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Magnolia officinalis (L.) Bark Extract Counteracts Oxidative Brain In-jury: A Proteomic Investigation into Neuroprotective Mechanisms

ABSTRACT: Neurodegenerative diseases involve progressive neuronal loss associated with oxidative stress (OS) and inflammation. Given the limited efficacy of current therapies, natural compounds with multitarget neuroprotective potential are of growing interest. In this study, we investigated the neuroprotective effects of a standardized Magnolia officinalis (L.) bark extract (MOE), rich in honokiol and magnolol (29.1 ± 1.39 mg/g and 16.2 ± 0.81 mg/g, HPLC-UV DAD analysis) in rat brain cortical slices exposed to hydrogen peroxide-induced OS. MOE significantly recovered tissue viability and reduced ROS and malondialdehyde levels caused by OS. Caspase-3, -8, and -9 activation was also attenuated, suggesting a role in modulating both intrinsic and extrinsic apoptotic pathways. Shotgun proteomics using LC-HRMS/MS identified OS-induced protein expression changes reversed by MOE. Thirty-three proteins significantly altered by OS were identified, fourteen of which were rescued by MOE co-treatment. These proteins participate in several processes, including neuronal survival, OS response, and proteostasis. Bioinformatic analysis demonstrated that genes responsible for protein synthesis regulated by MOE are subjected to transcriptional regulation by factors associated with OS, including FOXO4, NRF2, and SP1. The present findings support the hypothesis that MOE exerts multitarget neuroprotective effects by modulating key proteins involved in OS responses and neuronal survival, suggesting a promising natural products-based strategy for pre-venting processes related to neurodegenerative diseases.

INSTRUMENT(S):

ORGANISM(S): Rattus Norvegicus (rat)

TISSUE(S): Brain

SUBMITTER: Roberto Stella

LAB HEAD: Roberto Angeletti

PROVIDER: PXD075711 | Pride | 2026-05-25

REPOSITORIES: Pride

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			Action	DRS
	06092022_Brain_C1_5ug.msf	Msf
	06092022_Brain_C1_5ug.raw	Raw
	06092022_Brain_C2_5ug.msf	Msf
	06092022_Brain_C2_5ug.raw	Raw
	06092022_Brain_C3_5ug.msf	Msf

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<i>Magnolia officinalis</i> (L.) Bark Extract Counteracts Oxidative Brain Injury: A Proteomic Investigation into Neuroprotective Mechanisms.

Mattioli Laura Beatrice LB Stella Roberto R Peggion Caterina C Cagnin Stefano S Pifferi Alice A Miraldi Elisabetta E Cappellucci Giorgio G Baini Giulia G Camarda Luca L Budriesi Roberta R Frosini Maria M

International journal of molecular sciences 20260408 8

Neurodegenerative diseases involve progressive neuronal loss associated with oxidative stress (OS) and inflammation. Given the limited efficacy of current therapies, natural compounds with multitarget neuroprotective potential are of growing interest. In this study, we investigated the neuroprotective effects of a standardized <i>Magnolia officinalis</i> (L.) bark extract (MOE) in rat brain cortical slices exposed to hydrogen peroxide-induced OS. MOE significantly recovered tissue viability and ...[more]

