Acteoside: Kev Tshawb Fawb Txog Antioxidant Thiab Antihypertensive Activity

Hu rau:joanna.jia@wecistanche.com

Antioxidant Thiab Antihypertensive Kev Ua Haujlwm Ntawm Acteoside Thiab Nws Analogs

Chao-Hsiang CHEN1,2, Yin-Shiou LIN3, Mei-Yin CHIEN2,4, Wen-Chi HOU5,6,*, and Miao-Lin HU1,*

Abstract. Acteoside(Txoj Cai), ib qho phenylethanoid glycoside, yog ib qho kev sib xyaw ua ke hauv ntau cov nroj tsuag thiab tshuaj ntsuab tshuaj ntsuab. Ua nrog nws cov qauv isomer,isoacteoside(Isoact), thiab analog, 6-O-acety-lacteoside (6-O-acetylac), tau siv hauv txoj kev tshawb fawb los tshawb xyuas covantioxidant, anti-angiotensin-hloov enzyme (ACE), thiab hemolysis inhibitory kev ua ub nohauv vitrothiab antihypertensive kev ua ub no tiv thaiv spontaneously hypertensive nas (SHR)hauv vivo. Peb tau pom tias Txoj Cai, Isoact, thiab 6-O-acetylact tau txais txiaj ntsig zoo 1, 1-diphenyl-2- picryl-hydrazyl radicals (nrog IC50 ntawm 11.4, 9.48, thiab 9.55 μM, feem) thiab superoxide radicals (nrog IC50 ntawm 66.5, 38. , thiab 39.1 μM, feem). Raws li Isoact thiab 6-O-acetylact muaj cov dej num zoo sib xws, tsuas yog Act thiab Isoact tau siv rau cov kev tshawb fawb hauv qab no. Ob Txoj Cai thiab Isoact inhibited xanthine oxidase kev ua haujlwm nrog IC50 ntawm 53.3 thiab 62.2 μM, feem. Ob Txoj Cai thiab Isoact kuj tseem cuam tshuam rau ACE kev ua haujlwm thiab cov hemolysis tshwm sim los ntawm 2,2'-azo-bis (2-amidinopropane) dihydrochloride, tab sis cov teebmeem ntawm Txoj Cai tau muaj zog dua Isoact. Tom qab ntawd peb tau txais ib koob tshuaj ntawm Txoj Cai lossis Isoact (10 mg / Kg lub cev hnyav) rau SHR thiab ntsuas qhov kev hloov pauv ntawm cov ntshav siab (SBP) thiab diastolic ntshav siab (DBP) dhau 24 teev. Txoj Cai, tab sis tsis yog Isoact, tau pom tias muaj kev tiv thaiv kev ua haujlwm hauv kev txo qis SBP thiab DBP. Cov txiaj ntsig tau qhia txog qhov muaj txiaj ntsig zoo ntawm Txoj Cai ua cov khoom noj khoom haus rau kev noj qab haus huvantioxidantkev tiv thaiv thiab kev tswj ntshav siab.

Ntsiab lus: Acteoside; Antihypertensive kev ua haujlwm; Angiotensin-hloov enzyme (ACE); Antioxidant; Hemolysis.

active ingredient acteoside nyob rau hauv cistanche

Taw qhia

Acteoside(Act), ib qho phenylethanoid glycoside uas muaj caffeic acid, 3',4'-dihydroxy phenylethanol, qabzib, thiab rhamnose, yog thawj zaug cais tawm ntawm paj ntawmSyringa Vul- garis ua(Birkofer li al., 1968), thiab ua ke nrog cov qauv isomer ntawmisoacteoside(Isoact) thiab derivative ntawm6-O- acetylacteoside(6-O-acetylact), tau pom nyob rau hauv ntau cov nroj tsuag thiab tshuaj ntsuab, xws liLigstrum purpurascens(Wong et al., 2001),Callicapa dichotoma(Koo et al., 2006; Lee et al., 2006),Cistanche deserticolathiabBoschniakia rossica(Wu et al., 2006),Scrophularia ningpoenis(Huang et al., 2008),Rehmannia gluten(Li et al., 2006). Txoj cai tau tshaj tawm los nthuav tawm cov haujlwm antimetastatic ntawm B16 melanoma hlwb hauv C57BL/6 nas qauv (Ohno et al., 2002). Txoj Cai, Isoact, thiab 6-O-acetylact tsis ntev los no tau pom tias inhibit IL-1 - qhib kev qhia ntawm intercellular CAM-1 thiab vascular CAM-1 nyob rau hauv tib neeg umbilical leeg endothelial hlwb (Chen li al., 2009). Txoj cai tseem tiv thaiv bovine pulmonary endothelial hlwb los ntawm hydroxyl radical-induced oxidative kev nyuaj siab (Chiou li al., 2004) thiab inhibits nitric oxide thiab TNF- ntau lawm los ntawm kev thaiv ntawm AP -1 ua kom nyob rau hauv lipopolysaccharide-stimulated macrophages (Rao li al. , 2009). Txoj Cai thiab Isoact nthuav tawm cov haujlwm neuroprotectivehauv vitro(Koo et al., 2005). Koj et al. (2006) tau tshaj tawm tias Txoj Cai thiab nws cov aglycones tau txais txiaj ntsig zoo 1, 1-diphenyl-2-picryl-hydrazyl (DPPH) thiab nitric oxidehauv vitro. Txawm li cas los xij, qee qhov kev tshawb fawb tau muab piv rau ib sabhauv vitro antioxidantKev ua ub no ntawm Txoj Cai thiab nws cov txheej txheem muaj feem cuam tshuam xws li Isoact thiab 6-O- acetylac.

