魏彥明,郭延生,曲亞玲,華永麗,鄧紅娟

甘肅農(nóng)業(yè)大學(xué)動(dòng)物醫(yī)學(xué)院,蘭州 730070

當(dāng)歸及其炮制品水提物體外抗脂質(zhì)過氧化作用

魏彥明＊,郭延生,曲亞玲,華永麗,鄧紅娟

甘肅農(nóng)業(yè)大學(xué)動(dòng)物醫(yī)學(xué)院,蘭州 730070

為了研究當(dāng)歸及其不同炮制品水提物抗脂質(zhì)過氧化的作用。采用體外小鼠肝組織自發(fā)性脂質(zhì)過氧化、H2O2誘導(dǎo)的紅細(xì)胞膜脂質(zhì)過氧化和溶血反應(yīng),評(píng)價(jià)了當(dāng)歸及其炮制品水提物對(duì)脂質(zhì)過氧化的抑制作用。結(jié)果表明當(dāng)歸及其不同炮制品水提物體外對(duì)肝組織自發(fā)性脂質(zhì)過氧化的抑制能力為當(dāng)歸碳 ＞酒當(dāng)歸 ＞生當(dāng)歸 ＞油當(dāng)歸 ＞土當(dāng)歸;對(duì) H2O2誘導(dǎo)的紅細(xì)胞膜脂質(zhì)過氧化的抑制能力為當(dāng)歸碳 ＞土當(dāng)歸 ＞生當(dāng)歸 ＞酒當(dāng)歸 ＞油當(dāng)歸;對(duì) H2O2誘導(dǎo)的溶血作用的抑制能力為酒當(dāng)歸 ＞當(dāng)歸碳 ＞土當(dāng)歸 ＞油當(dāng)歸 ＞生當(dāng)歸,且抑制效果均呈現(xiàn)良好的劑量依賴關(guān)系。說明當(dāng)歸及其不同炮制品水提物體外都具有一定的抗脂質(zhì)過氧化的作用,其中抗肝組織自發(fā)性脂質(zhì)過氧化和 H2O2誘導(dǎo)的紅細(xì)胞膜脂質(zhì)過氧化的能力以當(dāng)歸碳最好,而抗 H2O2誘導(dǎo)的溶血作用以酒當(dāng)歸最好。

當(dāng)歸;炮制品;水提物;脂質(zhì)過氧化

當(dāng)歸為傘形科多年生草本植物當(dāng)歸Angelicasinesis的根,主產(chǎn)于甘肅岷縣,歷代多以甘肅岷縣所產(chǎn)作為道地藥材。此外,四川、云南、湖北等省也有栽培。其藥用歷史悠久,歷代本草均有記載,《神農(nóng)本草經(jīng)》謂之“當(dāng)歸味溫,主呃逆上氣”被列為中品。有補(bǔ)血、活血、調(diào)經(jīng)止血、潤腸滑腸之功效[1],為醫(yī)家常用,素有“十方九歸”之稱。目前臨床常用的炮制品有生當(dāng)歸、酒當(dāng)歸、土當(dāng)歸和當(dāng)歸碳[2],除此之外,甘肅習(xí)用油當(dāng)歸,并被載入《甘肅省中藥炮制規(guī)范》[3],前人有“油當(dāng)歸偏于養(yǎng)血潤腸,酒當(dāng)歸偏于活血,當(dāng)歸碳偏于止血之說”?，F(xiàn)代藥理研究表明,當(dāng)歸在心血管系統(tǒng)、血液系統(tǒng)、免疫系統(tǒng)、抗損傷及保護(hù)方面均顯示良好的藥理作用,且具有一定的抗氧化和清除自由基的作用,對(duì)腦缺氧、缺血后再灌注腦組織脂質(zhì)過氧化增高具有明顯的抑制作用[4],但能否在體外重現(xiàn)這種作用、提供直接證據(jù),尚需進(jìn)行研究,目前關(guān)于上述炮制品抗脂質(zhì)過氧化的作用的研究報(bào)道較少。因此,探討當(dāng)歸不同炮制品對(duì)小鼠肝勻漿脂質(zhì)過氧化、紅細(xì)胞膜脂質(zhì)過氧化和溶血的抑制作用,可為當(dāng)歸臨床用藥和炮制理論提供更加科學(xué)合理的理論依據(jù)。