PMID: 42073995

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Project description:Background: Heat stress is an increasing global health concern associated with high mortality and multi-organ dysfunction. The brain is particularly vulnerable, leading to behavioral impairments. At the molecular level, heat stress disrupts proteins involved in synaptic communication, mitochondrial function, and cellular homeostasis. Current treatments are mainly symptomatic, highlighting the need for targeted neuroprotective strategies. Edaravone, a potent free-radical scavenger with anti-inflammatory properties, has demonstrated neuroprotective effects in various neurological conditions. This study aimed to evaluate the neuroprotective effects of edaravone against heat stress–induced behavioral dysfunction and to investigate the underlying molecular mechanisms using proteomic analysis. Methodology: Male Wistar rats (n = 54) were assigned to four groups: control, heat stress (HS), edaravone (Edv), and heat stress plus edaravone (HS+Edv). Heat stress and treatment were administered for 12 weeks. Behavioral assessments, including radial arm water maze (RAWM), open field test (OFT), elevated plus maze (EPM), and tail suspension test (TST), were conducted. Proteomic analysis of the cortex, hippocampus, and cerebellum was performed using UHPLC–QTOF-MS. Result: Heat stress induced significant impairments in memory, learning, anxiety-like, and depressive-like behaviors. Proteomic analysis revealed region-specific alterations, with the cerebral cortex showing the most pronounced changes, particularly in pathways related to mitochondrial function, oxidative stress, synaptic signaling, and protein quality control. The HS+Edv group showed partial normalization of behavioral outcomes and modulation of key proteomic pathways, including improved mitochondrial function, reduced oxidative stress, and preservation of synaptic and cytoskeletal integrity. Conclusion: Edaravone attenuates heat stress–induced brain dysfunction by promoting adaptive proteomic remodeling rather than complete restoration.

Project description:Background: Cerebral ischemia/reperfusion injury is a common secondary effect of cardiac arrest which is largely responsible for postresuscitative mortality. Therefore development of therapies which restore and protect the brain function after cardiac arrest is essential. Methylene blue (MB) has been experimentally proven neuroprotective in a porcine model of global ischemia-reperfusion in experimental cardiac arrest. However, no comprehensive analyses have been conducted at gene expression level. Methods: Pigs underwent either untreated cardiac arrest (CA) or CA with subsequent cardiopulmonary resuscitation (CPR) accompanied with an infusion of saline or an infusion of saline with MB. Genome-wide transcriptional profiling using the Affymetrix porcine microarray was performed to 1) gain understanding of delayed neuronal death initiation in porcine brain during ischemia and after 30, 60 and 180 min following reperfusion, and 2) identify the mechanisms behind the neuroprotective effect of MB after ischemic injury (at 30, 60 and 180 min). Results: Our results show that restoration of spontaneous circulation (ROSC) induces major transcriptional changes related to stress response, inflammation, apoptosis and even cytoprotection. In contrast, the untreated ischemic and anoxic insult affected only few genes mainly involved in intra-/extracellular ionic balance. Furthermore, our data show that the neuroprotective role of MB is diverse and fulfilled by regulation of the expression of soluble guanylate cyclase and biological processes accountable for inhibition of apoptosis, modulation of stress response, neurogenesis and neuroprotection. Conclusions: Our results support that MB could be a valuable intervention and should be investigated as a therapeutic agent against neural damage associated with I/R injury induced by cardiac arrest. One group of pigs underwent cardiac arrest (CA) without subsequent cardiopulmonary resuscitation (CPR) and the brain of the animals was removed after 5, 20 or 30 min post CA for genome-wide expression study. Two groups of pigs underwent first CA for 12 min with a subsequent 8 min-long CPR and received either an infusion of saline or an infusion of saline with MB from one minute after the start of CPR until 50 min after return of spontaneous circulation (ROSC). In both latter groups the brains were removed for microarray analysis at the following time points: 30, 60, 180 min.