Ntau chav kawm ntawm cov kws tshuaj tau siv rau hauv kev kho mob ntshav siab (Mark thiab Davis, 2000). Ib chav kawm ntawm cov tshuaj tiv thaiv kab mob siab, hu ua angiotensin I converting enzyme (ACE) inhibitors (ie peptidase inhibitors), muaj qhov tshwm sim tsis zoo ntawm cov kev mob tshwm sim thiab yog cov chav kawm nyiam ntawm kev tiv thaiv hypertensive.

cov neeg sawv cev thaum kho cov neeg mob uas muaj cov kab mob sib thooj (Fotherby thiab Panayiotou, 1999). ACE (peptidyl- dipeptide hydrolase EC 3.4.15.1) yog ib qho dipeptide-liberating Zn-muaj exopeptidase, uas tshem tawm cov dipeptide los ntawm C-terminus ntawm angiotensin I los tsim angiotensin II, ib qho tshuaj tiv thaiv kab mob siab heev. Ob pebantioxidantpeptides (txo glutathione thiab carnosine-txog peptides) nthuav tawm ACE inhibitory kev ua ub no (Hou li al., 2003). Thawj qhov chaw kho mob muaj, qhov ncauj nquag ACE inhibitor, captopril, tau tsim rau kev kho mob ntshav siab (Ondetti li al., 1977; Borer, 2007). Txoj cai tau tshaj tawm kom siv nitric oxide-mediated relaxing teebmeem ntawm endothelium- tsis zoo aortic rings ntawm SD nas (Wong et al., 2001). Ahmad et al. (1995) tau tshaj tawm tias Txoj Cai ua rau muaj qhov txo qis hauv cov ntshav systolic (SBP) thiab diastolic ntshav siab (DBP) tom qab nws cov tshuaj txhaj rau hauv cov tshuaj loog tsis muaj zog Wistar nas. Txawm li cas los xij, nws tsis paub meej tias qhov ncauj tswj hwm txoj cai thiab / lossis nws cov isomers muaj feem xyuam yog cov tshuaj tiv thaivhauv vivo. Hauv qhov kev tshawb fawb tam sim no, peb tau tshawb xyuas qhovhauv vitro antioxidantmuaj peev xwm thiab ACE inhibitory kev ua ub no thiabhauv vivoAntihypertensive kev ua ntawm Act, Isoact, thiab/los yog 6-O-acetylact siv cov spontaneous hypertensive nas (SHRs). Cov kev tshawb fawb no yuav tsum muab cov ntaub ntawv muaj txiaj ntsig zoo rau kev txhim kho Txoj Cai ua khoom noj khoom haus noj qab haus huv.

Cov ntaub ntawv thiab cov txheej txheem

Khoom siv

2,2'-azo-bis(2-amidinopropane)dihydrochloride (AAPH), ACE (I unit, luav lub ntsws), butylated hydroxytoluene (BHT), DPPH, N-(3-[{{7 }}furyl]acryloyl)-Phe-Gly- Gly (FAPGG), NADH, phenazinemethosulfate (PMS), xanthine, thiab xanthine oxidase tau yuav los ntawm Sigma Chemical Co. (St. Louis, MO, USA). Captopril tau yuav los ntawm Calbiochem Co. (CA, USA). Txoj Cai, Isoact, thiab 6-O-acetylact (Daim duab 1) tau yuav los ntawm Equal Corp. (purities> 98 feem pua, Shanghai, Tuam Tshoj). Lwm yam tshuaj thiab reagents yog los ntawm Sigma Chemical Co. (St. Louis, MO, USA).

