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Fluimucil, N-acetyl-cystein, NAC, neuroprotective, antioxidant, bibliometric, trend.
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SALEH AY, Susanto TD, Valentina R and Saputra DAY. Fluimucil as a neuroprotective, is there anything new? Bibliometric study from 1996 to 2024 [version 1; peer review: awaiting peer review]. F1000Research 2025, 14:46 (https://doi.org/10.12688/f1000research.156696.1)
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Systematic Review
Fluimucil as a neuroprotective, is there anything new? Bibliometric study from 1996 to 2024
[version 1; peer review: awaiting peer review]
PUBLISHED 08 Jan 2025
OPEN PEER REVIEW
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Abstract
Corresponding author:
ARMAN YURISALDI SALEH
Competing interests:
No competing interests were disclosed.
Grant information:
The author(s) declared that no grants were involved in supporting this work.
Copyright:
© 2025 SALEH AY et al.
This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
How to cite: SALEH AY, Susanto TD, Valentina R and Saputra DAY. Fluimucil as a neuroprotective, is there anything new? Bibliometric study from 1996 to 2024 [version 1; peer review: awaiting peer review]. F1000Research 2025, 14:46 (https://doi.org/10.12688/f1000research.156696.1)
First published: 08 Jan 2025, 14:46 (https://doi.org/10.12688/f1000research.156696.1)
Latest published: 08 Jan 2025, 14:46 (https://doi.org/10.12688/f1000research.156696.1)
Introduction
Fluimucil, or better known by its chemical name N-acetylcysteine (NAC), was originally developed as a mucolytic drug that functions to thin mucus in patients with respiratory disorders. However, recent studies have revealed that NAC has potential as a neuroprotective agent, which can protect nerve cells from oxidative damage and inflammation. This discovery opens up new opportunities in the use of NAC for the treatment of neurodegenerative diseases such as Alzheimer’s and Parkinson’s.1
This study aims to conduct a bibliometric analysis of documents related to the use of NAC as a neuroprotective agent, taken from the Scopus database. This bibliometric analysis has never been done before and is expected to provide in-depth insight into the development of research in this field.
Bibliometric research plays an important role in evaluating and understanding scientific developments in a field. Qualitatively, this analysis can identify research trends, emerging topics, and collaborations between researchers and institutions.2 By understanding these patterns, researchers can identify unexplored research gaps and direct their research in more innovative and relevant directions.
Quantitatively, bibliometric analysis allows researchers to measure scientific productivity, the impact of publications, and the influence of particular researchers or institutions.2 These data can be used to evaluate the effectiveness of the research strategies that have been carried out and plan the next steps. In the clinical context, a deeper understanding of the development of NAC research as a neuroprotective agent can help in designing more effective and evidence-based therapies for patients with neurodegenerative diseases.
Thus, this bibliometric study not only provides an overview of the development of NAC research, but also provides a strong foundation for the development of better clinical therapies in the future.
Methods
Bibliometric research is a methodological approach that employs scientific publishing data to delineate and examine the evolution of a scientific discipline. This research seeks to find and delineate trends, patterns, and correlations within scientific texts pertaining to specific subjects. This research focusses on fluimucil, NAC, N-acetylcysteine, and their neuroprotective properties. This study utilises data from www.scopus.com, a prominent and reputable database for scientific articles. This research was conducted in September 2024. To do bibliometric research, the subsequent steps must be adhered to:
1. Identify search keywords. This research employs the keywords fluimucil, NAC, N-acetylcysteine, and neuroprotective. These keywords are inputted into the search area on the www.scopus.com website by selecting the topic category (title, abstract, keywords).
2. Refine search outcomes. In this investigation, the data were not filtered. Extract the data from the search results. This study entails the extraction of search result data in three various forms, specifically:
• CSV (comma-separated values), which encompasses fundamental information regarding the document, including title, author, affiliation, year, source, abstract, and keywords.
• RIS (Research Information System), which encompasses comprehensive details regarding a document, including its cited references.
Data collection
A search was conducted on the Scopus website using the provided criteria, recognising that this platform encompasses research deemed credible. The current evaluation pertains to the designations: TITLE – ABS – KEY (fluimucil), TITLE – ABS – KEY (n-acetylcysteine), TITLE – ABS – KEY (N-acetylcysteine), and TITLE – ABS – KEY (neuroprotective). We received three hundred forty-three documents. We then save the Scopus document as a file with the designated extension. CSV in accordance with this procedure.
