版權(quán)說(shuō)明:本文檔由用戶提供并上傳,收益歸屬內(nèi)容提供方,若內(nèi)容存在侵權(quán),請(qǐng)進(jìn)行舉報(bào)或認(rèn)領(lǐng)
文檔簡(jiǎn)介
1、AIM to investigate the effect of sweet-potato anthocyanins on oxidation conditions in aging mice and cytotoxicity of PC- 12 cells induced by Amyloid β protein (Aβ). METHODS we use the natural aging Wistar rats as experim
2、ental models. The animals were randomly divided into six groups, including normal young control group, aging model group, low concentration, middle concentration and high concentration sweet-potato anthocyanins groups an
3、d vitmin E as positive control group. We measured the total antioxidative capacity (T-AOC), activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-px), reactive oxygen species (ROS) and malondialdehyde (MD
4、A) of different organs from the animals. And we also established the cytotoxicity of PC-12 cell model induced by Aβ. By using cell culture, MTT assays, flow cytometry, we measured the cell viability, apoptosis, activity
5、of caspase-3, and mitochondria membrane potential, intracellular Ca2+ in PC12 cells. RESULTS sweet-potato anthocyanins can increase the activities of T-AOC, SOD and GSH-px and decrease the amount of ROS and MDA in severa
6、l organs from the animal in a dose-dependent manner (p<0.05, p<0.01). MTT assays showed that the PC-12 cell viability decreased under A β treatment. Sweet-potato anthocyanins can increase the PC-12 cell viability, stabil
7、ize the mitochondria membrane potential, and decrease the concentration of intracellular Ca2+ dose dependently (p<0.05, p<0.01). CONCLUSION sweet-potato anthocyanins modulate the oxidation condition of aging rats through
8、 its ability of compensating the decline in T-AOC and the activities of antioxidant enzymes and thereby inhibit the aging process. Also sweet-potato anthocyanins can protect the PC-12 cell from A β induced injury. Thus i
溫馨提示
- 1. 本站所有資源如無(wú)特殊說(shuō)明,都需要本地電腦安裝OFFICE2007和PDF閱讀器。圖紙軟件為CAD,CAXA,PROE,UG,SolidWorks等.壓縮文件請(qǐng)下載最新的WinRAR軟件解壓。
- 2. 本站的文檔不包含任何第三方提供的附件圖紙等,如果需要附件,請(qǐng)聯(lián)系上傳者。文件的所有權(quán)益歸上傳用戶所有。
- 3. 本站RAR壓縮包中若帶圖紙,網(wǎng)頁(yè)內(nèi)容里面會(huì)有圖紙預(yù)覽,若沒有圖紙預(yù)覽就沒有圖紙。
- 4. 未經(jīng)權(quán)益所有人同意不得將文件中的內(nèi)容挪作商業(yè)或盈利用途。
- 5. 眾賞文庫(kù)僅提供信息存儲(chǔ)空間,僅對(duì)用戶上傳內(nèi)容的表現(xiàn)方式做保護(hù)處理,對(duì)用戶上傳分享的文檔內(nèi)容本身不做任何修改或編輯,并不能對(duì)任何下載內(nèi)容負(fù)責(zé)。
- 6. 下載文件中如有侵權(quán)或不適當(dāng)內(nèi)容,請(qǐng)與我們聯(lián)系,我們立即糾正。
- 7. 本站不保證下載資源的準(zhǔn)確性、安全性和完整性, 同時(shí)也不承擔(dān)用戶因使用這些下載資源對(duì)自己和他人造成任何形式的傷害或損失。
最新文檔
- 鎘對(duì)大鼠大腦皮質(zhì)神經(jīng)細(xì)胞毒性損傷的機(jī)制.pdf
- 乙醛誘導(dǎo)的神經(jīng)細(xì)胞毒性機(jī)制及蝦青素的保護(hù)作用.pdf
- 白術(shù)多糖對(duì)衰老大鼠神經(jīng)細(xì)胞SODmRNA表達(dá)及DNA損傷影響的研究.pdf
- 墊料物質(zhì)的細(xì)胞毒性及其對(duì)大鼠肝臟細(xì)胞色素P450酶系誘導(dǎo)作用的研究.pdf
- 自噬在鎘致大鼠神經(jīng)細(xì)胞毒性中的作用及調(diào)控機(jī)制.pdf
- MANF對(duì)Aβ和tau蛋白過(guò)度磷酸化誘導(dǎo)的神經(jīng)細(xì)胞毒性的抑制作用.pdf
- DON對(duì)仔豬海馬神經(jīng)細(xì)胞的毒性作用研究.pdf
- 血管緊張素Ⅱ誘導(dǎo)神經(jīng)細(xì)胞衰老的作用及藥物干預(yù).pdf
- 青紫薯色素保護(hù)小鼠抗60Coγ-射線輻射所致氧化損傷的作用研究.pdf
- 魚藤酮對(duì)大鼠多巴胺神經(jīng)和PC12細(xì)胞毒性作用研究.pdf
- 尼古丁致大鼠睪丸間質(zhì)細(xì)胞毒性的體內(nèi)外研究.pdf
- 何首烏飲對(duì)自然衰老大鼠精子質(zhì)量的影響.pdf
- 淫羊藿總黃酮對(duì)喹啉酸誘導(dǎo)的人神經(jīng)母細(xì)胞瘤細(xì)胞毒性的保護(hù)作用.pdf
- 左旋多巴對(duì)帕金森病神經(jīng)細(xì)胞毒性作用及相關(guān)保護(hù)因素的研究.pdf
- 限制能量攝入對(duì)衰老大鼠抗氧化水平、IL-2、MAO、NO及肝細(xì)胞凋亡的影響.pdf
- 自然衰老大鼠糖耐量變化及其機(jī)理的研究.pdf
- 青紫薯色素對(duì)39;60coγ射線輻射小鼠胸腺淋巴細(xì)胞的保護(hù)作用及其機(jī)制研究
- 補(bǔ)氣活血法對(duì)衰老大鼠ALI的作用機(jī)理研究.pdf
- LeukameninE對(duì)原代培養(yǎng)大鼠腦星形神經(jīng)膠質(zhì)細(xì)胞毒性作用的研究.pdf
- 中樞神經(jīng)系統(tǒng)損傷后谷氨酸的神經(jīng)細(xì)胞毒性作用的機(jī)理研究.pdf
評(píng)論
0/150
提交評(píng)論