Kev khawb av kev ua si ntawm Txoj cai, Isoact, thiab 6-O- acetylact tawm tsam dPPH ua radicals los ntawm spectrophotometric

Ib ntim (0.3 mL) ofAct, Isoact, thiab 6-O-acetylact (qhov kawg concentrations yog 1.56 txog 50 µM), BHT thiab ascorbic acid (kawg concentrations yog 2.4 txog 60 µM) tau ntxiv rau 0.1 mL ntawm 1 M Tris-HCl tsis (pH 7.9). ) thiab tom qab ntawd tov nrog 0.6 mL ntawm 100 µM DPPH hauv methanol mus rau qhov kawg ntawm 60 µM rau 20 min nyob rau hauv kev tiv thaiv lub teeb ntawm chav tsev kub (Liu li al., 2004; Lin li al., 2008). Qhov txo qis ntawm qhov nqus ntawm 517 nm tau ntsuas thiab qhia tias ΔA517 nm. Cov dej deionized tau siv los ua kev sim dawb. Qhov kev ua si ntawm DPPH radical (feem pua ​​​​) tau suav nrog qhov sib npaug: (ΔA517blank − ΔA517sample) ÷ ΔA517blank × 100. Lub IC50 sawv rau qhov concentration ntawm ib nrab-inhibition.

Inhibitory kev ua si ntawm Ua thiab Isoact tawm tsam xanthine oxidase

Kev ua haujlwm xanthine oxidase tau ntsuas los ntawm kev txiav txim siab ntawm uric acid tsim ntawm 295 nm siv xanthine ua substrate (Kalckar, 1947). Qhov sib txawv ntawm Txoj Cai thiab Isoact (qhov kawg concentrations yog 25, 50, thiab 75 µM) tau ua ntej sib xyaw nrog 50 μL ntawm 1 mU / mL xanthine oxidase ntawm 4 degree rau 1 h, thiab tom qab ntawd 300 μL ntawm 1 mM xanthine tau ntxiv. Cov kev hloov ntawm absorbance ntawm 295 nm tau sau tseg tshaj 2 min thiab qhia raws li ΔA295 nm / min. Lub xanthine oxidase inhibitory kev ua si (feem pua) raug xam raws li hauv qab no: (ΔA295 nm / min dub − ΔA295 nm / min qauv) ÷ ΔA295 nm / min dub × 100. Deionized dej tau siv es tsis txhob siv cov qauv tov raws li kev sim dawb paug. IC50 stands rau qhov concentration ntawm ib nrab-inhibition.

Kev khawb av kev ua si ntawm Txoj cai, Isoact, thiab 6-O- acetylact tawm tsam superoxide radicals los ntawm spectrophotometric

Lub superoxide radical yog tsim los ntawm PMS-NA- DH system (Liu et al., 2004; Lin et al., 2008). Tag nrho cov qauv 0.2 mL, muaj ntau qhov sib txawv ntawm Txoj Cai, Isoact, thiab 6-O-acetylate (qhov kawg concentration yog 15.6, 31.3, 62.5, 125, thiab 250 µM), tau ntxiv rau hauv ib ntu rau 0.2 mL ntawm 630 µM nitroblue tetrazolium, 0.2 ml ntawm 33 µM PMS, thiab 0.2 ml ntawm 156 µM NADH hauv 100 mM phosphate tsis (pH 7.4). Cov dej deionized tau siv los hloov cov qauv kev daws teeb meem raws li kev sim dawb. Ascorbic acid (qhov kawg concentration yog 6, 9, 12, thiab 24 µM) tau siv los ua kev tswj xyuas zoo. Cov kev hloov ntawm absorbance ntawm 560 nm tau sau tseg thaum 2 min thiab qhia raws li ΔA560 nm / min. Cov kev ua si ntawm superoxide radicals (feem pua) raug xam raws li hauv qab no: (ΔA560 nm / min dub − ΔA560 nm / min qauv) ÷ ΔA560 nm / min dub × 100. IC50 stands rau qhov concentration ntawm ib nrab-inhibition.

kev txiav txim siab ntawm AcE inhibitory kev ua si ntawm Ua thiab Isoact los ntawm HPLC

