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您的检索式：作者名="Ranjana Patnaik"
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| 1 | Resveratrol inhibits matrix metalloproteinases to attenuate neuronal damage in cerebral ischemia:a molecular docking study exploring possible neuroprotection显示文摘The main pathophysiology of cerebral ischemia is the structural alteration in the neurovascular unit, coinciding with neurovascular matrix degradation. Resveratrol has been reported to be one of the most potent chemopreventive agents that can inhibit cellular processes associated with ischemic stroke. Matrix metalloproteinases(MMPs) has been considered as a potential drug target for the treatment of cerebral ischemia. To explore this, we tried to investigate the interaction of resveratrol with MMPs through molecular docking studies. At 30 minutes before and 2 hours after cerebral ischemia/reperfusion induced by occlusion of the middle cerebral artery, 40 mg/kg resveratrol was intraperitoneally administered. After resveratrol administration, neurological function and brain edema were significantly alleviated, cerebral infarct volume was significantly reduced, and nitrite and malondialdehyde levels in the cortical and striatal regions were significantly decreased. The molecular docking study of resveratrol and MMPs revealed that resveratrol occupied the active site of MMP-2 and MMP-9. The binding energy of the complexes was –37.848672 k J/mol and –36.6345 k J/mol for MMP-2 and MMP-9, respectively. In case of MMP-2, Leu 164, Ala 165 and Thr 227 were engaged in H-Bonding with resveratrol and in case of MMP-9, H-bonding was found with Glu 402, Ala 417 and Arg 424 residues. These findings collectively reveal that resveratrol exhibits neuroprotective effects on cerebral ischemia through inhibiting MMP-2 and MMP-9 activity. | Anand Kumar Pandey Pallab Bhattacharya Swet Chand Shukla Sudip Paul Ranjana Patnaik | 2015 | Neural Regeneration Research2015，10，4： | 12 |
| 2 | Piroxicam-mediated modulatory action of 5-hydroxytryptamine serves as a “brake” on neuronal excitability in ischemic stroke显示文摘Our previous studies indicated an increase in extracellular γ-aminobutyric acid(GABA) in rodent's ischemic brain after Piroxicam administration, leading to alleviation of glutamate mediated excitotoxicity through activation of type A GABA receptor(GABAA). This study was to investigate if GABAA activation by Piroxicam affects extracellular 5-hydroxytryptamine or not. High performance liquid chromatography revealed that there was a significant decrease in extracellular 5-hydroxytryptamine release in ischemic cerebral cortex and striatum in Piroxicam pre-treated rat brains. This suggests a probable role of Piroxicam in reducing extracellular 5-hydroxytryptamine release in ischemic cerebral cortex and striatum possibly due to the GABAA activation by Piroxicam. | Pallab Bhattacharya Anand Kumar Pandey Sudip Paul Ranjana Patnaik | 2015 | Neural Regeneration Research2015，10，9： | 4 |
| 3 | A possible therapeutic potential of quercetin through inhibition of μ-calpain in hypoxia induced neuronal injury:a molecular dynamics simulation study显示文摘The neuroprotective property of quercetin is well reported against hypoxia and ischemia in past studies.This property of quercetin lies in its antioxidant property with blood-brain barrier permeability and anti-inflammatory capabilities.μ-Calpain,a calcium ion activated intracellular cysteine protease causes serious cellular insult,leading to cell death in various pathological conditions including hypoxia and ischemic stroke.Hence,it may be considered as a potential drug target for the treatment of hypoxia induced neuronal injury.As the inhibitory property of μ-calpain is yet to be explored in details,hence,in the present study,we investigated the interaction of quercetin with μ-calpain through a molecular dynamics simulation study as a tool through clarifying the molecular mechanism of such inhibition and determining the probable sites and modes of quercetin interaction with the μ-calpain catalytic domain.In addition,we also investigated the structure-activity relationship of quercetin with μ-calpain.Affinity binding of quercetin with μ-calpain had a value of –28.73 k J/mol and a Ki value of 35.87 μM that may be a probable reason to lead to altered functioning of μ-calpain.Hence,quercetin was found to be an inhibitor of μ-calpain which might have a possible therapeutic role in hypoxic injury. | Anand Kumar Pandey Swet Chand Shukla Pallab Bhattacharya Ranjana Patnaik | 2016 | Neural Regeneration Research2016，11，8： | 3 |
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