Data analysis
Both the Biblioshiny and Vosviewer software packages were utilised in the analysis process.
Quantitative analysis
Documents by Year
According to Figure 1, there has been a growth in the number of papers, culminating at 23 documents by 2021. The earliest document, dated 1996, is titled “Prevention of Dopamine-Induced Cell Death by Thiol Antioxidants: Possible Implications for Treatment of Parkinson’s Disease,” authored by Daniel Offen et al. Additionally, “On the Track of Cell Survival Pharmaceuticals in the Oligodendrocyte Type-2 Astrocyte Lineage” was authored by Noble, M., and Mayer-Próschel, M. The most recent document from 2024 is titled “Catalpol Inhibits HHcy-Induced EndMT in Endothelial Cells by Modulating ROS/NF-κB Signalling,” authored by Chengyan Wu et al. Atmospheric pressure plasma preconditioning mitigates death in human neuronal SH-SY5Y cells generated by oxygen and glucose deprivation by activating protective autophagy and the ROS/AMPK/mTOR pathway, as reported by Xu Yan et al. The neuroprotective benefits of chlorogenic acid involve the modulation of Akt/Erk1/2 signalling to avert neuronal death in Parkinson’s disease, as articulated by Shuai He et al. H2S inhibits the compromise of the blood-brain barrier in rats exhibiting prenatal hyperhomocysteinemia, authored by A.V. Yakovlev et al.8 The impact of N-acetylcysteine on the neurotoxicity of sevoflurane in developing hippocampal cells, authored by Esra Adiyeke et al.9 N-Acetylcysteine Mitigates Cisplatin Toxicity in the Cerebrum and Lungs of Young Rats with Induced Protein Deficiency by David Calderón Guzmán et al.10 NADPH and NAC collaboratively reduce neurodegeneration and neuroinflammation generated by chronic ocular hypertension via modulating the p38/MAPK pathway and peroxidation, as articulated by Naiji Yu et al.11 Polysaccharides from Lycium barbarum mitigate oxidative stress and neurotransmitter dysfunction produced by nonylphenol and octylphenol in PC-12 cells, authored by Linjing Xu et al.12 Recent advancements in the management of primary and secondary progressive Multiple Sclerosis authored by Shitiz Sriwastava et al.13 The molecular interaction, aggregation, and neurotoxicity of α-synuclein upon interaction with glycyrrhizic acid: Modulation of synucleinopathies authored by Zhang, L., Zhang, N., Pang, C.14 Argininyl-fructosyl-glucose (AFG) mitigates D-galactose-induced cellular senescence in neuro-2a cells by decreasing endoplasmic reticulum stress and apoptosis, as shown by Shan Tang et al.15 Topical Treatment Options for Oxidative Eye Diseases, with a Particular Emphasis on Retinopathies, authored by Cristina Russo et al.16 The neuroprotective effects of cerebroprotein hydrolysate and its synergistic application with antioxidants against oxidative stress-induced HT22 cell death, authored by Yang, E.-J., Kim, J.C., and Na, D. H, and the enhancement of dopamine release by N-acetylcysteine, which mitigates the adverse effects of 6-OHDA on the expression of VMAT2, α-synuclein, and tyrosine hydroxylase, authored by El-Habta, R., af Bjerkén, S., and Virel, A.
Figure 1. Documents by Year.
Documents by Author
According to Figure 2, the three most prolific authors, each with six documents, are as follows: Sandhir, R. titled the article The protective impact of N-acetylcysteine supplementation on mitochondrial oxidative stress and mitochondrial enzymes in the cerebral cortex of streptozotocin-treated diabetic rats. Hyperglycemia-induced modifications in synaptosomal membrane fluidity and the activity of membrane-bound enzymes: advantageous impact of N-acetylcysteine supplementation. The neuroprotective effect of N-acetylcysteine on the progression of diabetic encephalopathy in streptozotocin-induced diabetes. Disrupted synaptosomal calcium equilibrium and behavioural impairments subsequent to carbofuran exposure: Neuroprotection afforded by N-acetylcysteine. The neuroprotective efficacy of N-acetylcysteine against carbofuran neurotoxicity: A biochemical and histological investigation. and Neurochemical and neurobehavioral changes in rats produced by carbofuran: Mitigation by N-acetylcysteine.19–24
Figure 2. Documents by Author.
