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姜酮酸在大鼠阿尔茨海默病实验模型中的神经保护作用。

Neuroprotective effects of carnosic Acid in an experimental model of Alzheimer's disease in rats.

机构信息

1. Cellular and Molecular Research Center, Tehran University of Medical Sciences (Hemmat Pardis), Tehran, Iran.

出版信息

Cell J. 2011 Spring;13(1):39-44. Epub 2011 Apr 21.

Abstract

OBJECTIVE

Alzheimer's disease is the most common type of neurodegenerative disorder. It has been suggested that oxidative stress can be one of the pathological mechanisms of this disease. Carnosic acid (CA) is an effective antioxidant substance and recent studies have shown that its electrophilic compounds play a role in reversing oxidative stress. Thus we tried to find out whether CA administration protects hippocampal neurons, preventing neurodegeneration in rats.

MATERIALS AND METHODS

ANIMALS WERE DIVIDED INTO FOUR GROUPS: Sham-operated (sham), CA-pretreated sham-operated (sham+CA), untreated lesion (lesion) and CA-pretreated lesion (lesion+CA). Animals in all groups received vehicle or vehicle plus CA (CA: 10mg/ kg) intra-peritoneally one hour before surgery, again the same solution injected 3-4 hours after surgery (CA: 3 mg/kg) and repeated each afternoon for 12 days. A lesion was made by bilateral intra-hippocampal injection of 4 µl of beta amyloid protein (1.5 nmol/µl) or vehicle in each side. 14 days after surgery, the brains were extracted for histochemical studies. Data was expressed as mean ± SEM and analyzed using SPSS statistical software.

RESULTS

Results showed that pretreatment with carnosic acid can reduce cellular death in the cornu ammonis 1 (CA1) region of the hippocampus in the lesion+CA group, as compared with the lesion group.

CONCLUSION

Carnosic acid may be useful in protecting against beta amyloid-induced neurodegeneration in the hippocampus.

摘要

目的

阿尔茨海默病是最常见的神经退行性疾病之一。有研究表明,氧化应激可能是这种疾病的病理机制之一。迷迭香酸(CA)是一种有效的抗氧化物质,最近的研究表明,其亲电化合物在逆转氧化应激方面发挥作用。因此,我们试图找出 CA 给药是否可以保护海马神经元,防止大鼠发生神经退行性变。

材料和方法

动物分为四组:假手术组(sham)、CA 预处理假手术组(sham+CA)、未治疗损伤组(lesion)和 CA 预处理损伤组(lesion+CA)。所有组的动物均在手术前 1 小时接受载体或载体加 CA(CA:10mg/kg)腹腔内注射,手术后 3-4 小时再次注射相同溶液(CA:3mg/kg),并在接下来的 12 天的每天下午重复注射。通过双侧海马内注射 4µlβ淀粉样蛋白(1.5nmol/µl)或载体在每侧制造损伤。手术后 14 天,提取大脑进行组织化学研究。数据表示为平均值±SEM,并使用 SPSS 统计软件进行分析。

结果

结果表明,与损伤组相比,损伤+CA 组中 CA 的预处理可以减少海马 CA1 区的细胞死亡。

结论

迷迭香酸可能有助于防止β淀粉样蛋白诱导的海马神经退行性变。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4191/3652539/de4f67653511/Cell-J-13-39-g01.jpg

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