Changes in Cyclin D1, cdk4, and Their Associated Molecules in Ischemic Pyramidal Neurons in Gerbil Hippocampus after Transient Ischemia and Neuroprotective Effects of Ischemic Preconditioning by Keeping the Molecules in the Ischemic Neurons

Inadequate activation of cell cycle proteins including cyclin D1 and cdk4 is involved in neuronal cell death induced by diverse pathological stresses, including transient global brain ischemia. The neuroprotective effect of ischemic preconditioning is well-established, but the underlying mechanism is still unknown. In this study, we examined changes in cyclin D1, cdk4, and related molecules in cells or neurons located in Cornu Ammonis 1 (CA1) of gerbil hippocampus after transient ischemia for 5 min (ischemia and reperfusion) and investigated the effects of IPC on these molecules after ischemia. Four groups were used in this study as follows: sham group, ischemia group, IPC plus (+) sham group, and IPC+ischemia group. IPC was developed by inducing 2-min ischemia at 24 h before 5-min ischemia (real ischemia). Most pyramidal cells located in CA1 of the ischemia group died five days after ischemia. CA1 pyramidal cells in the IPC+ischemia group were protected. In the ischemia group, the expressions of cyclin D1, cdk4, phosphorylated retinoblastoma (p-Rb), and E2F1 (a transcription factor regulated by p-Rb) were significantly altered in the pyramidal cells with time after ischemia; in the IPC+ischemia group, they were controlled at the level shown in the sham group. In particular, the expression of p16INK4a (an endogenous cdk inhibitor) in the ischemia group was reversely altered in the pyramidal cells; in the IPC+TI group, the expression of p16INK4a was not different from that shown in the sham group. Our current results indicate that cyclin D1/cdk4-related signals may have important roles in events in neurons related to damage/death following ischemia and reperfusion. In particular, the preservation of p16INK4a by IPC may be crucial in attenuating neuronal death/damage or protecting neurons after brain ischemic insults.

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Neuroprotective Effect of Nilotinib on Cortical Pyramidal Cells, Histological, Morphometric and Biochemical Study

Annual Research & Review in Biology ◽

10.9734/arrb/2020/v35i330197 ◽

2020 ◽

pp. 23-33

Author(s):

Ahmed S. Ahmed

Keyword(s):

Cell Death ◽

Antioxidant Enzymes ◽

Antiepileptic Drug ◽

Neuroprotective Effect ◽

Latency Period ◽

Neuronal Cell ◽

Pyramidal Cells ◽

Male Rats ◽

Control Group ◽

Cortical Tissue

Introduction: Death of neuronal cell and gliosis are the two main pathological hallmarks induced by nervous tissue stress like conditions such as status epilepticus. Previous studies have mentioned that neuronal cell death occur as a result of different mechanisms, namely, necrosis and apoptosis. Although more recent studies have explained the cell death on the basis of autophagy. Many antiepileptic drugs are marketed, taking into consideration the antioxidant role of nilotinib and support its use as a favorable antiepileptic drug. The aim of the present study is to assess the neuroprotective effect of antiepileptic drug nilotinib on cortical tissue in rats. Materials and Methods: Sixty adult male rats were divided into three groups: (1) Control group, (2) pentylenetetrazol group (injected with pentylenetetrazol 60 mg/kg, subcutaneously), (3) nilotinib and pentylenetetrazol group (pretreated with nilotinib, 25 mg/kg daily for seven days prior to pentylenetetrazol administration). Latency of seizure and level of either oxidant or antioxidant enzymes in the cortical tissue was assessed. The histopathological changes in the cerebral cortex were studied also using hematoxylin and eosin stain. Results: Nilotinib increased the latency period of convulsions, increased the antioxidant enzymes levels with regain of the normal histological features. Conclusions: Nilotinib proved to promote the antioxidant, antiapoptotic pathways, anti-inflammatory and inhibiting autophagy which favor its use as an anti-epileptic drug.

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Neuroprotective Effect of Cudrania tricuspidata Fruit Extracts on Scopolamine-Induced Learning and Memory Impairment

International Journal of Molecular Sciences ◽

10.3390/ijms21239202 ◽

2020 ◽

Vol 21 (23) ◽

pp. 9202

Author(s):

Seung-Cheol Jee ◽

Kwang Min Lee ◽

Min Kim ◽

Yoo-Jung Lee ◽

Soee Kim ◽

...