Txhua 50 µL ntawm Txoj Cai (0.2, 0.4, 0.5, thiab 2.0 µmole) thiab Isoact ({{ 11}}.1, 0.2, 0.5, 1.0, thiab 2.0 µmole) tau premixed nrog 15 µL ntawm 1U/mL ACE rau 5 feeb, thiab tom qab ntawd 200 µL ntawm 0.5 mM FAPGG tau ntxiv thiab hnov ​​​​mob hauv chav sov li 10 min (Anzenbacherova li al., 2001). Lub 800 µL methanol tau ntxiv los nres cov tshuaj tiv thaiv. Qhov kev sim dawb yog FAPGG nkaus xwb. Hauv kev sim tswj, ACE tau hnov ​​​​mob nrog FAPGG nyob rau hauv tib lub sijhawm. Chromatographic sib cais ntawm FAPGG thiab FAP tau ua tiav ntawm Hitachi (Nyiv) chromatographic system nrog 10 µL-voj. Kev tshuaj xyuas HPLC tau ua tiav ntawm Biosil Aqua-ODS-W 5 µ kem (Biotic Chemical Co., Ltd., Taiwan, 250 × 4.6 mm id), particle loj 5 µm. Cov tshuaj reacted sib tov yog sib cais isocratically nrog ib tug mobile theem muaj xws li 0.02 M nonylamine (hloov rau pH 2.4 nrog phosphoric acid) thiab acetonitrile nyob rau hauv ib tug ratio ntawm 67.5:32.5 (V / V) (Anzenbacherova li al., 2001). Tus nqi ntws yog 1 mL / min; lub ntim ntim yog 10 µL; Lub ntes tau teeb tsa ntawm 345 nm. Cov ACE inhibitions (feem pua) ntawm Txoj Cai thiab Isoact raug xam raws li hauv qab no: [(Area of ​​FAPGGblank − Area of ​​FAPGGcontrol) − (Area of ​​FAPGGblank − Area of ​​FAPGGsample) ÷ (Area of ​​FAPGGblank − Area of ​​FAPGGcontrol) × 100.

Inhibitory kev ua si ntawm Ua thiab Isoact tawm tsam AAPH-mediated hemolysis

Cov kab mob dawb-radical oxidation ntawm cov qe ntshav liab (RBC) los ntawm AAPH-mediated hemolysis (Miki li al., 1987). Cov ntshav nas tau muab tso rau hauv cov hlab ntsha heparinized thiab centrifuged ntawm 1000 ×grau 10 min. Tom qab ntxuav nrog 0.15 M NaCl thrice, lub ntim RBC tau txais los ntawm centrifugation ntawm 1000 ×grau 10 min. Qhov sib txawv ntawm Act thiab Isoact (qhov kawg concentrations yog 2, 5, thiab 10 µM) tau tov 25 μL ntawm 20 feem pua ​​​​RBC ncua (V / V, hauv 10 mM PBS) thiab 25 μL ntawm 500 mM AAPH tov ntawm 37 degree rau 0 , 1, 1.5, 2, 2.5, 3, thiab 3.5 h nrog maj mam co. Txhua qhov sib tov tau centrifuged ntawm 1000 ×grau 10 min, thiab tus supernatant tau ntsuas ntawm 536 nm. Cov dej deionized tau siv los hloov cov tshuaj AAPH los yog cov qauv kev daws teeb meem, feem, raws li ib pawg neeg dawb huv los yog pab pawg tswj. Lub hemolysis inhibition (feem pua) ntawm Act thiab Isoact ntawm 3 h lossis ntawm 3.5 h raug xam raws li hauv qab no: (ΔA536 nmcontrol − ΔA536 nmsample) ÷ ΔA536 nmcontrol × 100.

Antihypertensive teebmeem ntawm Ua thiab Isoact ntawm SHr

Cov teebmeem ntawm qhov ncauj tswj hwm txoj cai, Isoact, thiab captopril los ntawm lub raj pub mis (2.0 × 80 mm) ntawm qhov txo SBP thiab qhov txo DBP tau txiav txim siab raws li cov txheej txheem ntawm cov ntaub ntawv dhau los (Lin et al., 2006; Lin et al., 2008; Han et al., 2011). Tag nrho cov txheej txheem kev sim tsiaj ua raws li cov lus qhia tau tshaj tawm (National Science Council, 1994). Cov txiv neej SHRs (8 lub lis piam hnub nyoog, National Laboratory Tsiaj Center, Taipei) tau nyob ib leeg hauv cov tawb steel khaws cia ntawm 24 degree nrog rau 12-h lub voj voog tsaus ntuj thiab muaj kev nkag mus rau tus qauv nas / nas chow ( Prolab RMH2500, 5P14 Diet, PMI Nutrition International, Brentwood, MO) thiab dej. SHRs tau muab faib rau hauv kev tswj hwm thiab qauv kev kho mob rau SBP thiab DBP kev txiav txim siab (rau nas rau ib pawg). Rau kev sim tshuaj tiv thaiv luv luv, 0.5 mL ntawm 10 mg Act lossis Iso-act / Kg ntawm SHR lossis 5 mg captopril / Kg ntawm SHR tau noj ib zaug, thiab tus Tsov tus tw ntshav siab tau ntsuas ntawm 2, 4, 6, thiab 24. h tom qab ib qho kev tswj qhov ncauj. 0.5 mL dej distilled yog siv rau kev sim dawb. Lub ntsuas ntshav siab tsis ncaj (BP-98A, Softron Co. Ltd. Tokyo, Nyiv) tau siv los ntsuas SBP thiab DBP plaub zaug ntawm txhua qhov kev txiav txim siab rau txhua qhov kev kho mob.

