The Potential of JWH-133 to Inhibit the TLR4/NF-κB Signaling Pathway in Uterine Ischemia-Reperfusion Injury

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dc.authoridINANDIKLIOGLU, NIHAL/0000-0001-7137-3929
dc.contributor.authorInandiklioglu, Nihal
dc.contributor.authorOnat, Taylan
dc.contributor.authorRaheem, Kayode Yomi
dc.contributor.authorKaya, Savas
dc.date.accessioned2025-05-04T16:45:42Z
dc.date.available2025-05-04T16:45:42Z
dc.date.issued2024
dc.departmentSivas Cumhuriyet Üniversitesi
dc.description.abstractIn recent years, significant progress has been made in understanding the biological and molecular pathways that regulate the effects of ischemia-reperfusion (I/R) injuries. However, despite these developments, various pharmacological agents are still being tested to either protect against or mitigate the damage caused by the IR's harmful consequences. JWH133 is a CB2R-selective agonist and belongs to the class of Delta 8-tetrahydrocannabinol. The present study aimed to determine the in vivo effect of JWH-133 on uterine IR injury via the TLR4/NF-kappa B, pathway. Female Wistar albino rats (n = 40) were randomly divided into five groups. Three different doses of JWH-133 (0.2, 1, and 5 mg/kg) were administered to the rats. RNA was isolated from uterine tissue samples, and gene expression was measured by RT-PCR using specific primers. The interaction energies and binding affinities of JWH-133 with IL-1 beta, IL-6, NF-kappa B, TLR-4, and TNF-alpha were calculated through molecular docking analysis. The expression analysis revealed that JWH-133 administration significantly reduced the expression levels of IL-1 beta, IL-6, NF-kappa B, TLR-4, and TNF-alpha (p < 0.05). Notably, in the 1 mg/kg JWH-133 group, all of the gene expression levels decreased significantly (p < 0.05). The molecular docking results showed that JWH-133 formed hydrogen bonds with GLU64 of IL-1 beta, SER226 of IL-6, and SER62 of TNF-alpha. This study highlights the molecular binding affinity of JWH-133 and its potential effects on inflammation in IR injury. These results pave the way for future research on its potential as a therapeutic target.
dc.identifier.doi10.3390/life14101214
dc.identifier.issn2075-1729
dc.identifier.issue10
dc.identifier.pmid39459513
dc.identifier.scopus2-s2.0-85207674390
dc.identifier.scopusqualityQ1
dc.identifier.urihttps://doi.org/10.3390/life14101214
dc.identifier.urihttps://hdl.handle.net/20.500.12418/35195
dc.identifier.volume14
dc.identifier.wosWOS:001343483600001
dc.identifier.wosqualityQ1
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherMDPI
dc.relation.ispartofLife-Basel
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_WOS_20250504
dc.subjectgene expression
dc.subjectischemia-reperfusion
dc.subjectJWH-133
dc.subjectmolecular docking
dc.subjectuterus
dc.titleThe Potential of JWH-133 to Inhibit the TLR4/NF-κB Signaling Pathway in Uterine Ischemia-Reperfusion Injury
dc.typeArticle

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