Inandiklioglu, NihalOnat, TaylanRaheem, Kayode YomiKaya, Savas2025-05-042025-05-0420242075-1729https://doi.org/10.3390/life14101214https://hdl.handle.net/20.500.12418/35195In 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.en10.3390/life14101214info:eu-repo/semantics/openAccessgene expressionischemia-reperfusionJWH-133molecular dockinguterusArticle1410394595132-s2.0-85207674390Q1WOS:001343483600001Q1