ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Safranal improves the anticancer efficacy of sorafenib via transcriptomic reprogramming and metabolomic changes in a rat model of diethylnitrosamine-induced cirrhosis-hepatocellular carcinoma.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Epigallocatechin-3-Gallate, the green tea polyphenol suppresses expression of CD31 and VEGFR2 and enhances the chemotherapeutic potential of irinotecan in AOM/DSS model of colorectal cancer in mice.Journal of the Egyptian National Cancer Institute · 2026Article
- Icariin-loaded liposomal nanoparticles alleviate streptozotocin-induced diabetic hepatopathy associated with modulation of ferroptosis-related and inflammatory signaling.BMC pharmacology & toxicology · 2026Article
- A novel dihydroisoxazole derivative DHI9 suppresses colorectal cancer cell survival by inducing oxidative stress, DNA damage, and mitochondrial apoptosis while targeting Akt and Wnt/β-catenin signalling.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Morin attenuates vancomycin-induced nephrotoxicity via Nrf-2/HO-1, SIRT1/PGC1α and AKT/FOXO1A pathways.Molecular biology reports · 2026Article
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Abstract
Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality. Sorafenib (SB) remains an option for advanced HCC in patients who cannot receive, or do not respond to, immunotherapy. Safranal (SF), a bioactive saffron compound, possesses anti-inflammatory and anticancer properties. This study evaluated SF with SB in a diethylnitrosamine-induced cirrhosis-HCC rat model. Rats were assigned to control, HCC, HCC + SB, HCC + SF, and HCC + SF + SB groups and treated for three weeks. Liver morphology, function, histology, apoptosis, cell proliferation, transcriptomics, and metabolomics analyses were assessed. Combination therapy inhibited hepatic nodules and restored liver architecture. Biochemical and histopathological analyses confirmed improved liver function, reduced fibrosis, vacuolation, and decreased α-SMA expression. Combined treatment improved apoptosis, antiproliferative effects and caused G2/M cell cycle arrest. Inflammatory markers (TNF-α, NF-κB, COX-2, MMP9, and β-catenin) were downregulated. Multiomics confirmed modulation of apoptosis, inflammation, oxidative stress, and metabolic pathways. SF potentiates a promising anti-HCC therapeutic efficacy of SB.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.