Protection of Cultured Cortical Neurons by Luteolin against Oxidative Damage through Inhibition of Apoptosis and Induction of Heme Oxygenase-1

Kim, Sun‐Young; Chin, Young‐Won; Cho, Jungsook

doi:10.1248/bpb.b16-00579

Cited by 35 publications

(25 citation statements)

References 51 publications

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“…We studied the role of HO-1 in our model system because it is expressed in the RVLM neurons (Mazza et al, 2001), exerts neuronal antioxidant and antiapoptotic effects (Spitz et al, 1987;Fouda and Abdel-Rahman, 2017;Kim et al, 2017), and mediates sympathoinhibition (Nassar et al, 2011). Our findings suggest H 2 S-dependent regulation of HO-1 in the RVLM contributes to the diabetes-evoked neurotoxicity and its alleviation by moxonidine for the following reasons.…”

Section: H 2 S-dependent Neuroprotection By Moxonidine In Diabetesmentioning

confidence: 98%

Restoration of Rostral Ventrolateral Medulla Cystathionine-γ Lyase Activity Underlies Moxonidine-Evoked Neuroprotection and Sympathoinhibition in Diabetic Rats

Fouda

El-Sayed

Abdel‐Rahman

2017

J Pharmacol Exp Ther

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We recently demonstrated a fundamental role for cystathionine- lyase (CSE)-derived hydrogen sulfide (HS) in the cardioprotective effect of the centrally acting drug moxonidine in diabetic rats. Whether a downregulated CSE/HS system in the rostral ventrolateral medulla (RVLM) underlies neuronal oxidative stress and sympathoexcitation in diabetes has not been investigated. Along with addressing this question, we tested the hypothesis that moxonidine prevents the diabetes-evoked neurochemical effects by restoring CSE/HS function within its major site of action, the RVLM. Ex vivo studies were performed on RVLM tissues of streptozotocin (55 mg/kg, i.p.) diabetic rats treated daily for 3 weeks with moxonidine (2 or 6 mg/kg; gavage), HS donor sodium hydrosulfide (NaHS) (3.4 mg/kg, i.p.), CSE inhibitor DL-propargylglycine (DLP) (37.5 mg/kg, i.p.), a combination of DLP with moxonidine, or their vehicle. Moxonidine alleviated RVLM oxidative stress, neuronal injury, and increased tyrosine hydroxylase immunoreactivity (sympathoexcitation) by restoring CSE expression/activity as well as heme oxygenase-1 (HO-1) expression. A pivotal role for HS in moxonidine-evoked neuroprotection is supported by the following: 1) NaHS replicated the moxonidine-evoked neuroprotection, and the restoration of RVLM HO-1 expression in diabetic rats; and 2) DLP abolished moxonidine-evoked neuroprotection in diabetic rats, and caused RVLM neurotoxicity, reminiscent of a diabetes-evoked neuronal phenotype, in healthy rats. These findings suggest a novel role for RVLM CSE/HS/HO-1 in moxonidine-evoked neuroprotection and sympathoinhibition, and as a therapeutic target for developing new drugs for alleviating diabetes-evoked RVLM neurotoxicity and cardiovascular anomalies.

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Section: H 2 S-dependent Neuroprotection By Moxonidine In Diabetesmentioning

confidence: 98%

Restoration of Rostral Ventrolateral Medulla Cystathionine-γ Lyase Activity Underlies Moxonidine-Evoked Neuroprotection and Sympathoinhibition in Diabetic Rats

Fouda

El-Sayed

Abdel‐Rahman

2017

J Pharmacol Exp Ther

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“…Indeed, an upregulation of Hsp70 detected in stressed hamsters fed with genistein tends to further underlie its protective measures in a similar fashion to that of other anti-apoptotic plus antidepressant compounds [39], and this is in line with its upregulatory trend reported during traumatic brain injuries [40] and during ischemic episodes [33]. Con textually, the downregulation of NF-κB1 transcripts in stressed hamsters treated with genistein appears to be tightly associated with a neuroprotective ability, as shown by diminished levels of such a factor observed in the HIP during recovery from stress-induced depression and inflammatory processes [41] as well as after treatment with antidepressants [42].…”

Section: Discussionmentioning

confidence: 75%

“…In addition, the morphofunctional effects of genistein seemed to tightly overlap the evident increased levels, aside NF-κB1, of stress factors (TrkB and Hsp70), thereby supporting their neuroprotective role against toxic agents, neurodegenerative diseases, anxiety, and depression-related phenomena [31-33]. In this case, upregulation of TrkB mRNA by genistein may be viewed as a turning on switch for the interaction of BDNF with its neuroreceptor [34], thereby supplying a compensatory ability of limbic cells to cope with reduced levels of BDNF-TrkB complex deriving from stressful conditions [35] in a comparable manner to its antidepressant effects [36] exhibited especially during the functional restoration of pathologies such as Parkinson’s disease [37].…”