Keyword(s):

Ache Activity ◽

Biological Activities ◽

Neuroprotective Effect ◽

Neuronal Cell ◽

Protective Effects ◽

Gene Expressions ◽

Differentiation Markers ◽

Neuroprotective Effects ◽

Cudrania Tricuspidata ◽

Fruit Extracts

Cudrania tricuspidata has diverse biological activities, such as antioxidant, anti-inflammatory, anticancer, and neuroprotective effects. This study investigated the protective effects of C. tricuspidata fruit extracts (CTFE) against scopolamine (SCO)-induced neuron impairment. The neuroprotective effects of CTFE on SCO-induced memory dysfunction were confirmed in mice using the Barnes maze test. The results showed that co-treatment of SCO and CTFE increased the stay time in the target zone compared with SCO treatment alone. Similarly, the results obtained by the fear conditioning test revealed that SCO-CTFE co-treatment induced the freezing action time under both the contextual fear condition and the cued fear condition compared with SCO treatment alone. Moreover, we showed that CTFE reduced the SCO-induced acetylcholinesterase (AChE) activity, thereby increasing the acetylcholine concentration in mice hippocampal tissues. Consistent with the improvement of memory and recognition function in vivo, our in vitro results showed that CTFE induced cAMP response element binding protein (CREB) and extracellular regulated kinase 1/2 (ERK1/2) activity in PC12 cells and reduced SCO-induced AChE activity. In addition, the microarray results of the hippocampal tissue support our data showing that CTFE affects gene expressions associated with neurogenesis and neuronal cell differentiation markers such as spp1 and klk6. Overall, CTFE exerts a neuroprotective effect via regulation of the CREB and ERK1/2 signaling pathways and could be a therapeutic candidate for neurodegenerative diseases.

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Contribution of ginsenosides Rg1, Rb1 to the neuroprotective effect of Panax notoginseng in mouse organotypic hippocampal slice cultures exposed to oxygen and glucose deprivation

Vietnam Journal of Science Technology and Engineering ◽

10.31276/vjste.63(2).64-69 ◽

2021 ◽

Vol 63 (2) ◽

pp. 64-69

Author(s):

Nguyen Thi Thanh Loan ◽

◽

Le Thi Xoan ◽

Pham Thi Nguyet Hang ◽

Nguyen Van Tai ◽

...

Keyword(s):

Hippocampal Slice ◽

Cell Damage ◽

Neuroprotective Effect ◽

Neuronal Cell ◽

Glucose Deprivation ◽

Panax Notoginseng ◽

Ginsenoside Rg1 ◽

Neuroprotective Effects ◽

Oxygen And Glucose Deprivation ◽

Mk 801

We previously demonstrated that Panax notoginseng (pNG) root extract treatments exertedneuroprotective effects on brain injuries using middle cerebral artery occlusion in mice. The present study aims to investigate the neuroprotective effects of PNG extract and its ginsenosides Rg1 and Rb1 on ischemic neuronal damage caused by oxygen and glucose deprivation (OGD) in mouse organotypic hippocampal slice cultures (OHSCs). Before the experiments, hippocampal slices collected from 7-day-old Swiss mice were cultured for 7 days. OGD was triggered in OHSCs for 30, 60, or 90 min with the aim of finding the optimal period of OGD for drug testing. PNG extract (10, 30 μg/ml), ginsenosides Rg1 and Rb1 (5, 25 μM), or MK-801 25 μM, a reference drug, was added to the culture medium 24 h before OGD and these treatments were continued for 24 h after the optimum 60-min period of OGD. After 24 h of OGD exposure, the measurement of propidium iodide uptake was analysed in OHSCs to evaluate neuronal cell damage. The results showed that OGD time-dependently increased PI uptake of the OHSCs. PNG 30 μg/ml treatment reduced the OGD-induced neuronal cell damage in OHSCs. Ginsenosides Rg1 25 μM, Rb1 (5, 25 μM), as well as MK-801 (25 μM) significantly inhibited PI uptake 24 h after OGD exposure. However, ginsenoside Rg1 5 μM did not show any significant effects on the OGD-induced neuronal cell damage. These findings indicated that ginsenosides Rg1 and Rb1 contributed to the neuroprotective effects of PNG against ischemic damage in OHSCs and the neuroprotective effect of ginsenoside Rb1 was stronger than that of ginsenoside Rg1.

