Effects of Bushen-Yizhi formula on age-related inflammation and oxidative stress in senescence-accelerated mice

被引:14
作者
Hou, Xue-Qin [1 ]
Song, Hou-Pan [2 ]
Chen, Yun-Bo [3 ]
Cheng, Shu-Yi [3 ]
Fang, Shu-Huan [3 ]
Zhang, Ji-Guo [1 ]
Wang, Qi [3 ]
机构
[1] Taishan Med Coll, Inst Pharmacol, 619 Chang Cheng Rd, Tai An 271016, Shandong, Peoples R China
[2] Hunan Univ Chinese Med, Hunan Prov Key Lab Diagnost Chinese Med, Changsha 410208, Hunan, Peoples R China
[3] Guangzhou Univ Chinese Med, Inst Clin Pharmacol, Design Measurement & Evaluat Clin Res Ctr, 12 Airport Rd, Guangzhou 510405, Guangdong, Peoples R China
基金
中国国家自然科学基金;
关键词
Bushen-Yizhi formula; aging; cognitive impairment; inflammation; oxidative stress; neuronal apoptosis; MILD COGNITIVE IMPAIRMENT; ALZHEIMERS-DISEASE; MOUSE MODEL; CYCLOOXYGENASE-2; EXPRESSION; PARKINSONS-DISEASE; MEMORY IMPAIRMENT; GAMMA AGONISTS; NITRIC-OXIDE; SAMP8; MICE; DEMENTIA;
D O I
10.3892/mmr.2018.8736
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The present study aimed to investigate the possible effects and underlying molecular mechanism of Bushen-Yizhi formula (BSYZ), a traditional Chinese medicine, on age-related degeneration of brain physiology in senescence-accelerated mouse prone 8 (SAMP8) mice. SAMP8 mice (age, 6 months) were administered BSYZ (1.46, 2.92 and 5.84 g/kg/day) for 30 days. Morris water maze and step-down tests demonstrated that BSYZ significantly improved memory impairments in SAMP8 mice. In addition, BSYZ significantly enhanced the expression levels of peroxisome proliferator-activated receptor-gamma and B-cell lymphoma extra-large, and downregulated the expression levels of inflammatory mediators, glial fibrillary acidic protein, cyclooxygenase-2, nuclear factor-kappa B and interleukin-1 beta in the brain compared with untreated SAMP8 mice. Furthermore, BSYZ reversed disordered superoxide dismutase activity, malondialdehyde content and glutathione peroxidase activity, and ameliorated apoptosis and histological alterations. The present study indicated that BSYZ may attenuate cognitive impairment in SAMP8 mice, and modulate inflammation, oxidative stress and neuronal apoptosis. These results suggested that BSYZ may have the potential to be further developed into a therapeutic agent for protection against age-related neurodegenerative diseases.
引用
收藏
页码:6947 / 6960
页数:14
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