Sulfatides were noted to protect hippocampal neurons from oxidative damage through the clearance of β-amyloid protein, with apolipoprotein E transporting and low-density lipoprotein receptor binding. Hippocampal formation and cerebral cortex also exhibited pathological changes, characterized by neurofibrillary tangle and reduced Nissl bodies. Long-term high-fat diet (HFD) in rats triggered cerebral oxidative stress, reflected by reactive oxygen species accumulation and antioxidant decline in peripheral and cerebral tissues, together with hippocampal lipid disturbance, particularly for triglyceride accumulation and sulfatide deficiency.
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