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A high-fat diet rich in corn oil exaggerates the infarct size and memory impairment in rats with cerebral ischemia and is associated with suppressing osteopontin and Akt, and activating GS3Kβ, iNOS, and NF-κB.
Journal of Physiology and Biochemistry ( IF 3.7 ) Pub Date : 2020-06-02 , DOI: 10.1007/s13105-020-00744-2
Dalia G Mostafa 1, 2 , Huda H Satti 3, 4 , Eman F Khaleel 1, 5 , Rehab M Badi 1, 6
Affiliation  

The increase in osteopontin (OPN) levels after stroke induces neural protection by activating Akt signaling and inhibiting GS3Kβ, iNOS, and NF-κB. This study investigated the effect of a high-fat diet rich in corn oil (CO-HFD) on infarct size and memory function in rats after induction of cerebral ischemia in rats and investigated its effect on the expression of OPN/Akt/iNOS/NF-κB signaling pathways. Rats were initially fed a standard diet (STD, 3.82 kcal/g; 9.4%, from fat) or a CO-HFD (5.4 kcal/g, 40% from fat) for 12 weeks. Then, both groups were further subdivided into either sham group or group exposed to cerebral ischemia by the middle cerebral artery occlusion (MCAO) protocol. Compared with sham-operated rats fed STD diet, neurological scores and both short- and long-term memory functions were significantly impaired in sham-operated CO-HFD-fed rats. In addition, brains collected from CO-HFD-fed rats showed lower protein levels of OPN, p-Akt (Thr308), p-GS3Kβ (Ser9), and Bcl-2 and had higher protein levels of iNOS, cleaved caspase-3, nuclear NF-κB p65, and cytoplasmic cytochrome C. However, once exposed to MCAO surgery, similar but more profound alterations of all these biochemical parameters with more severe impairment in short- and long-term memory functions and larger infarct size were noticed in the brains of CO-HFD-fed rats as compared with STD-fed rats exposed to MCAO. In conclusion, chronic consumption of CO-HFD induces memory impairments and worsens memory function recovery and infarct size after cerebral ischemia in rats by reducing levels of OPN, inhibiting the activation of Akt and activating iNOS and NF-κB.

中文翻译:

富含玉米油的高脂饮食会加剧脑缺血大鼠的梗死面积和记忆障碍,并与抑制骨桥蛋白和Akt以及激活GS3Kβ,iNOS和NF-κB有关。

中风后骨桥蛋白(OPN)水平的升高通过激活Akt信号传导并抑制GS3Kβ,iNOS和NF-κB诱导神经保护。本研究探讨了富含玉米油的高脂饮食(CO-HFD)对大鼠脑缺血后脑梗死面积和记忆功能的影响,并研究了其对OPN ​​/ Akt / iNOS / NF表达的影响-κB信号通路。首先给大鼠喂食标准饮食(STD,3.82 kcal / g; 9.4%,来自脂肪)或CO-HFD(5.4 kcal / g,40%,脂肪),持续12周。然后,将两组进一步分为假组或通过大脑中动脉闭塞(MCAO)方案暴露于脑缺血的组。与接受STD饮食的假手术大鼠相比,假手术的CO-HFD喂养的大鼠的神经系统评分以及短期和长期记忆功能均明显受损。此外,从接受CO-HFD喂养的大鼠收集的大脑中,OPN,p-Akt(Thr308),p-GS3Kβ(Ser 9)和Bcl-2并具有较高的iNOS,caspase-3裂解,核NF-κBp65和细胞质细胞色素C的蛋白水平。但是,一旦进行了MCAO手术,相似但更多与暴露于MCAO的STD喂养的大鼠相比,CO-HFD喂养的大鼠的大脑中所有这些生化参数发生了深刻变化,短期和长期记忆功能受损更严重,梗塞面积更大。总之,长期服用CO-HFD会降低大鼠的OPN水平,抑制Akt的激活以及激活iNOS和NF-κB,从而导致脑缺血后记忆障碍,并使记忆功能恢复和梗死面积恶化。
更新日期:2020-06-02
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