ArticleMetabolic brain disease2025
The potential of alphapinene as a therapeutic agent for maternal hypoxia-induced cognitive impairments: a study on HO-1 and Nrf2 gene expression in rats.
Article in Metabolic brain disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Epimedin C: A promising neuroprotective agent that can participate in mediating the JNK/Nrf2/HO-1 signaling pathway to prevent neurodegenerative diseases.Experimental and therapeutic medicine · 2026Article
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4 authors.
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Abstract
This research seeks to address the gap in past studies by examining the role of the Nrf2 (nuclear factor erythroid 2-related factor 2) and HO-1 (heme oxygenase-1) signaling pathways in hypoxia and the potential effects of alpha-pinene on these factors. Wistar rats were divided into 7 experimental groups (n = 7): 1) control, 2 and 3) groups receiving alpha-pinene 5 and 10 mg/kg (i.p., for 21 days), 4) hypoxia group (7% O2 and 93 N2, 3 h, GD14 to GD18), 5 and 6) groups receiving alpha-pinene 5 and 10 after hypoxia. Memory and cognition were evaluated using the Morris water maze and novel object recognition tests. Inflammation was assessed by ELISA method and Nrf2 and HO-1 Nrf2 gene expression was evaluated using real-time PCR in the hippocampus. Recognition index, spatial memory, and Nrf2-H0-1 gene expression significantly reduced in the hypoxia group compared to the control group, and alpha-pinene injection in the offspring improved cognition, memory, and Nrf2- HO-1 gene expression in the groups were affected by hypoxia. Inflammation factors in the hypoxia group were higher than the control, but alpha-pinene significantly decreased inflammation ( all cases p < 0.05). Based on the results, it seems that alpha-pinene prevents cognitive and memory loss by increasing Nrf2 and H0-1 gene expression and reducing inflammation.
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