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    <Journal>
      <PublisherName>isfcppharmaspire</PublisherName>
      <JournalTitle>Pharmaspire</JournalTitle>
      <PISSN>C</PISSN>
      <EISSN>o</EISSN>
      <Volume-Issue/>
      <PartNumber/>
      <IssueTopic>Multidisciplinary</IssueTopic>
      <IssueLanguage>English</IssueLanguage>
      <Season/>
      <SpecialIssue>N</SpecialIssue>
      <SupplementaryIssue>N</SupplementaryIssue>
      <IssueOA>Y</IssueOA>
      <PubDate>
        <Year>-0001</Year>
        <Month>11</Month>
        <Day>30</Day>
      </PubDate>
      <ArticleType>Pharmacology</ArticleType>
      <ArticleTitle>Modulating the Nrf-2/NF-κB pathway as a potential strategy for neuroprotection against traumatic brain injury: insights from animal models</ArticleTitle>
      <SubTitle/>
      <ArticleLanguage>English</ArticleLanguage>
      <ArticleOA>Y</ArticleOA>
      <FirstPage>0</FirstPage>
      <LastPage>0</LastPage>
      <AuthorList>
        <Author>
          <FirstName>Shamsher</FirstName>
          <LastName>Singh</LastName>
          <AuthorLanguage>English</AuthorLanguage>
          <Affiliation/>
          <CorrespondingAuthor>N</CorrespondingAuthor>
          <ORCID/>
        </Author>
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      <DOI/>
      <Abstract>Traumatic brain injury (TBI) is a major public health concern that can result in significant long-term disability and mortality. Neuroprotection strategies that can mitigate the effects of TBI are urgently needed. The Nrf-2/NF-κB pathway has emerged as a promising target for neuroprotection in TBI due to its role in regulating inflammation, oxidative stress, and mitochondrial dysfunction. This review summarizes the current preclinical evidence supporting the role of the Nrf-2/NF-κB pathway in TBI and the mechanisms underlying its regulation in this context. Pharmacological and genetic approaches have been used to modulate the pathway in animal models of TBI, resulting in improved functional, histological, and molecular outcomes. The molecular mechanisms underlying the Nrf-2/NF-κB pathway in TBI involve its regulation of inflammation, oxidative stress, and mitochondrial dysfunction. Future studies should focus on identifying safe and effective agents for modulating this pathway, optimizing dosing regimens, and exploring combination therapies that target multiple pathways involved in TBI. While preclinical studies have shown promising results, further research is needed to determine the safety and efficacy of modulating the Nrf-2/NF-κB pathway in human TBI patients. Overall, the Nrf-2/NF-κB pathway represents a promising target for neuroprotection in TBI, and further research is needed to translate these preclinical findings into effective treatments for human patients.</Abstract>
      <AbstractLanguage>English</AbstractLanguage>
      <Keywords>Traumatic brain injury,neuroprotection,Nrf-2,inflammation,oxidative stress,mitochondrial dysfunction</Keywords>
      <URLs>
        <Abstract>https://isfcppharmaspire.com/ubijournal-v1copy/journals/abstract.php?article_id=14860&amp;title=Modulating the Nrf-2/NF-κB pathway as a potential strategy for neuroprotection against traumatic brain injury: insights from animal models</Abstract>
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      <References>
        <ReferencesarticleTitle>References</ReferencesarticleTitle>
        <ReferencesfirstPage>16</ReferencesfirstPage>
        <ReferenceslastPage>19</ReferenceslastPage>
        <References/>
      </References>
    </Journal>
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