1 實(shí)驗(yàn)材料

1.1 實(shí)驗(yàn)動(dòng)物

SPF級(jí)昆明小鼠,18～22 g,雌雄各半,由蘭州大學(xué)醫(yī)學(xué)院實(shí)驗(yàn)動(dòng)物中心提供,實(shí)驗(yàn)設(shè)施合格證號(hào)和動(dòng)物合格證號(hào)為 SCXK(甘)20050007。

1.2 試劑

三氯醋酸、鹽酸、H2O2和 L-抗壞血酸等均為國產(chǎn)分析純,硫代巴比妥酸 (TBA),三 (羥甲基)氨基甲烷 (Tris)為進(jìn)口上海分裝。

1.3 儀器

Lambda7島津紫外/可見光分光光度計(jì) (日本),T10組織勻漿機(jī) (德國),AL104電子分析天平(德國),加樣器(Eppendorf公司),TBZ5-WS多管架自動(dòng)平衡離心機(jī) (湘儀),CW-2000型超聲-微波協(xié)同萃取儀 (上海),RE-6000旋轉(zhuǎn)蒸發(fā)儀 (上海), SHA-B水浴恒溫振蕩器(江蘇)。

1.4 藥物

當(dāng)歸的原藥材采于甘肅岷縣,經(jīng)甘肅中醫(yī)學(xué)院中藥學(xué)系龍全江副教授和甘肅農(nóng)業(yè)大學(xué)動(dòng)物醫(yī)學(xué)院中獸醫(yī)教研組作生藥學(xué)鑒定。取原藥材,除去雜質(zhì),洗凈,潤透,切成薄片,曬干作為為生當(dāng)歸。其炮制品油當(dāng)歸、酒當(dāng)歸、當(dāng)歸碳、土當(dāng)歸均按《甘肅省中藥炮制規(guī)范》和《全國中藥炮制規(guī)范》要求,由甘肅中醫(yī)學(xué)院龍全江副教授指導(dǎo)炮制。

2.3 當(dāng)歸及其炮制品水提物對(duì) H2O2誘導(dǎo)的紅細(xì)胞膜脂質(zhì)過氧化的抑制作用

2 實(shí)驗(yàn)方法

2.1 當(dāng)歸及其炮制品水提物的制備

取生當(dāng)歸及其炮制品各 100 g,加蒸餾水 300 mL,85℃超聲-微波協(xié)同提取 2次,每次 30 min。合并兩次提取液,減壓濃縮至質(zhì)量濃度 1 g/mL浸膏,4℃保存?zhèn)溆?測試時(shí)精密吸取,作適當(dāng)稀釋。

2.2 當(dāng)歸及其炮制品水提物對(duì)小鼠肝組織自發(fā)性脂質(zhì)過氧化的抑制作用

采用 TBA比色法略作修改[5],實(shí)驗(yàn)設(shè)空白管、對(duì)照管、加藥管和藥物底管。取 5%肝組織勻漿上清液 1 mL分別加入對(duì)照管和加藥管,空白管和藥物底管加 1 mL生理鹽水。加藥管和藥物底管加入不同濃度的生當(dāng)歸及其炮制品水提液 0.05 mL,空白管和對(duì)照管加入蒸餾水 0.05 mL,搖勻 37℃恒溫水浴振蕩 2 h,各管加入 20%TCA 0.3 mL,0.1 mol/L HCl 2 mL,0.67%TBA 1 mL,沸水浴 15 min,自來水流水冷卻,3000 r/min離心 10 min,以空白管標(biāo)零,取上清液于 532 nm處測定吸光度A,按下式計(jì)算抑制率:

參照文獻(xiàn)方法略作修改[6],實(shí)驗(yàn)設(shè)空白管、對(duì)照管、加藥管和藥物底管,取 0.5%紅細(xì)胞懸液 0.5 mL加入到空白管、對(duì)照管和加藥管,藥物底管加生理鹽水 0.5 mL,各管再加入生理鹽水 1 mL,加藥管和藥物底管加入不同濃度的生當(dāng)歸及其炮制品水提液 0.05 mL,對(duì)照管和加藥管分別加入 300 mmol/L H2O20.1 mL,空白管和藥物底管加 0.1 mL生理鹽水,搖勻,37℃恒溫水浴振蕩 2 h,加入 20%TCA 0.3 mL,0.1 mol/L HCl 2 mL,3500 r/min離心 15 min,取上清液 3 mL加入 0.67%TBA 1 mL,沸水浴15 min,自來水流水冷卻,以空白管標(biāo)零,于 535 nm處測定吸光度A,按下式計(jì)算抑制率:

