Journal
PHARMACOLOGICAL REPORTS
Volume 63, Issue 2, Pages 381-391Publisher
POLISH ACAD SCIENCES INST PHARMACOLOGY
DOI: 10.1016/S1734-1140(11)70504-7
Keywords
diabetes mellitus; minocycline; beta-amyloid protein; NF-kappa B
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Funding
- Clinical Research Institute, Guangdong Medical College
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Activation of the NF-kappa B pathway plays an important role in the pathophysiology of Alzheimer's disease (AD), and blocking NF-kappa B pathway activation has been shown to attenuate cognitive impairment. Diabetic metabolic disorder contributes to beta-amyloid protein (A beta) generation. The goal of this study was to determine the effect of minocycline on A beta generation and the NF-kappa B pathway in the hippocampus of diabetic rats and to elucidate the neuroprotective mechanisms of minocycline for the treatment of diabetic metabolic disorder. The diabetic rat model was established using a high-fat diet and an intraperitoneal injection of streptozocin (STZ). Behavioral tests showed that the capacity of learning and memory was significantly lower in diabetic rats. The levels of NF-kappa B, COX-2, iNOS, IL-1 beta and TNF-alpha after the STZ injection were significantly increased in the hippocampus. Significant increases in A beta, BACE1, NF-kappa B, COX-2, iNOS, IL-1 beta and TNF-alpha were found in diabetic rats. The levels of A beta, NF-kappa B, COX-2, iNOS, IL-1 beta and TNF-alpha were significantly decreased after minocycline administration; however, minocycline had no effect on BACE1 expression. In sum, diabetes contributes to the activation of the NF-kappa B pathway and upregulates BACE I and A beta. Minocycline downregulates A beta in the hippocampus by inhibiting NF-kappa B pathway activation.
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