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SHAH, Fawad-Ali,GIM, Sang-Ah,KIM, Myeong-Ok,KOH, Phil-Ok The Japanese Society of Veterinary Science 2014 The Journal of veterinary medical science Vol.76 No.10
<P><B>ABSTRACT</B></P><P>Resveratrol has a neuroprotective effect against cerebral ischemia. The objective of this study was to identify proteins that are differentially expressed in the cerebral cortex of vehicle- and resveratrol-treated animals during ischemic injury. Focal cerebral ischemia was induced as middle cerebral artery occlusion (MCAO) in male rats. Rats were treated with vehicle or resveratrol before MCAO, and cerebral cortex was collected 24 hr after MCAO. Cerebral cortex proteins were identified by two-dimensional gel electrophoresis and mass spectrometry. Several proteins were identified as differentially expressed between vehicle- and resveratrol-treated animals. Among these proteins, expression of peroxiredoxin-5, isocitrate dehydrogenase [NAD<SUP>+</SUP>], apolipoprotein A-I and ubiquitin carboxy terminal hydrolase L1 was decreased in the vehicle-treated group, whereas resveratrol attenuated the injury-induced decrease in expression of these proteins. However, expression of collapsing response mediator protein 2 was increased in the vehicle-treated group, whereas resveratrol prevented the injury-induced increase in the expression of this protein. These findings suggest that resveratrol modulates the expression of various proteins that associated with oxidative stress and energy metabolism in focal cerebral ischemia.</P>
Shah, Fawad Ali,Zeb, Amir,Ali, Tahir,Muhammad, Tahir,Faheem, Muhammad,Alam, Sayed Ibrar,Saeed, Kamran,Koh, Phil-Ok,Lee, Keun Woo,Kim, Myeong Ok Frontiers Media S.A. 2018 Frontiers in neuroscience Vol.12 No.-
<P>Ischemic stroke is characterized by permanent or transient obstruction of blood flow, which initiates a cascading pathological process, starting from acute ATP loss to subsequent membrane depolarization, glutamate excitotoxicity, and calcium overload. Melatonin is a potent antioxidant that exerts protective effects in different experimental stroke models. In this study, melatonin effects were demonstrated by a proteomic and <I>in silico</I> approach. The proteomic study identified differentially expressed proteins by 2D gel electrophoresis in the striatum 24 h after middle cerebral artery occlusion. Proteomic analysis revealed several proteins with aberrant expression and was validated by western blot and immunofluorescence analysis. Homology modeling was performed to build 3D structures for γ-enolase, thioredoxin (TRX), and heat shock 60 (HSP60) by the template crystal structures using a protein data bank as a sequence database. The structure refinement of each model was achieved by energy minimization via molecular dynamic simulation, and the generated models were further assessed for stability by Procheck and ProSA. The models were processed for docking analysis using AutoDock Vina, and post-docking analysis was determined by discovery studio. The proteomic study showed decreased expression of γ-enolase, TRX, and protein phosphatase 2A subunit B and increased expression of collapsin response mediator protein 2 and HSP60 in the striatum after ischemic injury. Treatment with melatonin modulated the expression profiles of these proteins. This study demonstrated the neuroprotective role of melatonin in the ischemic striatum using a proteomic and <I>in silico</I> approach. Collectively, melatonin may act in a multimechanistic way by modulating the expression of several proteins in the ischemic striatum.</P>
박동주,강주빈,Fawad-Ali Shah,고필옥 한국실험동물학회 2019 Laboratory Animal Research Vol.35 No.3
Cerebral ischemia is a major cause of neurodegenerative disease. It induces neuronal vulnerability and susceptibility, and leads to neuronal cell death. Resveratrol is a polyphenolic compound that acts as an anti-oxidant. It exerts a neuroprotective effect against focal cerebral ischemic injury. Akt signaling pathway is accepted as a representative cell survival pathway, including proliferation, growth, and glycogen synthesis. This study investigated whether resveratrol regulates Akt/glycogen synthase kinase-3β (GSK-3β) pathway in a middle cerebral artery occlusion (MCAO)-induced ischemic brain injury. Adult male rats were intraperitoneally injected with vehicle or resveratrol (30 mg/kg) and cerebral cortices were isolated 24 h after MCAO. Neurological behavior test, corner test, brain edema measurment, and 2,3,5-triphenyltetrazolium chloride staining were performed to elucidate the neuroprotective effects of resveratrol. Phospho-Akt and phospho-GSK-3β expression levels were measured using Western blot analysis. MCAO injury led to severe neurobehavioral deficit, infraction, and histopathological changes in cerebral cortex. However, resveratrol treatment alleviated these changes caused by MCAO injury. Moreover, MCAO injury induced decreases in phospho-Akt and phospho-GSK-3β protein levels, whereas resveratrol attenuated these decreases. Phosphorylations of Akt and GSK-3β act as a critical role for the suppression of apoptotic cell death. Thus, our finding suggests that resveratrol attenuates neuronal cell death in MCAO-induced cerebral ischemia and Akt/GSK-3β signaling pathway contributes to the neuroprotective effect of resveratrol.