2.4 當(dāng)歸及其炮制品水提物對(duì) H2O2誘導(dǎo)的紅細(xì)胞溶血的抑制作用

參照文獻(xiàn)方法略作修改[7,8],實(shí)驗(yàn)設(shè)為為對(duì)照管、加藥管和藥物底管,取 0.5%紅細(xì)胞懸液 1 mL分別加入對(duì)照管和加藥管,藥物底管加入 1 mL生理鹽水,加藥管加入不同濃度的生當(dāng)歸及其炮制品水提液 0.05 mL,搖勻,37℃水浴 10 min,對(duì)照管和加藥管分別加入 300 mmol/L H2O20.05 mL,藥物底管加 0.05 mL生理鹽水,搖勻 37℃恒溫水浴振蕩 1 h,各管加生理鹽水 4 mL,3000 r/min離心 10 min,以生理鹽水標(biāo)零,取各管上清液于 415 nm處測定吸光度A,按下式計(jì)算抑制率:

2.5 數(shù)據(jù)統(tǒng)計(jì)處理

用 SPSS 13.0統(tǒng)計(jì)軟件進(jìn)行方差分析和回歸分析,測定結(jié)果以±s表示。

3 實(shí)驗(yàn)結(jié)果

3.1 當(dāng)歸及其炮制品水提物對(duì)小鼠肝組織自發(fā)性脂質(zhì)過氧化的抑制效果

從表 1可以看出,生當(dāng)歸、油當(dāng)歸、酒當(dāng)歸、土當(dāng)歸和當(dāng)歸碳水提物在 25～200 mg/mL劑量范圍內(nèi)都對(duì)小鼠肝組織自發(fā)性脂質(zhì)過氧化有一定的抑制作用,且隨藥物濃度增加,抑制率顯著升高 (P＜0.05),即藥物濃度 (X)與抑制率(Y)之間存在良好的依賴關(guān)系,擬合曲線,計(jì)算回歸方程,生當(dāng)歸:y= e4.294-49.497/x,R2=0.994;油當(dāng)歸:y=e4.284-54.059/x,R2= 0.969;酒當(dāng)歸:y=0.579x-0.001x2-1.201,R2= 0.999;土當(dāng)歸:y=0.567x-0.001x2-1.943,R2= 0.995;當(dāng)歸碳:y=23.776lnX-50.315,R2=0.998。從圖 1可以看出,不同炮制品 IC50從小到大依次為當(dāng)歸碳、酒當(dāng)歸、生當(dāng)歸、油當(dāng)歸和土當(dāng)歸,即生當(dāng)歸及其炮制品水提物對(duì)小鼠肝組織自發(fā)性脂質(zhì)過氧化能力依次為當(dāng)歸碳 ＞酒當(dāng)歸 ＞生當(dāng)歸 ＞油當(dāng)歸 ＞土當(dāng)歸。表明當(dāng)歸經(jīng)炒碳和酒炒后對(duì)其抑制肝組織自發(fā)性脂質(zhì)過氧化的能力增強(qiáng),而當(dāng)歸經(jīng)油炒和土炒后抑制能力降低。在此試驗(yàn)條件下L-抗壞血酸在 4～10 mg/mL劑量范圍內(nèi)能有效抑制肝組織自發(fā)性脂質(zhì)過氧化作用,I C50為 4.64 mg/mL(圖 1)。

表 1 當(dāng)歸炮制品水提物體外對(duì)小鼠肝組織自發(fā)性脂質(zhì)過氧化的抑制作用Table 1 Inhibitory effects ofwater extracts from processed products of Chinese angelica on mouse liver homogenates spontaneous antilipid peroxidationin vitro(±s)

表 1 當(dāng)歸炮制品水提物體外對(duì)小鼠肝組織自發(fā)性脂質(zhì)過氧化的抑制作用Table 1 Inhibitory effects ofwater extracts from processed products of Chinese angelica on mouse liver homogenates spontaneous antilipid peroxidationin vitro(±s)

注:1.a,b……表示同一炮制品不同濃度之間比較,不同字母表示差異顯著(P＜0.05),相同字母,表示差異不顯著(P＞0.05)。Notes:1.a,b… represents the Comparison between different Concentrations of same processed product,and difference letter has significant difference (P＜0.05),the same letter no significant difference(P＞0.05).

