Purpose The purpose of this study was to investigate the effect of dexmedetomidine (DEX) on hypotension-induced neuronal damage in a chronic cerebral hypoperfusion (CCH) model of rats, an established model of cerebral white matter lesions (WML) in humans, which is prevalent in the elderly and closely related to cognitive decline. Methods The CCH model rats were randomly assigned to one of four groups: normotension + no DEX (NN) group (n = 6), normotension + DEX (ND) group (n = 6), hypotension + no DEX (HN) group (n = 6), or hypotension + DEX (HD) group (n = 6). Under isoflurane anesthesia, mean arterial blood pressure was maintained at or above 80 mmHg (normotension) or below 60 mmHg (hypotension) for a duration of two hours. The DEX groups received 50 μg of DEX intraperitoneally. Two weeks later, the Y-maze test and, after preparing brain slices, immunohistochemical staining were performed using antibodies against neuronal nuclei (NeuN), microtubule-associated protein 2 (MAP2), glial fibrillary acidic protein (GFAP), and Ionized calcium-binding adapter molecule 1 (Iba1). Results Behavioral observations showed no significant differences among the groups. Significant reductions of both NeuN-positive cells and the MAP2-positive area were found in the hippocampal CA1 in the HN group compared with NN and ND groups, but not in the HD group. GFAP and Iba-1-positive areas were significantly increased in the HN group, but not in the HD group. Conclusion DEX significantly ameliorated hypotension-induced neuronal damage and both astroglial and microglial activation in the CA1 region of CCH rats.

UNASSIGNED: Low-density polyethylene microplastics are ingested into the bloodstream and distributed to all the organ tissue, including the hippocampus, causing toxic effects. This research aimed to elucidate the responses of hippocampal neurons to microplastic in the blood based on the expressions of superoxide dismutase (SOD), catalase (CAT) enzymes, malondialdehyde (MDA), 8-oxo-7,8-dihydro-2-deoxyguanosine (8-OHdG) in hippocampal neurons, and blood serum amyloid beta 1-42 (Aβ42) levels using SMART PLS pathway analysis.
UNASSIGNED: This was a pure experimental research on Wistar rats with a post-test control group design. Five experimental groups (X1, X2, X3, X4, X5) were given 0.0375 mg, 0.075 mg, 0.15 mg, 0.3 mg, and 0.6 mg of low-density polyethylene microplastics mixed in 2cc distilled water, respectively. Furthermore, except for control (C), the groups received microplastics an oral probe for 90 days.
UNASSIGNED: The molecular response of hippocampal neurons of Wistar rats to microplastics in the blood significantly decreased SOD enzyme expression, while CAT enzyme was unaffected. It considerably increased neuronal membrane damage (expression of MDA), increased considerably neuronal deoxyribonucleic acid damage (expression of 8-OHdG), and decreased blood serum Aβ42 levels (pathway analysis, all t-value >1.96).
UNASSIGNED: The pathway analysis showed that hippocampal neurons were significantly affected by microplastic particles in the blood.