ArticleFrontiers in pharmacology2025
α-Bisabolol alleviates doxorubicin-induced cognitive dysfunction in rats via enhancing the hippocampal BDNF/TrKB signaling and inhibiting neuroinflammation.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Chemofog is a serious sequela commonly manifested among cancer patients receiving doxorubicin (DOX) chemotherapy. Our goal was to explore the abrogative action of α-Bisabolol (BISA), a phytochemical sesquiterpene, against DOX-induced cognitive deficit. Rats were allocated into 5 groups: Group I: control; Group II received BISA orally (100 mg/kg/day for 4 weeks); Group III received DOX (2 mg/kg/week/i.p.) for 4 weeks; Groups IV and V were administered BISA orally at 50 and 100 mg/kg, respectively plus DOX, i. p. Results: 1) BISA attenuated DOX-induced chemofog as shown in memory-related behavioral tests. 2) BISA restored the hippocampal histological structure and redox homeostasis via diminishing MDA content and upregulating Nrf2 and HO-1 genes. 3) BISA mitigated DOX-induced neuroinflammation through reducing NF-kB, TNF-α, IL-6, IL-1β, and GFAP expressions. 4) BISA repressed the hippocampal apoptosis via downregulating Bax gene and upregulating Bcl-2 gene. 5) BISA enhanced the synaptic plasticity by activating the BDNF/TrKB signaling and increasing the levels of neurotransmitters that enhance memory, i.e., ACh, 5-HT, and DA. BISA at 100 mg/kg/day exerted a better neuroprotection than BISA at 50 mg/kg/day. Thus, BISA may protect cancer patients from cognitive disorders caused by DOX.
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