1 Department of Neurology, Lu’an People’s Hospital, the Fifth Clinical College, Anhui Medical University, Lu’an 237005, China 
2 Department of Neurology, the First Affiliated Hospital, Chongqing Medical University, Chongqing Key Laboratory of Neurology, Chongqing 400016, China

Abstract 

Objective 
To study the neuroprotective mechanism of minocycline against vascular cognitive impairment after cerebral ischemia. 
Methods 
The rat model with vascular cognitive impairment was established by permanent bilateral common carotid artery occlusion (BCCAO). The observing time-points were determined at 4, 8 and 16 weeks after BCCAO. Animals were randomly divided into sham-operated group (n = 6), model group (subdivided into 3 groups: 4 weeks after BCCAO, n = 6; 8 weeks after BCCAO, n = 6; and 16 weeks after BCCAO, n = 6), and minocycline group (subdivided into 3 groups: 4 weeks after BCCAO, n = 6; 8 weeks after BCCAO, n = 6; and 16 weeks after BCCAO, n = 6). Minocycline was administered by douche via stomach after BCCAO until sacrifice. Glial fibrillary acidic protein (GFAP) was examined by Western blotting and immunohistochemistry. Levels of cyclooxygenase-2 (COX-2) and nuclear factor-kappaB (NF-κB) were measured by immunohistochemistry. IL-1β and TNF-α levels were tested with ELISA method. 
Results 
Levels of GFAP, COX-2, NF-κB, IL-1β and TNF-α were all up-regulated after permanent BCCAO, which could be significantly inhibited by minocycline. 
Conclusion 
Minocycline could ameliorate the inflammation and oxidative stress in the hippocampus of the vascular cognitive impairment rat model.

Keywords

vascular cognitive impairment; minocycline; inflammation; astrocyte

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