详细信息

ICARIIN PROTECTS NEURONS FROM ISCI-TENEC BRAIN INJURY BY UP-REGULATING SIRTLMHDI AT HD PGC-1A EXPRESSION  ( SCI-EXPANDED收录)  

文献类型:期刊文献

英文题名:ICARIIN PROTECTS NEURONS FROM ISCI-TENEC BRAIN INJURY BY UP-REGULATING SIRTLMHDI AT HD PGC-1A EXPRESSION

作者:Zhou, Qiang[1];Xiao, Yuxia[2];Wen, Xin[3];Li, Shurui[4];Feng, Xilian[3];Wang, Qiong[5];Zhang, Jingjing[6];Liu, Naijia[3];Zhao, Feng[5]

第一作者:周强

通信作者:Zhao, F[1]

机构:[1]Gansu Univ Tradit Chinese Med, Integrated Chinese Med Treatment Area, Affiliated Hosp, Lanzhou 730020, Gansu Province, Peoples R China;[2]Gansu Univ Tradit Chinese Med, Changjiaxiang TCM Clin, Affiliated Hosp, Lanzhou 730000, Gansu Province, Peoples R China;[3]Gansu Univ Tradit Chinese Med, Dept Acupuncture & Moxibust, Affiliated Hosp, Lanzhou 730020, Gansu Province, Peoples R China;[4]Gansu Univ Tradit Chinese Med, Dept Disinfect, Affiliated Hosp, Lanzhou 730020, Gansu Province, Peoples R China;[5]Gansu Univ Tradit Chinese Med, Dept Neurol, Affiliated Hosp, Lanzhou 730020, Gansu Province, Peoples R China;[6]Gansu Univ Tradit Chinese Med, Dept Otolaryngol & Head Surg, Affiliated Hosp, Lanzhou 730020, Gansu Province, Peoples R China

第一机构:甘肃中医药大学第二附属医院

通信机构:[1]corresponding author), 732 Jiayuguan West Rd, Lanzhou City, Gansu Province, Peoples R China.

年份:2022

卷号:38

期号:6

起止页码:4089

外文期刊名:ACTA MEDICA MEDITERRANEA

收录:;WOS:【SCI-EXPANDED(收录号:WOS:000908447100058)】;

语种:英文

外文关键词:Icariin; Sirtl; PGC-l alpha; ischemic brain injury; neuron.

摘要:Objective: To analyze the protective effect of icariin on neurons from chernic brain injury by up -regulating the expression of PGC-1 a mediated by Sits]. Methods: The mouse middle cerebral artery ischemic model was made by the suture method, which was divided into sham operation group (only the common carotid artery was isolated without ligation), a model group, and low (50 mg/kg), medium (100 kg) and high (200 mg/kg) dose icariin groups. We observed the changes in the neurological function and the number of dopaminergic neurons in the substantia nigra of the mice in each group. Western blot was used to detect the PGC-la and Sirt1 proteins in the cerebral cortex of each group. Expression; Sirt1 inhibitor was used to treat cells and PGC-la plasmid transfection technology to detect the survival and apoptosis rate of dopaminergic neurons in the substantia nigra of the mouse brain. Western blot was used to detect the effect of Sirt1 inhibitor on the expression of PGC-la protein influences. Results: After treatment for 3 d and 7 d, the neurological scores of the mice is the low, medium, and high dose icariin groups were significantly lower than the model group, and the difference was statistically significant (P<0.05). Compared with the sham operation group, the number of dopaminergic neurons in the substantia nigra of mice in the model group was significantly reduced (P<0.05), and the number of dopcuninergic neurons in the substantia nigra of mice in the low, medium, and high -dose icariin groups was significantly more titan in the model group (P<0.05). The expression of PGC-la and Sirt 1 protein in the cortex of mice in the low, medium, and high close icariin groups was significantly higher than that in the model group (P<0.05). The Sinrt1 inhibitor group and PGC-1 alpha interference group significantly reduced icariin and increased the survival rate of dopaminergic neurons in the substantia nigra of mice (P<0.05). Also, the Sirt1 inhibitor group and PGC-1 alpha interference group significantly increased icariin and reduced the apoptosis rate of dopaminergic neurons in the substantia nigra of mice (P<0.05). Finally, the Sirt1 inhibitor group blocked the increase of PGC-la protein expression in the mouse cortex by icariin, compared with the control group, and the difference was statistically significant (P<0.05). Conclusion: Icariin has a protective effect on ischemic brain injury neurons, and the mechanism of action may be related to the up -regulation of Sirt1 -mediated PGC-1 alpha expression, suggesting that icariin may become a new type of ischemic brain injury protection agent.

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