ArticleDrug design, development and therapy2026
Sacubitril/Valsartan Fails to Ameliorate Cisplatin-Induced Cognitive Impairment.
Article in Drug design, development and therapy, 2026. 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
Background: Chemotherapy-induced cognitive impairment ("chemobrain") is mechanistically linked to oxidative stress, neuroinflammation, and apoptotic pathway dysregulation. Angiotensin receptor-neprilysin inhibitors and angiotensin II type-1 receptor blockers, such as sacubitril/valsartan (VS), have demonstrated neuroprotective potential; however, their effects in cisplatin (CIS)-induced neurotoxicity models remain poorly characterized. Methods: Forty male Wistar rats were randomized into four groups: Control, CIS (5 mg/kg, i.p). VS alone (≈40 mg/kg/day in drinking water), and CIS+VS, receiving three doses over 7 days. Cognitive performance was assessed 24 hours after the final dose via the Y-maze and novel object recognition test (NORT). Survival and body weight were monitored throughout. Hippocampal levels of reactive oxygen species (ROS), malondialdehyde (MDA), TNF-α, IL-1β, IL-6, total NF-κB, BAX, and total caspase-3 were quantified by ELISA, complemented by histopathological analysis. Results: CIS produced dose-limiting toxicity, with 40% mortality and approximately 13% body weight loss over 8 days. The CIS+VS group exhibited greater toxicity, with 50% mortality and approximately 16% weight loss, while the control and VS animals gained weight. Both CIS and CIS+VS groups demonstrated significant impairment in spatial and recognition memory, as reflected by reduced novel-arm entries and time spent in the Y-maze, and diminished novel object exploration in NORT relative to controls. Hippocampal oxidative stress, neuroinflammatory, and apoptosis-related signaling markers were markedly elevated following CIS and remained comparably elevated in the CIS+VS group, consistent with persistent neuroinflammation. Histopathological examination confirmed severe hippocampal tissue damage in both CIS-treated groups, with no attenuation observed in the CIS+VS group. Conclusion: CIS induces significant cognitive deficits accompanied by elevated neurotoxicity markers. Under the tested dosing schedule, adjunctive VS failed to rescue cognitive function or attenuate hippocampal neuro-injury. These findings reinforce oxidative stress, neuroinflammation, and apoptotic signaling as key mechanistic drivers of chemobrain and indicate that VS confers no neuroprotective benefit in this model.
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