Abstract

 
 
 
 Purpose: To study the effect minocycline on learning and memory functions in ischemic stroke rats, and the underlying mechanism.
 Methods: 60 adult male SD rats were randomly divided into control group, ischemic brain damage (6 and 24 h MACO) groups; and 6 and 24 h minocycline groups, with 12 rats in each group. The volume of cerebral infarction, neuronal cell apoptosis, NF-κB protein expression, learning and memory ability, and the number of Iba-1+CD206-positive cells, and CD206/CD68 mRNA expressions in sham group, 6 h MACO group and 6 h minocycline group were determined and compared.
 Results: The number of iba-1 +CD206-positive cells, expression level of CD206 mRNA, frequency of platform crossing, and percentage of third quadrant route in 6 h minocycline group were significantly higher than the corresponding values in 6 h MACO group. However, the cerebral infarction volume, number of Nini-positive cells, and the NF- B protein expression levels were markedly reduced, relative to corresponding values in 6 h MACO rats. The number of iba-1+CD206-positive cells was significantly lower in 6 h MACO rats than in sham rats, while the expression level of CD68 mRNA was significantly higher (p < 0.05). The number of TUNEL-positive cells in 6 and 24 h minocycline groups were markedly lower than that in 6 h MACO group (p < 0.05).
 Conclusion: Minocycline improves learning and memory of ischemic stroke rats by relieving the neuroinflammation induced by cerebral ischemia and cell apoptosis. Thus, the compound can be further developed for management learning and memory deficits in stroke patients.
 
 
 
Highlights
Cerebrovascular disease is one of the three major fatal diseases of human beings, and the treatment time window is extremely short
Impairment of cerebral blood supply leads to ischemia and hypoxia, necrosis and
Other reports have shown that minocycline effectively reduces neuronal apoptosis induced by middle cerebral artery occlusion and ischemic brain injury in rats, but its therapeutic target and related molecular mechanism have not been elucidated [7]
Summary
Cerebrovascular disease is one of the three major fatal diseases of human beings, and the treatment time window is extremely short. Elucidation of the pathological mechanism of ischemic stroke is of great significance for evolving new treatment methods and intervention targets for the disease. The purpose of this study was to investigate the effect of minocycline on learning and memory function in ischemic stroke rats, and the mechanism involved. Cerebral infarction areas of the rats in each group with ischemic stroke were determined using TTC staining. Apoptosis in each group was determined using TUNEL staining and Nidner staining to detect apoptosis of nerve cells in rats with ischemic stroke. Real-time fluorescence quantitative PCR and immunoblotting were used to assay the mRNA and protein expressions of microglia-specific (M1 microglial CD206) and nuclear transcription factor-κB (NF-κB) in brain tissues of sham group and 6h minocycline. Values of p < 0.05 were regarded as indicating significant differences
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