cov ntaub ntawv tsom xam

Cov txiaj ntsig tau nthuav tawm raws li txhais tau tias ± SD thiab tshuaj xyuas siv ib-txoj kev ANOVA, ua raws li cov post hoc Tukey qhov kev xeem rau ntau qhov kev sib piv. Cov tub ntxhais kawm ntawvt-test tau ua, thaum tsuas yog ob pawg ntawm cov ntaub ntawv raug muab piv (xws li ntawm Txoj Cai thiab Isoact ntawm tib qhov concentration). P-tus nqi < 0.05="" yog="" suav="" tias="" yog="" qhov="" tseem="" ceeb.="" kev="" txheeb="" xyuas="" txheeb="" cais="" tau="" ua="" tiav="" siv="" spss="" rau="" windows,="" version="" 10="" (spss,="" inc.,="" chicago,="" il,="">

acteosidehauv cistanche los txhim kho kev nco

Cov txiaj ntsig

Kev khawb av kev ua si ntawm PPH thiab superoxide radicals

Txoj Cai, Isoact, thiab 6-O-acetylact nthuav tawm koob tshuaj-dependent DPPH scavenging kev ua ub no ntawm pH 7.9 (Daim duab 2). IC50 qhov tseem ceeb yog 11.4, 9.48, thiab 9.55 µM, ntsig txog, rau Txoj Cai, Isoact, thiab 6-O- acetylact. IC50 qhov tseem ceeb ntawm kev tswj hwm zoo ntawm ascorbic acid thiab BHT yog 13.1 thiab 18.5 µM, feem.

Inhibition ntawm xanthine oxidase kev ua si

Txoj Cai thiab Isoact tau pom tias muaj cov tshuaj tiv thaiv kab mob ntawm xanthine oxidase (Daim duab 3). IC50 tau suav tias yog 53.3 thiab 62.2 µM, raws li txoj cai thiab Isoact.

Inhibition ntawm superoxide dismutase kev ua si

Vim hais tias ob qho tib si Act thiab Isoact inhibited xanthine oxidase kev ua, peb siv PMS-NADH system los tsim superoxide radicals (Liu li al., 2004; Lin li al., 2008). Txoj cai,

Isoact, thiab 6-O-acetylact nthuav tawm koob tshuaj-dependent superoxide radical scavenging kev ua ub no (Daim duab 4). IC50 qhov tseem ceeb yog 66.0, 38.5, thiab 39.1 µM, ntsig txog, rau Txoj Cai, Isoact, thiab 6-O- acetylact. IC50 qhov tseem ceeb ntawm kev tswj zoo ntawm ascorbic acid yog 9.0 µM. Los ntawm cov txiaj ntsig ntawm daim duab 2 thiab 4, nws tau pom tseeb tias Isoact thiab 6-O-acetylate muaj cov kev ua si radical-scavening zoo sib xws tiv thaiv DPPH thiab superoxide radicals, thiab yog li tsuas yog Txoj Cai thiab Isoact raug xaiv rau kev tshuaj ntsuam xyuas kev lom neeg ntxiv.

AcE inhibitory kev ua si ntawm Ua thiab Isoact

Hauv kev sim ua ntej, peb pom tias Txoj Cai thiab Isoact cuam tshuam nrog kev nqus ntawm ACE substrate FAPGG thiab nws cov khoom siv hydrolyzed FAP ntawm 345 nm raws li siv rau kev soj ntsuam spectrophotometric txuas ntxiv (Holmquist li al., 1979). Yog li, kev sib cais ua ke nrog kev tshawb pom ntawm Txoj Cai lossis Isoact thiab FAPGG los ntawm HPLC tau siv los saib xyuas cov haujlwm ACE inhibitory. Daim duab 5A rau daim duab 5D yog cov HPLC chromatograms ib txwm los ntawm 10 µl cov tshuaj tiv thaiv sib tov ntawm ib qho kev sim dawb paug (FAPGG nkaus xwb, Daim duab 5A); tswj kev xeem (ACE rov ua nrog FAPGG los tsim FAP, Daim duab 5B); 0.5 µmole ofAct (312.5 µg), ACE thiab FAPGG (Daim duab 5C); thiab 0.5 µmole ntawm Isoact (312.5 µg), ACE thiab FAPGG (Daim duab 5D). Qhov chaw ntawm FAPGG hauv daim duab 5B yog qhov qis tshaj plaws thiab hauv daim duab 5A qhov siab tshaj plaws ntawm plaub yam HPLC chromatograms. Cov cheeb tsam ntawm FAPGG hauv daim duab 5C thiab 5D yog nyob ntawm ACE inhibitory kev ua ub no ntawm ntau qhov sib txawv ntawm Txoj Cai thiab Isoact. Kev suav ACE inhibitions ntawm Txoj Cai thiab Isoact tau qhia hauv daim duab 5E. Qhov kev coj ua tau pom tias ACE inhibitory kev ua haujlwm siab dua li Isoact, thiab IC50 ntawm qhov qub tau suav tias yog 472 µM los ntawm cheeb tsam hauv HPLC chromatograms.

