RGD Reference Report - Polydatin modulates inflammation by decreasing NF-kappaB activation and oxidative stress by increasing Gli1, Ptch1, SOD1 expression and ameliorates blood-brain barrier permeability for its neuroprotective effect in pMCAO rat brain.

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Polydatin modulates inflammation by decreasing NF-kappaB activation and oxidative stress by increasing Gli1, Ptch1, SOD1 expression and ameliorates blood-brain barrier permeability for its neuroprotective effect in pMCAO rat brain.
Authors:	Ji, H Zhang, X Du, Y Liu, H Li, S Li, L
Citation:	Ji H, etal., Brain Res Bull. 2012 Jan 4;87(1):50-9. doi: 10.1016/j.brainresbull.2011.09.021. Epub 2011 Oct 6.
RGD ID:	8657021
Pubmed:	PMID:22001340 (View Abstract at PubMed)
DOI:	DOI:10.1016/j.brainresbull.2011.09.021 (Journal Full-text)
Inflammation and oxidative stress play an important role in cerebral ischemic pathogenesis. Polydatin has been proved to elicit numerous biological effects through its anti-inflammatory and anti-oxidant properties. However, little is known regard to the mechanism of polydatin's neuroprotection in ischemic stroke. We therefore investigated the potential neuroprotective effects of polydatin and explored the underlying mechanisms. Male, Sprague-Dawley rats were subjected to permanent middle cerebral artery occlusion (pMCAO). Experiment 1 was used to evaluate the expression of glioma-associated oncogene homolog1 (Gli1), Patched-1 (Ptch1) and Superoxide dismutase 1 (SOD1) after pMCAO, six time points were included. Experiment 2 was used to detect polydatin's neuroprotection after pMCAO. Neurological deficit, brain water content and infarct size were measured at 24h and 72 h after pMCAO. Immunohistochemistry, reverse transcription-polymerase chain reaction (RT-PCR), Western Blotting, activity assay and confocal microscope were used to analyse the expression of Gli1, Ptch1, SOD1 and nuclear factor-kappa B (NF-kappaB). Experiment 3 was used to detect polydatin's influence on blood-brain barrier (BBB). Compared with Sham group, the expression of Gli1, Ptch1 and SOD1 were up-regulated shortly after pMCAO (P<0.05). Compared with Vehicle group, high dose of polydatin (50mg/kg) up-regulated Gli1, Ptch1, SOD1 and down-regulated NF-kappaB, and reduced infarct volume, brain water content and behavioral deficits (P<0.05). Meanwhile, BBB permeability was also ameliorated. The results indicated that polydatin protected the brain from damage caused by pMCAO, and this effect may be through up-regulating the expression of Gli1, Ptch1 and SOD1 and down-regulating the expression of NF-kappaB, and ameliorating BBB permeability.

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Object Symbol	Species	Term	Qualifier	Evidence	With	Notes	Source	Original Reference(s)
SOD1	Human	middle cerebral artery infarction	treatment	ISO	Sod1 (Rattus norvegicus)		RGD
Sod1	Rat	middle cerebral artery infarction	treatment	IDA			RGD
Sod1	Mouse	middle cerebral artery infarction	treatment	ISO	Sod1 (Rattus norvegicus)		RGD

Objects Annotated

Genes (Rattus norvegicus)

Sod1 (superoxide dismutase 1)

Genes (Mus musculus)

Sod1 (superoxide dismutase 1, soluble)

Genes (Homo sapiens)

SOD1 (superoxide dismutase 1)

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Polydatin modulates inflammation by decreasing NF-kappaB activation and oxidative stress by increasing Gli1, Ptch1, SOD1 expression and ameliorates blood-brain barrier permeability for its neuroprotective effect in pMCAO rat brain.