3.2 當(dāng)歸及其炮制品水提物對(duì) H2O2誘導(dǎo)的紅細(xì)胞膜脂質(zhì)過氧化的抑制效果

從表 2可以看出,生當(dāng)歸、油當(dāng)歸、酒當(dāng)歸、土當(dāng)歸和當(dāng)歸碳水提物對(duì) H2O2誘導(dǎo)的紅細(xì)胞膜脂質(zhì)過氧化具有一定的抑制效果,除生當(dāng)歸外,其余炮制品在 25～200 mg/mL的劑量范圍內(nèi),抑制率隨著藥物濃度的增高而顯著增高 (P＜0.05),即炮制品藥物濃度(X)與抑制率(Y)之間存在著良好的依賴關(guān)系。擬合曲線,計(jì)算回歸方程,生當(dāng)歸:y=34.207-0.1x+0.001x2,R2=0.997;油當(dāng)歸:y=2.665x0.495, R2=0.972;酒當(dāng)歸:y=e3.817-41.086/x,R2=0.977;土當(dāng)歸:y=9.633+0.275x,R2=0.999;當(dāng)歸碳:y= 4.097+0.410x,R2=0.989。不同炮制品對(duì) H2O2誘導(dǎo)的紅細(xì)胞膜脂質(zhì)過氧化的 I C50由小到大依次為當(dāng)歸碳、土當(dāng)歸、生當(dāng)歸、酒當(dāng)歸、油當(dāng)歸 (圖 1),即抗氧化能力當(dāng)歸碳 ＞土當(dāng)歸 ＞生當(dāng)歸 ＞酒當(dāng)歸 ＞油當(dāng)歸。表明當(dāng)歸炒碳和土炒后增強(qiáng)了對(duì) H2O2誘導(dǎo)的紅細(xì)胞膜脂質(zhì)過氧化的抑制能力,而經(jīng)酒炒和油炒后抗紅細(xì)胞膜脂質(zhì)過氧化的能力降低。在此試驗(yàn)條件下L-抗壞血酸在 4～10 mg/mL劑量范圍內(nèi)能有效抑制 H2O2誘導(dǎo)的紅細(xì)胞膜脂質(zhì)過氧化作用,I C50為 6.52 mg/mL(圖 1)。

表 2 當(dāng)歸及其炮制品水提物對(duì) H2O2誘導(dǎo)的紅細(xì)胞膜脂質(zhì)過氧化的抑制作用Table 2 Inhibitory effects ofwater extracts from processed products of Chinese angelica on erythrocytic membrane anti-lipid peroxidation induced by H2O2in vitro(x ±s)

注:1.a,b……表示同一炮制品不同濃度之間比較,不同字母表示差異顯著(P＜0.05),相同字母,表示差異不顯著(P＞0.05)。Notes:1.a,b… represents the Comparison between different Concentrations of same processed product,and difference letter has significant difference (P＜0.05),the same letter no significant difference(P＞0.05).