Inhibitory kev ua si ntawm Ua thiab Isoact tawm tsam AAPH-mediated hemolysis

Cov haujlwm inhibitory ntawm Txoj Cai thiab Isoact tawm tsam AAPH-mediated hemolysis ntawm qhov ntau ntawm 2, 5, thiab 10 µM tau soj ntsuam ntau dua 3.5 h (Miki li al., 1987). Cov txiaj ntsig ntawm daim duab 6A qhia tau tias hemolysis hauv nas RBC nce siab heev (qhia raws li ΔA536 nm) tom qab 3-h lossis 3.5-h cov tshuaj tiv thaiv nyob rau hauv muaj AAPH radicals (raws li pab pawg tswj, lub voj voog dawb ). Me me lossis tsis muaj hemolysis tau pom thaum tsis muaj AAPH radicals thaum lub sij hawm 3.5-h cov tshuaj tiv thaiv (raws li pab pawg dawb paug, lub voj voog dub). Yog li ntawd, hemolysis inhibition of Act thiab Isoact ntawm 3 h lossis ntawm 3.5 h tau xam raws li hauv qab no: (ΔA536 nmcontrol − ΔA536 nmsample) ÷ ΔA536 nmcontrol × 100. Daim duab 6B

qhia tau hais tias ob qho tib si Act thiab Isoact ntawm 2, 5 thiab 10 µM nthuav tawm cov concentration-dependent inhibition ntawm AAPH-induced hemolysis, nrog rau cov teebmeem inhibitory ntawm Act muaj zog dua li cov Isoact ntawm txhua qhov concentration siv.

Antihypertensive teebmeem ntawm Ua thiab Isoact ntawm SHr

SHRs tau txais ib qho kev tswj hwm qhov ncauj ntawm Txoj Cai thiab Isoact (10 mg / Kg SHR), thiab kev hloov pauv hauv SBP thiab DBP tau sau tseg dhau 24 teev. Peb yav dhau los tau tshaj tawm tias cov ntshav siab (SBP thiab DBP) ntawm SHR tau hloov pauv thaum lub sijhawm 24-h (Lin et al., 2006; Han et al., 2011). Yog li ntawd, kev sib piv ntawm lub sijhawm teem tseg (xws li 2, 4, 6, 8, thiab 24 h) ntawm qhov khoob thiab cov qauv es tsis txhob siv ua ntej thiab tom qab qhov ncauj nws tus kheej tau siv. Nws tau pom tias Txoj Cai, tab sis tsis yog Isoact, tau txo qis SBP thiab DBP ntawm SHR piv rau pawg dawb paug (dej distilled). SBP tau txo qis hauv pawg Act ntawm 2, 4, thiab 6 h los ntawm 18.8, 16.5, thiab 14.9 mmHg, raws li, tab sis qhov txo qis ntawm SBP (3.3 mmHg) ntawm 24 teev tom qab Txoj Cai Kho Mob tsis yog nyob rau hauv SBP.

artically tseem ceeb (Daim duab 7A). Raws li pom hauv daim duab 7B, DBP tau txo qis hauv pawg Act ntawm 2, 4 thiab 6 h (los ntawm 8.5, 7.6, thiab 12.0 mmHg, raws li), txawm hais tias tsuas yog cov txiaj ntsig tau los ntawm 6 h yog qhov tseem ceeb hauv kev txheeb cais. (P< 0.05).="" nws="" tau="" sau="" tseg="" tias="" txoj="" cai="" thiab="" captopril="" (raws="" li="" kev="" tswj="" hwm="" zoo)="" muaj="" cov="" txiaj="" ntsig="" zoo="" sib="" xws="" ntawm="" sbp="" thaum="" ntxov="" (2,="" 4,="" thiab="" 6="" h)="" tom="" qab="" kev="" tswj="" hwm="" qhov="">

