<?xml version="1.0" encoding="ISO-8859-1"?><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
<front>
<journal-meta>
<journal-id>0535-5133</journal-id>
<journal-title><![CDATA[Investigación Clínica]]></journal-title>
<abbrev-journal-title><![CDATA[Invest. clín]]></abbrev-journal-title>
<issn>0535-5133</issn>
<publisher>
<publisher-name><![CDATA[Instituto de Investigaciones Clínicas "Dr. Américo Negrette", Facultad de Medicina, Universidad del Zulia]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0535-51332025000100004</article-id>
<article-id pub-id-type="doi">10.54817/ic.v66n1a01</article-id>
<title-group>
<article-title xml:lang="en"><![CDATA[Phillygenin reduced neuropathic pain by inhibiting the rats&#8217; TLR4/MyD88/NF-&#954;B pathway.]]></article-title>
<article-title xml:lang="es"><![CDATA[Filigenina reduce el dolor neuropático en ratas inhibiendo la vía del TLR4/MyD88/NF-&#954;B.]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Hua]]></surname>
<given-names><![CDATA[Lei]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Zhou]]></surname>
<given-names><![CDATA[Waiping]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Li]]></surname>
<given-names><![CDATA[Mengjie]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Li]]></surname>
<given-names><![CDATA[Rongchun]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Wuhan Fourth Hospital Department of Pain ]]></institution>
<addr-line><![CDATA[Wuhan ]]></addr-line>
<country>China</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>03</month>
<year>2025</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>03</month>
<year>2025</year>
</pub-date>
<volume>66</volume>
<numero>1</numero>
<fpage>4</fpage>
<lpage>15</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://ve.scielo.org/scielo.php?script=sci_arttext&amp;pid=S0535-51332025000100004&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://ve.scielo.org/scielo.php?script=sci_abstract&amp;pid=S0535-51332025000100004&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://ve.scielo.org/scielo.php?script=sci_pdf&amp;pid=S0535-51332025000100004&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract To elucidate the effects of phillygenin (PHI) and the potential mechanism on TLR4 and MyD88/NF-&#954;B signalling in neuropathic pain in animal studies, chronic constriction injury (CCI) models were constructed for neuropathic pain induction using male Sprague-Dawley rats. PHI (20 mg/kg) was delivered through intragastric administration. Von Frey and Hargreaves tests were implemented to determine the 50% paw-withdrawal threshold (PWT) and paw-withdrawal latency (PWL). A nitric oxide (NO) assay was used for NO level detection, and an ELISA assay was employed to measure the expression of proinflammatory cytokines. Western blotting and RT-qPCR were conducted for protein and mRNA level detection. Treatment with PHI significantly enhanced 50% of PWT and PWL. PHI significantly decreased the levels of NO and reduced the levels of TNF-&#945;, IL -1&#946;, and IL -6. PHI also downregulated TLR4 and MyD88 expressions and inhibited the phosphorylation of NF-&#954;B. PHI ameliorated inflammatory status and alleviated neuropathic pain in CCI rats, targeting TLR4 and suppressing MyD88/NF-&#954;B signalling.]]></p></abstract>
<abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen Para dilucidar los efectos de la filigenina (PHI) y el mecanismo potencial en la señalización de TLR4 y MyD88/NF-&#954;B en el dolor neuropático en estudios con animales, se construyeron modelos de lesión por constricción crónica (CCI) para la inducción del dolor neuropático utilizando ratas Sprague-Dawley macho. La PHI (20 mg/kg) se administró por vía intragástrica. Se implementaron las pruebas de von Frey y Hargreaves para determinar el 50% del umbral de retracción de la pata (PWT) y la latencia de retracción de la pata (PWL). Se utilizó un ensayo de óxido nítrico (NO) para la detección del nivel de NO, y se empleó un ensayo ELISA para medir la expresión de citocinas proinflamatorias. Se realizaron transferencia Western y RT-qPCR para la detección del nivel de proteína y ARNm. El tratamiento con PHI mejoró significativamente el 50% del PWT y la PWL. La PHI disminuyó significativamente los niveles de NO y redujo los niveles de TNF-&#945;, IL -1&#946; e IL -6. PHI también disminuyó la expresión de TLR4 y MyD88 e inhibió la fosforilación de NF-&#954;B. PHI mejoró el estado inflamatorio y alivió el dolor neuropático en ratas con CCI, actuando sobre TLR4 y suprimiendo la señalización MyD88/NF-&#954;B.]]></p></abstract>
<kwd-group>
<kwd lng="en"><![CDATA[neuropathic pain]]></kwd>
<kwd lng="en"><![CDATA[phillygenin]]></kwd>
<kwd lng="en"><![CDATA[proinflammatory cytokines]]></kwd>
<kwd lng="en"><![CDATA[TLR4]]></kwd>
<kwd lng="en"><![CDATA[MyD88]]></kwd>
<kwd lng="es"><![CDATA[dolor neuropático]]></kwd>
<kwd lng="es"><![CDATA[filigenina]]></kwd>
<kwd lng="es"><![CDATA[citocinas proinflamatorias]]></kwd>
<kwd lng="es"><![CDATA[TLR4]]></kwd>
<kwd lng="es"><![CDATA[MyD88]]></kwd>
</kwd-group>
</article-meta>
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