The subsequent author is Wiberg, M., with the title: The effects of N-acetyl-cysteine and acetyl-l-carnitine on neuronal survival, neuroinflammation, and regeneration following spinal cord injury. Mitochondrial participation in the apoptosis and preservation of sensory nerve cells. Neuroprotective effects of N-acetylcysteine and acetyl-L-carnitine following spinal cord damage in adult rats. N-Acetylcysteine modifies apoptotic gene expression in axotomized primary sensory afferent subpopulations. Impact of N-acetyl-cysteine on the viability and regeneration of sural sensory neurones in adult rats, along with its neuroprotective effects, mitochondrial preservation, and therapeutic potential following nerve injury.25–30
The subsequent author is Chamorro, B., with the article titled: Neuroprotective and Antioxidant Properties of Novel Quinolylnitrones in in vitro and in vivo Cerebral Ischaemia Models. Neuroprotective and Antioxidant Properties of CholesteroNitrone ChN2 and QuinolylNitrone QN23 in an Experimental Model of Cerebral Ischaemia: Involvement of Necrotic and Apoptotic Cell Death. Nucleobase-Derived Nitrones: Synthesis and Antioxidant and Neuroprotective Activities in an in vitro Model of Ischemia–Reperfusion, along with the Synthesis, Neuroprotection, and Antioxidant Activity of 1,1′-Biphenylnitrones as α-Phenyl-n-tert-butylnitrone Analogues in in vitro Ischaemia Models.31–34
Documents by Affiliations
According to Figure 3, the Universidad Complutense de Madrid and Umeå Universitet each produced 8 records, followed by the College of Medicine and Panjab University, which each produced 7 documents. Medical University of South Carolina includes seven documents.
Figure 3. Documents by Affiliations.
Documents by country or territory
According to Figure 4, the United States has the highest number of document creators, totalling 85 documents. China has 75 documents, followed by India with 25, South Korea with 23, and Japan with 15.
Figure 4. Documents by country or territory.
Documents by funding sponsor
According to Figure 5, the National Natural Science Foundation of China is the funding sponsor with the highest number of document creators, totalling 28 documents. Subsequently, the National Institutes of Health produced 26 documents. National Institute of Neurological Disorders and Stroke with 21 documents and National Council for Scientific and Technological Development with 12 documents.
Figure 5. Documents by funding sponsor.
Factorial map of the documents with the highest contributes
Figure 6 illustrates that the publication with the highest contribution is titled “Purinergic Modulation of Extracellular Glutamate Levels in the Nucleus Accumbens In Vivo.” released by the International Journal of Developmental Neuroscience in 2004. The writers of this journal are U. Krügel, T. Schraft, R. Regenthal, P. Illes, and H. Kittner. This research examined the influence of P2 receptors on extracellular glutamate levels in the nucleus accumbens (NAc) of freely moving rats. Microdialysis techniques were employed to quantify glutamate concentrations in the nucleus accumbens (NAc). The findings indicated that activation of P2 receptors by the agonist 2-methylthioadenosine 5′-triphosphate (2-MeSATP) elevated extracellular glutamate concentrations in a dose-dependent manner. Furthermore, pretreatment with the P2 receptor antagonist, pyridoxalphosphate-6-azophenyl-2′,4′-disulphonic acid (PPADS), reduced basal glutamate levels and obstructed the 2-MeSATP-induced elevation in glutamate concentrations.
Figure 6. Factorial map of the documents with the highest contributes.
Figure 7. Documents by Subject Area.
Documents by Subject Area
Supplementary Table 1. Documents by subject area (Refer extedned data).