acteosideHauv cistanche muaj cov txiaj ntsig zoo ntawm antioxidant

Kev sib tham

Cov kab mob oxygen nquag thiab cov tshuaj dawb radical-mediated yog koom nrog hauv cov txheej txheem degenerative lossis pathological xws li kev laus, mob qog noj ntshav, kab mob plawv, thiab Alzheimer's disease (Ames, 1983; Gey, 1990; Smith et al., 1996). Ntau cov ntawv ceeb toom tau tsom mus rau kev tshuaj xyuas covantioxidantkev ua ub no los ntawm natural resources. Hauv kev tshawb fawb tam sim no, peb thawj zaug piv covantioxidantCov haujlwm ntawm Txoj Cai, Isoact, thiab 6-O- acetylate. Txoj Cai thiab Isoact yog cov qauv isomers uas cov ntsiab lus ntawm caffeic acid moiety yog sib koom ua ke rau C-4 hydroxyl pawg ntawm cov piam thaj hauv yav dhau los thiab rau C-6 hydroxyl pawg ntawm qabzib tom kawg. Thaum cov ntsiab lus ntawm rhamnose thiab 3',4'- dihydroxy phenyl ethanol, feem, yog sib txuas rau C-3 thiab C-1 pawg hydroxyl ntawm cov piam thaj moiety nyob rau hauv tib txoj cai thiab Isoact molecule, { {8}}O-acetylact yog ib qho Act derivative uas acetic acid yog sib koom nrog C-6 hydroxyl pawg hauv cov piam thaj moiety (Daim duab 1). Koj et al. (2006) tau tshaj tawm tias Txoj Cai thiab nws cov aglycones tau nthuav tawm DPPH-scavenging cov dej num, thiab qhov kev txiav txim ntawm cov dej num no (qhia raws li IC50) yog Txoj Cai (1.28 µM) > caffeic acid (2.22 µM) > 3',4'-dihydroxy phenyl ethanol ( 7.72 µM) > -tocopherol (15.1 µM). Hauv daim ntawv tshaj tawm tam sim no (Daim duab 2), qhov kev txiav txim ntawm DPPH scavenging kev ua ub no (qhia raws li IC50) yog 6-O-acetylate (9.55 µM) ≈ Isoact (9.48 µM) > Act (11.4 µM). Cov txiaj ntsig no tau muab piv rau lossis zoo dua li cov ascorbic acid (IC50 ntawm 13.1 µM) thiab BHT (IC50 ntawm 18.5 µM) rau kev tshem tawm DPPH radicals. Qhov siab dua IC50 ntawm Txoj Cai hauv daim ntawv tshaj tawm tam sim no yuav yog los ntawm qhov kawg ntawm 60 µM DPPH es tsis txhob siv 30 µM siv ntawm Koo li al. qhia (2006). Raws li DPPH radical as-hais belongs rau electron-hloov cov tshuaj tiv thaiv (Huang li al., 2005), nws yog speculated tias cov derivative hauv C-6 hydroxyl pawg ntawm cov piam thaj moiety, xws li acetyl pawg hauv {{21. }}O- acetylate thiab caffeic acid moiety hauv Isoact, tuaj yeem muab cov tshuaj tiv thaiv hluav taws xob hloov tau yooj yim dua li cov C-6 dawb hydroxyl pab pawg hauv cov piam thaj moiety ofAct rau DPPH scavenging assay.

Txoj Cai, 6-O-acetylate thiab Isoact tau tshaj tawm tias muaj superoxide-scavenging kev ua hauv vitro siv xanthine / xanthine oxidase system los tsim cov superoxide radicals (Wang li al., 1996; Gao et al., 1999). Txawm li cas los xij, peb txoj kev tshawb fawb tam sim no tau qhia tias Txoj Cai tau nthuav tawm xanthine oxidase inhibitory kev ua ub no (Daim duab 3). Yog li, cov superoxide radical tau tsim los ntawm kev siv PMS-NADH system hauv daim ntawv tshaj tawm tam sim no (Liu li al., 2004; Lin li al., 2008) es tsis txhob xanthine/xanthine oxidase system. Tseeb, siv xanthine / xanthine oxidase system los tsim superoxide radicals, Wang li al. (1996) tau txais IC50 ntawm 63 µM Txoj Cai tiv thaiv superoxide radicals, thiab tus nqi no nyob ze rau qhov inhibition ntawm xanthine oxidase kev ua los ntawm Txoj Cai, raws li qhia hauv txoj kev tshawb no (53.3 µM). Nws tau tshaj tawm tias caffeic acid nthuav tawm xanthine oxidase inhibitory kev ua ub no (Chiang li al., 1994). Tej zaum nws yuav xav tias superoxide-scavenging kev ua ub no siv xanthine / xanthine oxidase generating system ntawm ib co phytochemicals nrog cov qauv txuam nrog caffeic acids, xws li Act los yog Isoact (Wang li al., 1996; Gao li al., 1999), tej zaum yuav muaj. tau pab, tsawg kawg hauv ib feem, ntawm xanthine oxidase inhibitions. Interestingly, Wang et al. (1996) pom tias Txoj Cai (0.5 thiab 2.5 mM) tsis cuam tshuam xanthine oxidase kev ua haujlwm uas tau txiav txim los ntawm cov pa oxygen electrode rau kev siv cov pa oxygen thaum xanthine oxidation. Yog li, nws yog ib qho tseem ceeb uas yuav tsum nco ntsoov tias ntau txoj hauv kev rau kev soj ntsuam cov haujlwm superoxide-scavenging yuav tsim cov ntaub ntawv tsis sib xws.