3.3 當(dāng)歸及其炮制品水提物對(duì) H2O2誘導(dǎo)的紅細(xì)胞溶血的抑制作用

從表 3可以看出,生當(dāng)歸、油當(dāng)歸、酒當(dāng)歸、土當(dāng)歸和當(dāng)歸碳對(duì) H2O2誘導(dǎo)的紅細(xì)胞溶血具有一定抑制作用,同一炮制品在 12.5～200 mg/mL的劑量范圍內(nèi),抑制率隨著藥物濃度的增高而呈現(xiàn)出不同的增高趨勢,其中生當(dāng)歸和油當(dāng)歸各濃度之間抑制率具有顯著差異性 (P＜0.05),酒當(dāng)歸 25 mg/mL與50 mg/mL之間抑制率差異不顯著 (P＞0.05),其余濃度之間差異顯著 (P＜0.05),土當(dāng)歸 12.5 mg/mL與 50 mg/mL之間差異不顯著 (P＞0.05),其余濃度之間差異顯著 (P＜0.05),當(dāng)歸碳表 50 mg/mL與100 mg/mL之間抑制率差異不顯著 (P＞0.05),其余濃度之間差異顯著 (P＜0.05)。擬合曲線,計(jì)算回歸方程,生當(dāng)歸:y=1.261x-0.004x2-12.349,R2=0.988;油當(dāng)歸:y= e4.77-31.466/x,R2=0.998;酒當(dāng)歸:y=e4.452-7.828/x,R2=0.966;土當(dāng)歸:y=12.786+ 1.038x-0.003x2,R2=0.983;當(dāng) 歸碳:y= e4.658-18.207/x,R2=0.969。不同炮制品對(duì) H2O2誘導(dǎo)的紅細(xì)胞溶血的 IC50由小到大依次為酒當(dāng)歸、當(dāng)歸碳、土當(dāng)歸、油當(dāng)歸和生當(dāng)歸 (圖 1),即抑制紅細(xì)胞溶血的能力酒當(dāng)歸 ＞當(dāng)歸碳 ＞土當(dāng)歸 ＞油當(dāng)歸 ＞生當(dāng)歸。表明當(dāng)歸經(jīng)炮制后對(duì) H2O2誘導(dǎo)的紅細(xì)胞溶血的抑制能力都有所增強(qiáng)。在此試驗(yàn)條件下L-抗壞血酸在 4～10 mg/mL劑量范圍能有效抑制H2O2誘導(dǎo)的紅細(xì)胞溶血作用,I C50為 6.89 mg/mL(圖 1)。

表 3 當(dāng)歸炮制品水提物對(duì) H2O2誘導(dǎo)的紅細(xì)胞溶血的抑制作用Table 3 Inhibitory effects ofwater extracts from processed products of Chinese angelica on erythrocyte hemolysis induced by H2O2in vitro(x ±s)

4 討論

氧自由基及其介導(dǎo)的脂質(zhì)過氧化反應(yīng)參與了許多疾病的發(fā)生與發(fā)展,如動(dòng)脈硬化癥、高血壓、冠心病、骨關(guān)節(jié)炎、白內(nèi)障以及帕金森氏病等?，F(xiàn)代研究表明,當(dāng)歸能有效地清除超氧自由基,減少脂質(zhì)過氧化反應(yīng)等。但對(duì)當(dāng)歸及其炮制品體外抗脂質(zhì)過氧化的研究較少,僅見吳慧平等報(bào)道了當(dāng)歸炭、焦當(dāng)歸、酒當(dāng)歸、生當(dāng)歸和炒當(dāng)歸水煎液對(duì) FRGS誘導(dǎo)肝組織過氧化脂質(zhì)的抑制作用[9]。因此,選擇臨床常用的當(dāng)歸炮制品種以及多種指標(biāo)評(píng)價(jià)當(dāng)歸不同炮制品體外抗脂質(zhì)過氧化作用,可為當(dāng)歸臨床用藥和炮制理論提供更加科學(xué)合理的理論依據(jù)。

體外實(shí)驗(yàn)表明,生當(dāng)歸及其炮制品水提物對(duì)小鼠肝組織自發(fā)性過氧化、H2O2誘導(dǎo)的紅細(xì)胞膜脂質(zhì)過氧化和紅細(xì)胞溶血作用均有一定的抑制作用,其抑制作用隨著藥物濃度的升高逐漸升高,呈現(xiàn)良好的劑量依賴關(guān)系。但當(dāng)歸及其炮制品抑制脂質(zhì)過氧化的能力因選擇的評(píng)價(jià)方法不同而具有一定的差別,其抑制肝組織自發(fā)性過氧化能力為當(dāng)歸碳 ＞酒當(dāng)歸 ＞生當(dāng)歸 ＞油當(dāng)歸 ＞土當(dāng)歸,這與吳慧平等報(bào)道當(dāng)歸碳 ＞酒當(dāng)歸 ＞生當(dāng)歸一致[9];抑制 H2O2誘導(dǎo)的紅細(xì)胞膜過氧化的能力為當(dāng)歸碳 ＞土當(dāng)歸 ＞生當(dāng)歸 ＞酒當(dāng)歸 ＞油當(dāng)歸,抑制 H2O2誘導(dǎo)紅細(xì)胞溶血的能力為酒當(dāng)歸 ＞當(dāng)歸碳 ＞土當(dāng)歸 ＞油當(dāng)歸 ＞生當(dāng)歸。

圖 1 當(dāng)歸炮制品水提液體外抗脂質(zhì)過氧化 I C50Fig.1 IC50ofwater extracts from processed productsof Chinese angelica on anti-lipid peroxidation in vitro