Network Visualization
Figure 8 indicates that the examined areas remain unassociated with other regions delineated by edges. This is the domain: free radicals, anti-inflammatory agents, streptozocin, animalia, dizocilpine, calcium transport, antiinflammatory agent, dizocilpine maleate, calcium ion, rattus, brain injuries, nitrites, zinc, cerebral cortex, calcium, cadmium, spinal ganglion, brain edema, memory, memory disorders, ascorbic acid, dna, in situ nick-end labelling, incubation time, cell culture, glucose, nick end labelling, concentration response, cell nucleus, cobalt, map kinase signalling system, cell line, cobalt chloride, mitochondrial membrane potential, ginsenoside rg 1, protein kinase b, protein cleavage, antineoplastic agent, sh-sy5y cells, antineoplastic activity, endoplasmic reticulum stress, autophagy, mtt assay, sh-sy5y cell line, cytology, chemistry, cell proliferation, neuroapoptosis, cell structure, neurodegeneration, oxidopamine, dopaminergic neurons, protein aggregation, staining, mice inbred c57bl, rotarod test, dopamine transporter, dopamine release, microdialysis, reward, dopamine uptake inhibitors, cocaine, brain depth stimulation, nucleus accumbens, locomotion, corpus striatum, immunofluorescence, astrocytes, astrocyte, drug potention, glia cell, animal behavior, forced swim test, convalescence, depression, prefrontal cortex, anxiety, psychosis, randomized controlled trial, aged, review, demyelination, treatment outcome, cognition, drug safety, brain protection, tumor necrosis factor, headache, ketamine, minocycline, interleukin 6, interleukin 1 beta, cognitive defect, thiol, cytokine, thiobarbituric acid reactive s, drug therapy and combination.
Figure 8. Network Visualization.
Overlay visualization of scopus, database using Vosviewer
According to Figure 9, the overlay visualisation indicates that the extensively researched keywords leading up to 2018, highlighted in yellow, include: wistar rat, ketamine, cognition, headache, drug safety, tumour necrosis factor, randomised controlled trial, psychosis, adult, aged, prefrontal cortex, forced swim test, metabolism, down regulation, western blotting, immunofluorescence, rotarod test, reward, neuroapoptosis, chemistry, autophagy, cell proliferation, mtt assay, sh-sy5y cell line, dopaminergic neurones, and
Figure 9. Overlay visualization of scopus, database using Vosviewer.
Density Visualization
According to Figure 10, in the visual circulation density, the area that is saturated with research is indicated in yellow, while the area that remains unsaturated is represented by a lighter yellow and predominantly green, specifically concerning the keywords: free radicals, anti-inflammatory agents, streptozocin, Animalia, dizocilpine, calcium transport, anti-inflammatory agent, brain cortex, dizocilpine maleate, calcium ion, rattus, brain injuries, rats, wistar, nitrites, calcium, zinc, cerebral cortex, cadmium, spinal ganglion, brain oedema, memory, malondialdehyde, memory disorders, wistar rat, catalase, ascorbic acid, DNA, cells, cultured, spinal ganglion, cytosol. in situ nick-end labelling, scavenger, drug interactions, in situ nick-end labelling, incubation time, drug interactions, cell culture, glucose, nick end labelling, cell death, concentration response, enzyme activation, cell nucleus, hypoxia, cobalt, map kinase signalling system, cell line, cobalt chloride, mitochondrial membrane potential, ginsenoside rg 1, protein kinase b, cytotocity, cell line tumor, protein cleavage, human cell, antineoplastic agent, sh-sy5y cells, antineoplastic activity, endoplasmic reticulum stress, autophagy, mtt assay, sh-sy5y cell line, cytology, chemistry, cell proliferation, neuroapoptosis, cell structure, Parkinson disease, neurodegeneration, oxidopamine, dopaminergic nerve cell, dopaminergic neurons, protein aggregation, dopamine uptake inhibitors, in vivo study, staining, mice inbred c57bl, rotarod test, dopamine, dopamine transporter, dopamine release, microdialysis, reward, dopamine uptake inhibitors, cocaine, brain depth stimulation, nucleus accumbens, locomotion, behaviour animal, corpus striatum, immunofluorescence, western bloating, Astrocytes, astrocyte, murine model, pharmacological potentiation, glial cell, animal behaviour, forced swim test, convalescence, in vitro investigation, adult, depression, prefrontal cortex, anxiety, psychosis, randomised controlled trial, aged subjects, review, demyelination, therapeutic outcome, cognition, drug safety, neuroprotection, tumour necrosis factor. headache, ketamine, minocycline, interleukin-6, interleukin-1 beta, superoxide dismutase, cognitive impairment, thiol, cytokine, thiobarbituric acid reactive substances, combination medication therapy, hippocampus, and 3-nitrotyrosine.
Figure 10. Density Visualization.
Thematic Map
According to Figure 11, thematic maps in Biblioshiny are often categorised into four quadrants according to two parameters: centrality and density. Below is a concise elucidation of the four categories of topics we referenced: The initial theme is Niche Themes, encompassing phrases such as ketamine, memantine, n-acetylcysteine, and spinal cord damage. This theme encompasses particular study domains that may be underdeveloped yet are significantly pertinent to various facets of neuroprotection.