Li et al. (1993) tau tshaj tawm qhov zoo sib xws ntawm inhibition of Act thiab Isoact tiv thaiv AAPH-mediated hemolysis hauv RBC ntawm nas. Txawm li cas los xij, peb tau pom ntawm no tias Txoj Cai tau nthuav tawm ntau dua inhibitory kev tiv thaiv AAPH-induced hemolysis hauv RBC ntawm nas dua li Isoact (Daim duab 6). Nws tsis paub meej tias qhov tsis sib xws yuav yog vim qhov sib txawv ntawm cov nas tsuag.

Kang et al. (2003) tau tshaj tawm tias Txoj Cai tau nthuav tawm ACE inhibitory kev ua ub no, thiab IC50 yog 373.3 µg / mL uas tau suav tias yog 598 µM siv Hip-His-Leu ua substrates. Hauv tsab ntawv tshaj tawm tam sim no, Txoj Cai tau pom tias muaj ACE inhibitory kev ua ub no ntau dua li Isoact, thiab IC50 ntawm qhov qub tau suav tias yog 472 µM los ntawm cheeb tsam hauv HPLC chromatograms (Daim duab 5). Txoj cai tau tshaj tawm kom siv nitric oxide-mediated relaxing teebmeem ntawm endothelium- intact aortic rings ntawm SD nas (Wong et al., 2001). Txawm hais tias Txoj Cai tau pom tias muaj tshuaj tiv thaiv kab mob hauv Wistar nas,

Txoj kev tshawb no tau siv cov tshuaj txhaj tshuaj ntawm Txoj Cai rau hauv cov tshuaj loog txhawm rau txhawm rau txiav txim qhov adsorption yam (Ahmad li al., 1995). Ntawm no, peb tswj hwm Txoj Cai hais lus rau SHRs thiab txiav txim siab hloov ntshav siab. Peb pom tias qhov kev tswj hwm qhov ncauj qhov tseeb, tab sis tsis yog ntawm Isoact, tau nthuav tawm cov tshuaj tiv thaiv kab mob los ntawm kev txo qis SBP thiab DBP dhau 24 teev tom qab kev tswj hwm ib leeg (Daim duab 7). Ua ntawm ib koob ntawm 10 mg / kg lub cev qhov hnyav muaj qhov cuam tshuam ze li ntawm captopril hauv koob tshuaj 5 mg / kg SHR hauv kev txo qis SBP thiab zoo dua li captopril ntawm kev txo DBP.

Hauv kev xaus, Act tau nthuav tawmantioxidantKev ua ub no, ACE inhibitory kev ua ub no, thiab cov tshuaj tiv thaiv kev mob ntshav siab ntawm SHRs. Cov txiaj ntsig tau nthuav tawm ntawm no yuav muaj txiaj ntsig rau kev siv zog los tsim cov tshuaj ntsuab lossis cov khoom lag luam ntsig txog siv Txoj Cai, uas tau pom muaj nyob hauv ntau cov nroj tsuag thiab tshuaj ntsuab, rau kev tiv thaiv oxidant thiab kho cov teebmeem yav tom ntej.

Cistancheacteosiderau antioxidation thiab anti-aging

1Department zaub mov Science thiab Biotechnology, National Chung Hsing University, Taichung, Taiwan

2Ko Da Pharmaceutical Co., Ltd., Tao-Yuan, Taiwan

3 Tsev Kawm Ntawv Pharmacy, Taipei Medical University, Taipei, Taiwan

4Graduate Institute of Biomedical Materials thiab Engineering, Taipei Medical University, Taipei, Taiwan

5Traditional Herbal Medicine Research Center, Taipei Medical University Hospital, Taipei, Taiwan

6Graduate Institute of pharmacognosy, Taipei Medical University, Taipei, Taiwan

(Tau Lub Peb Hlis 12, 2012; Txais Lub Plaub Hlis 20, 2012)

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