據(jù)文獻(xiàn)報(bào)道,當(dāng)歸水溶性成分阿魏酸和多糖都具有一定的抗氧化作用,如吳建農(nóng)等報(bào)道阿魏酸不僅能對(duì)抗氧自由基,使超氧自由基、羥自由基和過氧化氫等氧自由基生成減少,而且還能與膜磷脂酰乙醇胺結(jié)合,使膜脂質(zhì)不受氧自由基的侵襲,從而發(fā)揮抗脂質(zhì)過氧化作用[10];李貴榮等報(bào)道,當(dāng)歸多糖能夠有效的清除氧自由基和羥自由基,且純化后的當(dāng)歸多糖對(duì)氧自由基和羥自由基的清除作用均小于其粗品多糖[11],凌小曼等還發(fā)現(xiàn),當(dāng)歸多糖能升高血瘀動(dòng)物心、腦、腎、胰四臟器超氧化物歧化酶 (SOD)活性,降低心、腦、腎、胰四臟器丙二醛 (MDA)含量,具有一定的抗氧化能力[12]。另據(jù)報(bào)道,生當(dāng)歸與炮制品之間阿魏酸含量有一定的差異,并且隨炮制溫度的升高,阿魏酸含量降低,以當(dāng)歸炭最為明顯[13]。劉漢珍等測定了當(dāng)歸及其炮制品中的多糖含量,以酒炙品中含量最高,當(dāng)歸炭中含量最低[14],即當(dāng)歸經(jīng)炒碳后阿魏酸和多糖含量均低于生當(dāng)歸,但本實(shí)驗(yàn)結(jié)果表明當(dāng)歸碳對(duì)肝組織自發(fā)性過氧化、H2O2誘導(dǎo)的紅細(xì)胞膜過氧化和 H2O2誘導(dǎo)紅細(xì)胞溶血的抑制能力均大于生當(dāng)歸。據(jù)此推測,當(dāng)歸不同炮制品抗氧化能力除與阿魏酸和多糖含量變化相關(guān)外,其抗氧化作用的成分可能還與其它未知的成分有密切關(guān)聯(lián),很有必要進(jìn)一步研究。

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Anti-lipid peroxida?tion of the Water Extracts from Processed Products of Chinese Angelicain vitro

WEI Yan-ming＊,GUO Yan-sheng,QU Ya-ling,HUA Yong-li,DENG Hong-juan
Gansu Agriculture University,College of Veterinary M edicine,Lanzhou 730070

To study the effect on Anti-lipid peroxidation of water extracts from processed products of Chinese angelica, mouse liver homogenates spontaneous lipid peroxidation,erythrocyticmembrane lipid peroxidation and erythrocyte hemolysis induced by H2O2in vitro were used to assess their capacity of Anti-lipid peroxidation.The results showed that the rate of inhibition on mouse liver homogenates spontaneous lipid peroxidation was in sequence of carbonized Angelica＞wine-broiled angelica＞raw Angelica＞oil-broiled Angelica＞Foci subsoil-broiled angelica;the rate of inhibition on erythrocytic membrane lipid peroxidation induced by H2O2was in sequence of carbonized Angelica ＞Foci subsoilbroiled angelica＞raw Angelica＞wine-broiled angelica＞oil-broiled Angelica;the rate of inhibition on erythrocyte hemolysis induced by H2O2was in sequence ofwine-broiled angelica＞carbonized Angelica＞Foci subsoil-broiled angelica＞oil-broiled Angelica＞raw Angelica.And inhibition effect showed a better dose-dependent relation.It was concluded that the water extracts from processed products of Chinese angelica showed certain inhibitory effect on anti-lipid peroxidation in vitro,and carbonized product had the best inhibition on liver homogenates spontaneous lipid peroxidation and erythrocytic membrane lipid peroxidation induced byH2O2,butwine-broiled angelica showed the best inhibitory effecton erythrocyte hemolysis induced by H2O2.

Chinese angelica;processed products;water extracts;anti-lipid peroxidation

R285.5;Q593.1

A

1001-6880(2010)05-0878-06

2009-07-17 接受日期:2009-09-21

國家自然科學(xué)基金項(xiàng)目“當(dāng)歸不同炮制品清除自由基和抗脂質(zhì)過氧化的作用”(30671541)

＊通訊作者 Tel:86-931-7632210;E-mail:weiym@gsau.edu.cn