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Minocycline Increases in-vitro Cortical Neuronal Cell Survival after Laser Induced Axotomy

Current Clinical Pharmacology ◽

10.2174/1574884714666190226093119 ◽

2020 ◽

Vol 15 (2) ◽

pp. 105-109 ◽

Cited By ~ 1

Author(s):

Burak Yulug ◽

Mehmet Ozansoy ◽

Merve Alokten ◽

Muzaffer B.C. Ozansoy ◽

Seyda Cankaya ◽

...

Keyword(s):

Cell Survival ◽

Cortical Neurons ◽

Neuroprotective Effect ◽

Neuronal Cell ◽

Neuroprotective Effects ◽

Therapeutic Trials ◽

Trauma Model ◽

Injury Models ◽

Translational Block

Background: Antibiotic therapies targeting multiple regenerative mechanisms have the potential for neuroprotective effects, but the diversity of experimental strategies and analyses of non-standardised therapeutic trials are challenging. In this respect, there are no cases of successful clinical application of such candidate molecules when it comes to human patients. Methods: After 24 hours of culturing, three different minocycline (Sigma-Aldrich, M9511, Germany) concentrations (1 μM, 10 μM and 100 μM) were added to the primary cortical neurons 15 minutes before laser axotomy procedure in order to observe protective effect of minocycline in these dosages. Results: Here, we have shown that minocycline exerted a significant neuroprotective effect at 1 and 100μM doses. Beyond confirming the neuroprotective effect of minocycline in a more standardised and advanced in-vitro trauma model, our findings could have important implications for future studies that concentrate on the translational block between animal and human studies. Conclusion: Such sophisticated approaches might also help to conquer the influence of humanmade variabilities in critical experimental injury models. To the best of our knowledge, this is the first study showing that minocycline increases in-vitro neuronal cell survival after laser-axotomy.

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Neuroprotective Effects of Salicin in a Gerbil Model of Transient Forebrain Ischemia by Attenuating Oxidative Stress and Activating PI3K/Akt/GSK3β Pathway

Antioxidants ◽

10.3390/antiox10040629 ◽

2021 ◽

Vol 10 (4) ◽

pp. 629

Author(s):

Joon Ha Park ◽

Tae-Kyeong Lee ◽

Dae Won Kim ◽

Hyejin Sim ◽

Jae-Chul Lee ◽

...

Keyword(s):

Oxidative Stress ◽

Brain Injury ◽

Pyramidal Neurons ◽

Glycogen Synthase ◽

Neuroprotective Effect ◽

Pyramidal Cells ◽

Ischemic Brain Injury ◽

Neuroprotective Effects ◽

Ischemic Brain ◽

Ca1 Pyramidal Neurons

Salicin is a major natural compound of willow bark and displays diverse beneficial biological properties, such as antioxidant activity. However, little information available for the neuroprotective potential of salicin against ischemic brain injury has been reported. Thus, this study was performed to investigate the neuroprotective potential of salicin against ischemia and reperfusion (IR) injury and its mechanisms in the hippocampus using a gerbil model of 5-min transient ischemia (TI) in the forebrain, in which a massive loss (death) of pyramidal neurons cells occurred in the subfield Cornu Ammonis 1 (CA1) among the hippocampal subregions (CA1-3) at 5 days after TI. To examine neuroprotection by salicin, gerbils were pretreated with salicin alone or together with LY294002, which is a phosphatidylinositol 3-kinase (PI3K) inhibitor, once daily for 3 days before TI. Treatment with 20 mg/kg of salicin significantly protected CA1 pyramidal neurons against the ischemic injury. Treatment with 20 mg/kg of salicin significantly reduced the TI-induced increase in superoxide anion generation and lipid peroxidation in the CA1 pyramidal neurons after TI. The treatment also reinstated the TI-induced decrease in superoxide dismutases (SOD1 and SOD2), catalase, and glutathione peroxidase in the CA1 pyramidal cells after TI. Moreover, salicin treatment significantly elevated the levels of phosphorylation of Akt and glycogen synthase kinase-3β (GSK3β), which is a major downstream target of PI3K, in the ischemic CA1. Notably, the neuroprotective effect of salicin was abolished by LY294002. Taken together, these findings clearly indicate that salicin protects against ischemic brain injury by attenuating oxidative stress and activating the PI3K/Akt/GSK3β pathway.

