetateDepletioninglycosylatedhemoglobin,bloodureanitrogen,andbloodglucose,andatthesametimeseruminsulincontentisenhanced[62]Eucalyptusglobulas(Nilgiri,Dinkumoil)LeafHydrocumin,phellandrene,andcuminaldehydeElevationofperipheralglucoseuptake[61,92,95]CurcumalongaLe.(Turmeric)ZingiberaceaeTuberCitronella,camphene,pinene,cineoleMentionedmedicineshowedpromisingoutcomesinthemanagementofdiabetes[13,62]3.6.民族醫(yī)學Table7:用于治療糖尿病的植物藥物制劑,植物部分應(yīng)具有高水平的藥理活性成分——為其治療作用確定的活性成分,以及可能的作用機制。(3)不同植物化學物質(zhì)及其作用方式的綜合表如(表7)所示,它們被加工成潛在的藥物(圖3)。PhytomedicinewithFamilyPortionActiveChemicalConstituentsMechanismofActionReferencesEugeniajambolana(jamun)MyrtaceaeDriedseedandpulpEssentialoil,dimethoxycurcumin,curcumin,andBtermennoneIntensifyingtheemissionofinsulininadditiontohindranceoftheliverandkidneyenzymeinsulinase[96]TrigonellafoenumGraecum(Methi)LeguminosaeSeedOleanolicacid,ellagicacid,alphaglucosidase,Malvidin3-laminaribiosideaandferulicacidValuabledischargeofinsulinalongsidetheinducementofinsulincoalescence[51,97]TinosporacrispaMenispermaceaeStemNicotinicacid,coumarin,saponin-peptideesters,trigonelline,andflavonoidsStimulationofinsulinsecretiononaccountofitsanti-diabeticeffectandfurther,thereistheregulationofcalciumconcentrationofbetacells[51,62]OcimumsanctumL.(Tulsi)LamiaceaeLeafFraxinuscoumarinalkaloids,ascoacid,eugenol,andglucosideSerumglucoselevelisdiminished[62]Lawsoniainermis(Henna)LythraceaeSeedandflowerXanthonesandtannin,alkaloidsandfattyoilConcentrationofcholesterol,glucose,andtriglyceridesisdepressed[98]Momordicacharantia(Karela)CucurbitaceaeLeafCharantin,momordicI,momordicII,andcucurbitacinBTheremayberejuvenationofmoderatelydamagedcellsalongwithimprovementofbetacellproductioninthepancreas.Inaddition,saidproductcontainslectin,whichmimicstheactionofinsulin[92]MangiferaindicaAnacardiaceaeLeafMangiferinIntestinalabsorptionofglucoseisdecreased[42]Musasapientum(Banana)MusaceaeFlowerGlycoside,flavonoids,andsteroidWorksbysimulatinginsulin-likeaction[99]TinosporaCardifolia(Guduchi)MenispermaceaeRoot,stem,andleavesDiterpenoidlactones,alkaloid,glycosides,andsteroidsAppreciabledepressionofbloodsugar[100]3.6.民族醫(yī)學Table7:用于治療糖尿病的植物藥物制劑,植物部分應(yīng)具有高水平的藥理活性成分——為其治療作用確定的活性成分,以及可能的作用機制。(4)不同

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