Section: Discussionmentioning

confidence: 99%

Genistein Modifies Hamster Behavior and Expression of Inflammatory Factors following Subchronic Unpredictable Mild Stress

et al. 2018

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Background: Previous studies have pointed to the protective role of genistein against stress adaptations although neuromolecular mechanisms are not yet fully known. With this work, we evaluated the influence of such a phytoestrogen on hamster behavioral and molecular activities following exposure to subchronic unpredictable mild stress. Methods: The motor behaviors of hamsters (n = 28) were analyzed using elevated plus maze (EPM) test, hole board (HB) test, and forced swim test (FST). In addition, neurodegeneration events were assessed with amino cupric silver stain, while expression variations of tropomyosin receptor kinase B (TrkB), nuclear factor kappa-B1 (NF-κB1), and heat shock protein 70 (Hsp70) mRNAs were highlighted in limbic neuronal fields via in situ hybridization. Results: Genistein accounted for increased motor performances in EPM and HB tests but reduced immobility during FST, which were correlated with diminished argyrophilic signals in some limbic neuronal fields. Contextually, upregulated Hsp70 and TrkB mRNAs occurred in hippocampal (HIP) and hypothalamic neuronal fields. Conversely, diminished NF-κB1 levels were mainly obtained in HIP. Conclusion: Hormonal neuroprotective properties of genistein corroborating anxiolytic and antidepressant role(s) through elevated expression levels of stress proteins and trophic factors may constitute novel therapeutic measures against emotional and stress-related motor performances.

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“…Exposure to METH also altered the expression of the mRNAs involved in the oxidative phosphorylation pathway (Wang et al, 2017b) in which cells use enzymes to oxidize nutrients and then to produce adenosine triphosphate. Some studies have reported that oxidative phosphorylation capacity in the mitochondria would be altered and would influence cellular function (Kim, Chin & Cho, 2017;Xia et al, 2014;Xu et al, 2015). It has been reported that NAFLD is associated with insulin resistance, metabolic syndrome and other metabolic dysfunctions (Jacobs et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

RNA-sequencing analysis of the effect of luteolin on methamphetamine-induced hepatotoxicity in rats: a preliminary study

Qu¹,

Zhang²,

Chen³

et al. 2020

PeerJ

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In this study, RNA-sequencing (RNA-seq) was utilized to investigate the effects of luteolin on hepatotoxicity caused by methamphetamine (METH). The rats in METH group were administrated with METH (15 mg/kg, two times per day) via intraperitoneal (i.p.) injections for four consecutive days. The rats in luteolin + METH group were firstly administrated with luteolin (100 mg/kg, once a day) by oral gavage for 3 days before METH treatment. Lueolin attenuated the hepatotoxicity induced by METH via histopathological and biochemical analysis. The results of RNA-seq showed that luteolin could regulate 497 differentially expressed genes (DEGs), and the selected DEGs were mainly enriched in eight pathways, according to KEGG analysis. Furthermore, qRT-PCR was utilized to verify the results of RNA-seq. Six genes were selected as follows: liver enriched antimicrobial peptide 2 (Leap2), fatty acid synthase (Fasn), fatty acid binding protein 5 (Fabp5), patatin like phospholipase domain containing 3 (Pnpla3), myelin basic protein (Mbp) and calmodulin 3 (Calm3). Though because of the design flaws, the luteolin group has not been included, this study demonstrated that luteolin might exert hepato-protective effects from METH via modulation of oxidative phosphorylation, cytochrome P450 and certain signaling pathways.

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Protection of Cultured Cortical Neurons by Luteolin against Oxidative Damage through Inhibition of Apoptosis and Induction of Heme Oxygenase-1

Cited by 35 publications

References 51 publications

Restoration of Rostral Ventrolateral Medulla Cystathionine-γ Lyase Activity Underlies Moxonidine-Evoked Neuroprotection and Sympathoinhibition in Diabetic Rats

Restoration of Rostral Ventrolateral Medulla Cystathionine-γ Lyase Activity Underlies Moxonidine-Evoked Neuroprotection and Sympathoinhibition in Diabetic Rats

Genistein Modifies Hamster Behavior and Expression of Inflammatory Factors following Subchronic Unpredictable Mild Stress

RNA-sequencing analysis of the effect of luteolin on methamphetamine-induced hepatotoxicity in rats: a preliminary study

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