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Ischemia-Reperfusion under Hyperthermia Increases Heme Oxygenase-1 in Pyramidal Neurons and Astrocytes with Accelerating Neuronal Loss in Gerbil Hippocampus

International Journal of Molecular Sciences ◽

10.3390/ijms22083963 ◽

2021 ◽

Vol 22 (8) ◽

pp. 3963

Author(s):

Tae-Kyeong Lee ◽

Jae-Chul Lee ◽

Dae Won Kim ◽

Bora Kim ◽

Hyejin Sim ◽

...

Keyword(s):

Heme Oxygenase ◽

Neuronal Death ◽

Sham Group ◽

Pyramidal Neurons ◽

Neuronal Damage ◽

Ischemia Reperfusion ◽

Heme Oxygenase 1 ◽

Transient Ischemia ◽

Expression Levels ◽

Ischemia Group

It has been studied that the damage or death of neurons in the hippocampus is different according to hippocampal subregions, cornu ammonis 1–3 (CA1–3), after transient ischemia in the forebrain, showing that pyramidal neurons located in the subfield CA1 (CA1) are most vulnerable to this ischemia. Hyperthermia is a proven risk factor for brain ischemia and can develop more severe and extensive brain damage related with mortality rate. It is well known that heme oxygenase-1 (HO-1) activity and expression is increased by various stimuli in the brain, including hyperthermia. HO-1 can be either protective or deleterious in the central nervous system, and its roles depend on the expression levels of enzymes. In this study, we investigated the effects of hyperthermia during ischemia on HO-1 expression and neuronal damage/death in the hippocampus to examine the relationship between HO-1 and neuronal damage/death following 5-min transient ischemia in the forebrain using gerbils. Gerbils were assigned to four groups: (1) sham-operated gerbils with normothermia (Normo + sham group); (2) ischemia-operated gerbils with normothermia (Normo + ischemia group); (3) sham-operated gerbils with hyperthermia (39.5 ± 0.2 °C) during ischemia (Hyper + sham group); and (4) ischemia-operated gerbils with hyperthermia during ischemia (Hyper + ischemia group). HO-1 expression levels in CA1–3 of the Hyper + ischemia group were significantly higher than those in the Normo + ischemia group. HO-1 immunoreactivity in the Hyper + ischemia group was significantly increased in pyramidal neurons and astrocytes with time after ischemia, and the immunoreactivity was significantly higher than that in the Normo + ischemia group. In the Normo + Ischemia group, neuronal death was shown in pyramidal neurons located only in CA1 at 5 days after ischemia. However, in the Hyper + ischemia group, pyramidal neuronal death occurred in CA1–3 at 2 days after ischemia. Taken together, our findings showed that brain ischemic insult during hyperthermic condition brings up earlier and severer neuronal damage/death in the hippocampus, showing that HO-1 expression in neurons and astrocytes is different according to brain subregions and temperature condition. Based on these findings, we suggest that hyperthermia in patients with ischemic stroke must be taken into the consideration in the therapy.

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Neuroprotective Effects of Chrysin Mediated by Estrogenic Receptors Following Cerebral Ischemia and Reperfusion in Male Rats

Basic and Clinical Neuroscience Journal ◽

10.32598/bcn.12.1.2354.1 ◽

2021 ◽

Vol 12 (1) ◽

pp. 149-162

Author(s):

Maryam Khombi Shooshtari ◽

◽

Yaghoob Farbood ◽

Seyed Mohammad Taghi Mansouri ◽

Mohammad Badavi ◽

...

Keyword(s):

