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Cancer Treatment and Pharmacology / Cancer Related Cognitive Impairment Studies · Journal article
Biomolecules · September 4, 2026
Early or partial results. Treat as a signal, not a conclusion.
This preclinical study reports that thymoquinone (5–10 mg/kg/day orally) prevented paclitaxel-induced mechanical allodynia in rats without compromising paclitaxel's anticancer activity in vitro. However, no meaningful structural neuroprotection or improvement in neurophysiological parameters was observed, suggesting analgesic rather than disease-modifying benefit.
Preclinical in vitro and in vivo animal study. Sprague–Dawley rats (embryonic and adult); MCF-7 and MDA-MB-231 breast cancer cell lines.. Intervention: Thymoquinone 5–10 mg/kg/day oral, co-administered with paclitaxel. Compared with: Paclitaxel alone; in vitro vehicle controls implied but not explicitly stated. DRG tissue from Envigo Laboratory (Udine, Italy); study location not otherwise specified..
TQ (5 μM) significantly attenuated PTX-induced neurite shortening at 24 h in embryonic DRG neurons in vitro TQ co-treatment fully prevented PTX-induced SIRT1 downregulation in embryonic DRG neurons TQ did not compromise PTX cytotoxicity in MCF-7 cells and significantly potentiated it in MDA-MB-231 triple-negative breast cancer cells
TQ did not compromise PTX cytotoxicity in MCF-7 cells and significantly potentiated it in MDA-MB-231 triple-negative breast cancer cells
This study does not provide sufficient evidence to guide clinical use of thymoquinone in paclitaxel-induced peripheral neuropathy. Translation to human trials would be premature given the limited structural neuroprotection observed and absence of efficacy data beyond analgesia in animal models.
Early-stage preclinical and animal study demonstrating analgesic efficacy of thymoquinone in paclitaxel-induced neuropathy, but with limited structural neuroprotection and no human data, requiring confirmation before clinical translation.
As stated by the source record.
Quoted from the source exactly as published.
This study does not provide sufficient evidence to guide clinical use of thymoquinone in paclitaxel-induced peripheral neuropathy. Translation to human trials would be premature given the limited structural neuroprotection observed and absence of efficacy data beyond analgesia in animal models.
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Chemotherapy-Induced Peripheral Neuropathy (CIPN) is a dose-limiting complication of paclitaxel (PTX) therapy, for which effective treatments are still lacking. This study evaluated the neuroprotective potential of Thymoquinone (TQ), a bioactive derivative of Nigella sativa, in mitigating chronic PTX-induced neurotoxicity without compromising antineoplastic activity. We first performed in vitro experiments using Sprague–Dawley rat embryonic (E15) Dorsal Root Ganglia (DRG) (Envigo Laboratory (Udine, Italy))to assess neurotoxicity through neurite outgrowth evaluation. To investigate the molecular mechanisms underlying TQ’s putative neuroprotective mechanisms, SIRT1 protein expression was additionally evaluated by western blot, while MCF-7 and MDA-MB-231 breast cancer cells were used to monitor cytotoxicity via MTT assay. We then moved to in vivo experiments, in which chronic neuropathy was induced in rats using PTX (10 mg/kg, i.v., weekly for 4 weeks). TQ was co-administered orally (5–10 mg/kg/day). The effects of TQ on peripheral neuropathy were assessed through behavioral testing, neurophysiological assessments, and histological analysis of Intraepidermal Nerve Fibre density (IENF), DRG and peripheral nerves. In vitro, TQ (5 μM) significantly attenuated PTX-induced neurite shortening at 24 h; TQ co-treatment fully prevented PTX-induced SIRT1 downregulation in embryonic DRG neurons and did not compromise PTX cytotoxicity in MCF-7 cells, while significantly potentiating it in MDA-MB-231 triple-negative breast cancer cells. In vivo results demonstrated that PTX-treated animals exhibited mild erythroid myelosuppression at the end of treatment. Regarding efficacy, TQ consistently prevented PTX-induced mechanical allodynia throughout the treatment period, and TQ (10 mg/kg) transiently mitigated IENF depletion at mid-treatment; however, no improvement in neurophysiological parameters or peripheral nerve morphology was observed at either time point. Collectively, these findings suggest that, under conditions of chronic PTX exposure, TQ exerts a predominantly analgesic effect in vivo, without conferring meaningful structural neuroprotection against PTX-induced peripheral nerve degeneration.
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