Rizvi, Syed Zaki Husain,Shah, Fawad Ali,Khan, Namrah,Muhammad, Iftikhar,Ali, Khan Hashim,Ansari, Muhammad Mohsin,Din, Fakhar ud,Qureshi, Omer Salman,Kim, Kyoung-Won,Choe, Yeong-Hwan,Kim, Jin-Ki,Zeb, A Elsevier 2019 International journal of pharmaceutics Vol.560 No.-
<P><B>Abstract</B></P> <P>The objective of current study was to develop solid lipid nanoparticles-loaded with simvastatin (SIM-SLNs) and investigate their <I>in vivo</I> anti-hyperlipidemic activity in poloxamer-induced hyperlipidemia model. Nano-template engineering technique was used to prepare SIM-SLNs with palmityl alcohol as lipid core and a mixture of Tween 40/Span 40/Myrj 52 to stabilize the core. The prepared SIM-SLNs were evaluated for physicochemical parameters including particle diameter, surface charge, morphology, incorporation efficiency, thermal behaviour and crystallinity. <I>In vitro</I> release profile of SIM-SLNs in simulated gastric and intestinal fluids was evaluated by using dialysis bag technique and anti-hyperlipidemic activity was assessed in hyperlipidemia rat model. SIM-SLNs revealed uniform particle size with spherical morphology, zeta potential of −24.9 mV and high incorporation efficiency (∼85%). Thermal behaviour and crystallinity studies demonstrated successful incorporation of SIM in the lipid core and its conversion to amorphous form. SIM-SLNs demonstrated a sustained SIM release from the lipid core of nanoparticles. SIM-SLNs significantly reduced the elevated serum lipids as indicated by ∼3.9 and ∼1.5-times decreased total cholesterol compared to those of untreated control and SIM dispersion treated hyperlipidemic rats. In conclusion, SIM-SLNs showed a great promise for improving the therapeutic outcomes of SIM via its effective oral delivery.</P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
Quercetin attenuates neuronal cells damage in a middle cerebral artery occlusion animal model
PARK, Dong-Ju,SHAH, Fawad-Ali,KOH, Phil-Ok The Japanese Society of Veterinary Science 2018 The Journal of veterinary medical science Vol.80 No.4
<P>Cerebral ischemia is a neurological disorder with high mortality. Quercetin is a flavonoid compound that is abundant in vegetables and fruits. It exerts anti-inflammatory and anti-apoptotic effects. This study investigated the neuroprotective effects of quercetin in focal cerebral ischemia. Male Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO) to induce focal cerebral ischemia. Quercetin or vehicle was injected 30 min before the onset of ischemia. A neurological function test, brain edema measurement, and 2,3,5-triphenyltetrazolium chloride staining were performed to elucidate the neuroprotective effects of quercetin. Western blot analysis was performed to observe caspase-3 and poly ADP-ribose polymerase (PARP) protein expression. MCAO leads to severe neuronal deficits and increases brain edema and infarct volume. However, quercetin administration attenuated the MCAO-induced neuronal deficits and neuronal degeneration. We observed increases in caspase-3 and PARP protein levels in MCAO-operated animals injected with vehicle, whereas quercetin administration attenuated these increases in MCAO injury. This study reveals the neuroprotective effect of quercetin in an MCAO-induced animal model and demonstrates the regulation of caspase-3 and PARP expression by quercetin treatment. These results suggest that quercetin exerts a neuroprotective effect through preventing the MCAO-induced activation of apoptotic pathways affecting caspase-3 and PARP expression.</P>