Cerebral Ischemia ◽

Cognitive Deficits ◽

Neuroprotective Effect ◽

Ischemia Reperfusion ◽

Neuronal Cell Death ◽

Neuronal Cell ◽

Male Rats ◽

Neuroprotective Effects ◽

Necrosis Factor Alpha ◽

Male Wistar Rats

Introduction: Ischemic stroke is one of the leading causes of morbidity and mortality worldwide. Neuroprotective strategies were reported to attenuate cognitive deficits after ischemic incidents. Here we studied the neuroprotective potential of chrysin in a rat model of cerebral Ischemia/Reperfusion (I/R) in the presence or absence of Estrogen Receptors (ERs). Methods: Adult male Wistar rats were pretreated with chrysin (CH) (CH; 30 mg/kg; gavage; for 21 consecutive days) alone or with selective ERs antagonists (ERα antagonist MPP; ERβ antagonist PHTPP; IP) or nonselective ERs antagonist (ICI182780; IP). Then, the bilateral common carotid arteries were occluded for 20 min, which was followed by 72 h reperfusion. Subsequently, cognitive performance was evaluated by Morris Water Maze (MWM) and shuttle box tasks, and afterward, their hippocampi were removed for ELISA assays and H&E staining. Oxidative indicators Malondialdehyde (MDA) and Glutathione Peroxidase (GPx), as well as inflammation mediators interleukin (IL)-1β and tumor necrosis factor-alpha (TNFα), were measured using commercial kits. Results: Results of the current study showed that the anti-oxidative and anti-inflammatory properties of CH are possible mechanisms that could improve cognitive deficits and prevent neuronal cell death following I/R (P<0.001). These effects were reversed by ICI182780 (P>0.05). Furthermore, when chrysin was co-treated with ERβ antagonist, PHTPP showed a weak neuroprotective effect in I/R rats. However, these parameters were not significantly different when chrysin was combined with ERα antagonist MPP. Conclusion: Our data confirm that chrysin could potentially serve as a neuroprotective agent against devastating effects of cerebral I/R injury, which may be mediated via its interaction with ERs, especially ERβ.

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Risperidone Treatment after Transient Ischemia Induces Hypothermia and Provides Neuroprotection in the Gerbil Hippocampus by Decreasing Oxidative Stress

International Journal of Molecular Sciences ◽

10.3390/ijms20184621 ◽

2019 ◽

Vol 20 (18) ◽

pp. 4621

Author(s):

Go Eun Yang ◽

Hyun-Jin Tae ◽

Tae-Kyeong Lee ◽

Young Eun Park ◽

Jeong Hwi Cho ◽

...

Keyword(s):

Oxidative Stress ◽

Ischemic Stroke ◽

Body Temperature ◽

Receptor Agonist ◽

Pyramidal Neurons ◽

Neuroprotective Effect ◽

Neuronal Cell ◽

Induced Hypothermia ◽

Transient Ischemia ◽

Ca1 Pyramidal Neurons

Compelling evidence from preclinical and clinical studies has shown that mild hypothermia is neuroprotective against ischemic stroke. We investigated the neuroprotective effect of post-risperidone (RIS) treatment against transient ischemic injury and its mechanisms in the gerbil brain. Transient ischemia (TI) was induced in the telencephalon by bilateral common carotid artery occlusion (BCCAO) for 5 min under normothermic condition (37 ± 0.2 °C). Treatment of RIS induced hypothermia until 12 h after TI in the TI-induced animals under uncontrolled body temperature (UBT) compared to that under controlled body temperature (CBT) (about 37 °C). Neuroprotective effect was statistically significant when we used 5 and 10 mg/kg doses (p < 0.05, respectively). In the RIS-treated TI group, many CA1 pyramidal neurons of the hippocampus survived under UBT compared to those under CBT. In this group under UBT, post-treatment with RIS to TI-induced animals markedly attenuated the activation of glial cells, an increase of oxidative stress markers [dihydroethidium, 8-hydroxy-2′ -deoxyguanosine (8-OHdG), and 4-Hydroxynonenal (4-HNE)], and a decrease of superoxide dismutase 2 (SOD2) in their CA1 pyramidal neurons. Furthermore, RIS-induced hypothermia was significantly interrupted by NBOH-2C-CN hydrochloride (a selective 5-HT2A receptor agonist), but not bromocriptine mesylate (a D2 receptor agonist). Our findings indicate that RIS-induced hypothermia can effectively protect neuronal cell death from TI injury through attenuation of glial activation and maintenance of antioxidants, showing that 5-HT2A receptor is involved in RIS-induced hypothermia. Therefore, RIS could be introduced to reduce body temperature rapidly and might be applied to patients for hypothermic therapy following ischemic stroke.

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Neuroprotection by Phytoestrogens in the Model of Deprivation and Resupply of Oxygen and Glucose In Vitro: The Contribution of Autophagy and Related Signaling Mechanisms

Antioxidants ◽

10.3390/antiox9060545 ◽

2020 ◽

Vol 9 (6) ◽

pp. 545

Author(s):

Giuseppe Abbruzzese ◽

Javier Morón-Oset ◽

Sabela Díaz-Castroverde ◽

Nuria García-Font ◽

Cesáreo Roncero ◽

...