Figure 11. Thematic Map.
Ketamine exhibits context-dependent neuroprotective and neurotoxic characteristics. At subanesthetic dosages, ketamine can stimulate neurotrophic signalling pathways that exhibit neuroprotective effects. Moreover, ketamine has been employed in the management of treatment-resistant depression (TRD) and has demonstrated anti-inflammatory and antioxidant properties that may enhance neuroprotective capabilities. NAC may be utilised alongside ketamine to mitigate the neurotoxic adverse effects of ketamine and augment its neuroprotective properties.
Memantine is an NMDA receptor antagonist utilised in the management of ischaemic stroke and traumatic brain damage. Memantine can impede the excitotoxic cascade and enhance motor and sensory outcomes. Research indicates that memantine may be utilised alongside NAC to augment neuroprotective effects by modulating the glutamatergic system and diminishing oxidative stress.
Spinal cord trauma can result in damage to neurones and glial cells. NAC and other neuroprotective drugs may mitigate secondary damage and enhance neuronal survival.
Specialised Topics Significance, These themes represent certain domains of inquiry that may have received limited exploration. While not crucial to the present study, these topics possess the potential to emerge as a primary focus in the future due to their contextual significance.
Motor Themes
This quadrant encompasses topics including glutathione, mitochondria, neuronal apoptosis, Alzheimer’s disease, SH-SY5Y cells, brain, NAC, antioxidants, and reactive oxygen species. These topics signify new and crucial domains within the subject that propel future research.
Glutathione is a crucial antioxidant that contributes to the detoxification of reactive oxygen species (ROS) and reactive nitrogen species (RNS). NAC serves as a precursor to glutathione and can elevate cellular glutathione levels, hence offering neuroprotective benefits.
Mitochondria Mitochondrial failure is pivotal in the onset of neuroinflammation and oxidative stress, which are critical contributors to the progression of brain illness. NAC can safeguard mitochondria from oxidative damage and enhance mitochondrial performance.
Neuronal Mortality, Neuronal death may occur via necrosis or apoptosis pathways. NAC can diminish neuronal mortality by obstructing the apoptotic pathway and alleviating oxidative stress.
Alzheimer’s Disease include neurovascular alterations, amyloid-β accumulation, and impaired glucose metabolism. NAC may assist in mitigating oxidative stress and inflammation linked to this condition.
SH-SY5Y cells are a human neuroblastoma cell line frequently employed in neuroprotection research pertaining to Parkinson’s and Alzheimer’s illnesses. NAC will be utilised in this study to evaluate its neuroprotective properties.
Cerebrum, The brain is a primary organ in neuroprotection research. NAC may safeguard the brain from oxidative injury and inflammation. NAC is a potent antioxidant that can diminish oxidative stress in neuronal cells.
Reactive Oxygen Species (ROS) are chemicals capable of inducing oxidative damage to neuronal cells. NAC can diminish the generation of ROS and safeguard neuronal cells from injury.
Definition of Motor Themes. This theme represents a well-established research domain and is a primary catalyst in neuroprotection studies. This issue is crucial and significantly influences the advancement of novel knowledge and cures.
Fundamental Themes
This quadrant encompasses keywords including Parkinson’s disease, n-acetyl-l-cysteine, neurodegeneration, inflammation, dopamine, oxidative stress, and apoptosis. These themes encapsulate the core principles and essential research domains in the investigation of neuroprotection associated with NAC.
Parkinson’s Disease entails the degeneration of dopaminergic neurones in the substantia nigra. NAC may assist in diminishing the oxidative stress and inflammation linked to this condition.
Oxidative Stress Oxidative stress refers to the disproportion between the generation of reactive oxygen species (ROS) and the organism’s capacity to neutralise them. NAC is a potent antioxidant that can diminish oxidative stress.
Apoptosis is a type of planned cell death that occurs without inducing inflammation. NAC can impede the apoptotic process by diminishing ROS levels.
Definition of Fundamental Themes. This theme encapsulates the essential and foundational principles in neuroprotection research. It establishes the foundational knowledge required to comprehend the processes and neuroprotective properties of NAC.
Emerging or Diminishing Themes
This quadrant encompasses terms including elevated glucose, hippocampus neurones, zebrafish, neuroprotection, PC cells, reactive oxygen species, memory, and endoplasmic reticulum stress. This subject highlights regions of emerging or diminishing interest in this academic discipline.
