Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04179 (MnSOD)
 2,777 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spatial learning ability was quantitated in young and aged Long-Evans rats, and molecular markers were assessed in the striatum and hippocampal formation using immunocytochemical, immunoblotting, and in situ hybridization histochemical procedures. The mRNA for beta-amyloid precursor protein (beta APP), most likely the transcript encoding the 695-amino acid form of this protein, was elevated in pyramidal and granule cells in the hippocampus of aged rats exhibiting poorer spatial learning. In immunoblots of hippocampal protein extracts, however, the level of beta APP-like immunoreactivity was depressed in the more impaired subjects. Similarly, the level in hippocampus of the mRNA for manganese-dependent superoxide dismutase (Mn-SOD), a marker of oxidative stress, was positively correlated with the degree of behavioral impairment, but immunoblotting revealed that Mn-SOD protein was depressed in the aged hippocampus compared with young. The mRNAs for the neuronal form of nitric oxide synthase and for the astrocyte marker glial fibrillary acidic protein (GFAP) were elevated in the hippocampus in correlation with the extent of learning impairment. In the striatum, the levels of mRNA and protein for several candidate genes, including GFAP, were elevated in parallel with the learning index, but these were age effects. Several hippocampal proteins were unchanged (GFAP) or depressed (beta APP and Mn-SOD) in level, despite elevations in corresponding mRNAs. In the aged cohort, hippocampal GFAP mRNA, Mn-SOD mRNA, and beta APP emerged as predictors of behavioral impairment, suggesting the involvement of these hippocampal systems in age-related cognitive impairment.
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PMID:Molecular indices of neuronal and glial plasticity in the hippocampal formation in a rodent model of age-induced spatial learning impairment. 862 77

We studied the alterations of MDA and three forms of SOD activities such as T-SOD, CuZn-SOD, and Mn-SOD in rat cerebral tissues injected by bordetella pertussis (BP) to elucidate protective mechanism of SOD against the infectious brain injury. The results were that water content(WC), Evans blue content(EB), MDA, and Mn-SOD activities in 4 h and 24 h BP-treated groups increased and T-SOD and CuZn-SOD decreased compared to corresponding normal saline(NS)-treated groups, respectively(P < 0.01); MDA increased and had a positive correlation with WC and EB in 4 h BP treated group (r = 0.9650, r = 0.9441, P < 0.01, P < 0.01, respectively); Mn-SOD activities were elevated and had a negative correlation with WC, EB, and MDA (r = -0.8650, r = -0.9021, r = -0.9346, P < 0.01, P < 0.01, P < 0.01, respectively) in 24 h BP-treated group. The results suggest that the increase of component Mn-SOD activities may play an important role in vivo endogenous protective mechanism against delayed infectious brain injury.
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PMID:[Endogenous protective effects of superoxide dismutases on infectious brain injury in rats]. 1208 Jun 38

The abundance of cellular superoxide dismutase (Mn-SOD) was examined immunocytochemically in different regions of the brain of Long-Evans Cinnamon (LEC) rats at 4 and 50 weeks of age. When all animals develop chronic hepatitis, the substantia nigra and striatum showed a marked increase in Mn-SOD immunoreactivity versus Long-Evans agouti (LEA) rats of the same age. Mn-SOD was localized predominantly in dopaminergic neurons. The elevation of Mn-SOD level in the dopaminergic neurons of LEC rats may reflect the oxidative stress caused by copper accumulation in this brain area. Our data suggest that LEC rats may contribute to the mechanistic study of neurological manifestations in nigro-striatal dopaminergic system of Wilson's disease.
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PMID:Enhanced Mn-SOD immunoreactivity in the dopaminergic neurons of long-evans cinnamon rats. 1607 18

Carnosic acid (CA) has been reported to exhibit a variety of bioactivities including antioxidation, neuroprotection, and anti-inflammation; however, the impact of CA on subarachnoid hemorrhage (SAH) has never been elucidated. The current study was undertaken to explore the role of CA in early brain injury (EBI) secondary to SAH and the underlying mechanisms. Adult male Sprague-Dawley rats were perforated to mimic a clinical aneurysm with SAH. CA or vehicle was administered intravenously immediately after the SAH occurred. Mortality, SAH grade, neurologic function scores, brain water content, Evans blue extravasation, and the levels of reactive oxygen species (ROS) levels in the ipsilateral cortex were determined 24 h after the SAH occurred. Western blot, immunofluorescence, Fluoro-Jade C (FJC) and TUNEL staining were also performed. Our results showed that CA decreased ROS levels, alleviated brain edema and blood-brain barrier permeability, reduced neuronal cell death, and promoted neurologic function improvement. To probe into the potential mechanisms. We showed that CA increased SIRT1, MnSOD, and Bcl-2 expression, as well as decreased p66shc, Bax, and cleaved caspase-3 expression. Interestingly, sirtinol, a selective inhibitor of SIRT1, abolished the anti-apoptotic effects of CA. Taken together, these data revealed that CA has a neuroprotective role in EBI secondary to SAH. The potential mechanism may involve suppression of neuronal apoptosis through the SIRT1/p66shc signaling pathway. CA may provide a promising therapeutic regimen for management of SAH.
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PMID:Carnosic Acid Mitigates Early Brain Injury After Subarachnoid Hemorrhage: Possible Involvement of the SIRT1/p66shc Signaling Pathway. 3089 Sep 4