Keyword(s):

Protein Kinase ◽

Therapeutic Potential ◽

Neuronal Damage ◽

Neuroprotective Effect ◽

Ischemia Reperfusion ◽

Neuronal Cell ◽

Mitogen Activated Protein Kinase ◽

Neuroprotective Effects ◽

Signaling Mechanisms ◽

Ribosomal S6 Kinase

Phytoestrogens can have a neuroprotective effect towards ischemia-reperfusion-induced neuronal damage. However, their mechanism of action has not been well described. In this work, we investigate the type of neuronal cell death induced by oxygen and glucose deprivation (OGD) and resupply (OGDR) and pinpoint some of the signaling mechanisms whereby the neuroprotective effects of phytoestrogens occur in these conditions. First, we found that autophagy initiation affords neuronal protection upon neuronal damage induced by OGD and OGDR. The mammalian target of rapamycin/ribosomal S6 kinase (mTOR/S6K) pathway is blocked in these conditions, and we provide evidence that this is mediated by modulation of both the 5′ AMP-activated protein kinase (AMPK) and phosphatidylinositol-3-kinase/protein kinase B (PI3K/AKT) pathways. These are dampened up or down, respectively, under OGDR-induced neuronal damage. In contrast, the MAPK-Erk kinase/extracellular signal-regulated kinase (MEK/ERK) pathway is increased under these conditions. Regarding the pathways affected by phytoestrogens, we show that their protective properties require autophagy initiation, but at later stages, they decrease mitogen-activated protein kinase (MAPK) and AMPK activation and increase mTOR/S6K activation. Collectively, our results put forward a novel mode of action where phytoestrogens play a dual role in the regulation of autophagy by acting as autophagy initiation enhancers when autophagy is a neuroprotective and pro-survival mechanism, and as autophagy initiation inhibitors when autophagy is a pro-death mechanism. Finally, our results support the therapeutic potential of phytoestrogens in brain ischemia by modulating autophagy.

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Momordica charantia L. Extract Protects Hippocampal Neuronal Cells against PAHs-Induced Neurotoxicity: Possible Active Constituents Include Stigmasterol and Vitamin E

Nutrients ◽

10.3390/nu13072368 ◽

2021 ◽

Vol 13 (7) ◽

pp. 2368

Author(s):

Nattaporn Pattarachotanant ◽

Anchalee Prasansuklab ◽

Tewin Tencomnao

Keyword(s):

Vitamin E ◽

In Silico ◽

Neuroprotective Effect ◽

Neuronal Cell ◽

In Silico Analysis ◽

Momordica Charantia ◽

Mitogen Activated Protein Kinase ◽

Active Components ◽

Neuroprotective Effects ◽

Silico Analysis

Polycyclic aromatic hydrocarbons (PAHs) have been recognized to cause neurobehavioral dysfunctions and disorder of cognition and behavioral patterns in childhood. Momordica charantia L. (MC) has been widely known for its nutraceutical and health-promoting properties. To date, the effect of MC for the prevention and handling of PAHs-induced neurotoxicity has not been reported. In the current study, the neuroprotective effects of MC and its underlying mechanisms were investigated in mouse hippocampal neuronal cell line (HT22); moreover, in silico analysis was performed with the phytochemicals MC to decipher their potential function as neuroprotectants. MC was demonstrated to possess neuroprotective effect by reducing reactive oxygen species’ (ROS’) production and down-regulating cyclin D1, p53, and p38 mitogen-activated protein kinase (MAPK) protein expressions, resulting in the inhibition of cell apoptosis and the normalization of cell cycle progression. Additionally, 28 phytochemicals of MC and their competence on inhibiting cytochrome P450 (CYP: CYP1A1, CYP1A2, and CYP1B1) functions were resolved. In silico analysis of vitamin E and stigmasterol revealed that their binding to either CYP1A1 or CYP1A2 was more efficient than the binding of each positive control (alizarin or purpurin). Together, MC is potentially an interesting neuroprotectant including vitamin E and stigmasterol as probable active components for the prevention for PAHs-induced neurotoxicity.

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