Elevated Glucose Levels, Elevated glucose levels can induce oxidative stress and neuronal injury. NAC may assist in safeguarding neurones from damage induced by hyperglycemia. Neurones of the hippocampus, Hippocampal neurones are crucial for learning and memory processes. NAC may safeguard hippocampus neurones from oxidative injury.
Zebrafish serve as an animal model frequently employed in neuroprotection studies due to their capacity for nerve tissue regeneration. NAC may be utilised in this investigation to evaluate its neuroprotective properties.
Significance of Ascendant or Descendant Themes, This subject signifies a nascent or waning domain of inquiry. It presents emerging trends in neuroprotection research, which may either become a primary emphasis in the future or diminish in significance.
Discussion
Bibliometric analysis of the neuroprotective properties of N-acetylcysteine (NAC) or fluimucil has many advantages and disadvantages that warrant consideration. This study integrates quantitative and qualitative analyses, offering a thorough examination of research trends and the mechanism of action of NAC as a neuroprotective agent. This study employs bibliometric analysis to discern research trends, encompassing publication volume, the countries of origin, and researcher collaboration.343 This study thoroughly examines the method by which NAC safeguards neurons from oxidative damage and inflammation, along with its function in elevating glutathione levels and mitigating oxidative stress.344 This study thoroughly examines the method by which NAC safeguards neurons from oxidative damage and inflammation, along with its function in elevating glutathione levels and mitigating oxidative stress.132
This study possesses certain limitations. The accessible data may be restricted to papers indexed in specific databases, thereby omitting significant investigations. The analyzed research may have employed varying approaches, complicating direct comparisons. Publication bias may occur, wherein research yielding good results is more frequently published than those with negative or neutral outcomes.343
This research holds considerable value for the future progression of science and therapy. This discovery may facilitate the advancement of novel therapeutics utilizing NAC as a neuroprotective agent, particularly for neurodegenerative disorders like Parkinson’s and Alzheimer’s. Comprehending the mechanism of action of NAC could facilitate additional study into its potential usage in conjunction with other medications to augment therapeutic efficacy. NAC may enhance the quality of life for people with neurodegenerative disorders and other chronic illnesses by mitigating oxidative stress and inflammation.
This research possesses substantial potential to yield important advancements in neuroprotection and the formulation of novel therapeutics in the future. This finding is significant in clinical practice as it may facilitate the development of novel therapeutics utilizing NAC as a neuroprotective drug, particularly for neurodegenerative illnesses like Parkinson’s and Alzheimer’s. Comprehending the mechanism of action of NAC may facilitate further investigation into its potential usage in conjunction with other medications to augment treatment efficacy.343 NAC may enhance the quality of life for people with neurodegenerative disorders and other chronic illnesses by mitigating oxidative stress and inflammation. This research offers substantial advantages for future scientific advancement, facilitating the development of novel medicines and enhancing comprehension of the mechanism of action of NAC.132
Conclusion
The investigation of the neuroprotective properties of N-acetylcysteine (NAC) or fluimucil presents several limits and advantages. It employs quantitative and qualitative analysis to deliver an exhaustive comprehension of the study process and NAC’s function as a neuroprotective agent. This research examines NAC’s function in mitigating oxidative stress and inflammation, thereby elevating glutathione levels and averting oxidative damage.
Nonetheless, the research possesses drawbacks, including potential bias in the published data and the application of varying methodology. The research has considerable promise for enhancing quality of life and therapeutic interventions in the future, especially for neurodegenerative disorders such as Parkinson’s and Alzheimer’s illnesses. Comprehending the NAC’s mechanism of action can offer significant insights for researchers into its possible application in conjunction with other therapies to augment therapy efficacy.
This finding holds substantial potential for advancing neuroprotection and therapeutic development in the future. It can facilitate the advancement of novel therapies and enhance comprehension of NAC’s mechanism of action.
Software availability
VOSviewer software is an open-access tool that can be used as a cost-effective method for any scientometric analysis.345
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how to cite this article
SALEH AY, Susanto TD, Valentina R and Saputra DAY. Fluimucil as a neuroprotective, is there anything new? Bibliometric study from 1996 to 2024 [version 1; peer review: awaiting peer review]. F1000Research 2025, 14:46 (https://doi.org/10.12688/f1000research.156696.1)
NOTE: If applicable, it is important to ensure the information in square brackets after the title is included in all citations of this article.
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