Project description:We investigated the effects of PACAP treatment, and endogenous PACAP deficiency, on infarct volume, neurological function, and the cerebrocortical transcriptional response in a mouse model of stroke, middle cerebral artery occlusion (MCAO). PACAP-38 administered i.v. or i.c.v. one hour after MCAO significantly reduced infarct volume, and ameliorated functional motor deficits measured 24 hours later in wild-type mice. Infarct volumes and neurological deficits (walking faults) were both greater in PACAP-deficient than in wild-type mice, but treatment with PACAP reduced lesion volume and neurological deficits in PACAP-deficient mice to the same level of improvement as in wild-type mice. A 35,546-clone mouse cDNA microarray was used to investigate cortical transcriptional changes associated with cerebral ischemia in wild-type and PACAP-deficient mice, and with PACAP treatment after MCAO in wild-type mice. 229 known (named) transcripts were increased (228) or decreased (1) in abundance at least 50% following cerebral ischemia in wild-type mice. 49 transcripts were significantly up-regulated only at one hour post-MCAO (acute response transcripts), 142 were up-regulated only at 24 hours post-MCAO (delayed response transcripts) and 37 transcripts were up-regulated at both times (sustained response transcripts). More than 50% of these are transcripts not previously reported to be associated with brain ischemia responses. Many of the acutely regulated neurotrauma-associated transcripts, but a larger percentage of the delayed ones, require endogenous PACAP for up-regulation by ischemia, suggesting a more prominent role for PACAP in later response to injury than in the initial response, and consistent with a neuroprotective role for PACAP in late response to injury and neuroprotective efficacy when given post-MCAO. Putative injury effector transcripts regulated by PACAP include Ã£Ã-actin, midline 2, and metallothionein 1. Potential neuroprotective transcripts include several demonstrated to be PACAP-regulated in other contexts. Prominent among these were transcripts encoding the PACAP-regulated gene Ier3, and the neuropeptides enkephalin, substance P (tachykinin 1), and neurotensin. In the hybridization method employed, equal amounts (2-5Ã£Ãg/15.5 Ã£Ãl) of total RNA obtained from brain tissue of different experimental groups were separately labeled with two different fluorescent dyes (Cy3 or Cy5) and applied on the same NIMH Mouse 36K cDNA microarray chip containing 13217 distinct Entrez gene IDs (formerly known as LocusLink) and 15888 distinct unigene IDs, the remainders are incompletely annotated IMAGE clones. Probe preparation and hybridization were performed as follows. The total RNA (15-50 Ã£Ãg in 15.5 Ã£Ãl) was incubated with amine-modified random primer (2 Ã£Ãg/Ã£Ãl, 2 Ã£Ãl) and RNase inhibitor (5 units/Ã£Ãl, 1 Ã£Ãl) at 70 Ã¤aC for 10 min. Primer-RNA solution was then incubated at 42 Ã¤aC for 2 hr with the reverse transcriptase mix containing 5X first-strand buffer, 50X aa-dUTP/dNTPs (25 mM dATP, 25 mM dGTP, 25 mM dCTP, 15 mM dTTP and 10 mM aminoallyl dUTP), 0.1 M DDT, and Superscript II reverse transcriptase. The cDNA were labeled with NHS-ester Cy3 or Cy5 dye in the presence of 1 M sodium bicarbonate. Array slides placed in a hybridization chamber (Corning, Corning, NY) were incubated at 42 Ã¤aC for 16-24 hr, and successively washed with 0.5X SSC, 0.01% SDS, and 0.06X SSC at room temperature for 10 min each. Arrays were scanned with a GenePix 4000A scanner (Axon, Foster City, CA), and the resulting images were analyzed using IPlab (Fairfax, VA) and a FileMaker Pro 5 (Santa Clara, CA) relational database designed by Zedong Chen, NHGRI. Following background subtraction and normalization, a calculated ratio of Cy3 to Cy5 signal intensities was used to define the relative increase or decrease of a particular transcript. Ratios were calculated only from those spots with a combined ratio quality above 0.3.

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Magnolia officinalis (L.) Bark Extract Counteracts Oxidative Brain In-jury: A Proteomic Investigation into Neuroprotective Mechanisms

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<i>Magnolia officinalis</i> (L.) Bark Extract Counteracts Oxidative Brain Injury: A Proteomic Investigation into Neuroprotective Mechanisms.

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Magnolia officinalis (L.) Bark Extract Counteracts Oxidative Brain In-jury: A Proteomic Investigation into Neuroprotective Mechanisms

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&lt;i&gt;Magnolia officinalis&lt;/i&gt; (L.) Bark Extract Counteracts Oxidative Brain Injury: A Proteomic Investigation into Neuroprotective Mechanisms.

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OmicsDI is part of the ELIXIR infrastructure

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<i>Magnolia officinalis</i> (L.) Bark Extract Counteracts Oxidative Brain Injury: A Proteomic Investigation into Neuroprotective Mechanisms.