Effect of ω-3PUFAs on cognitive deficit in rats with schizophrenia
Maosheng Fang, Hong Qian, Kuan Zeng, Meng Ye, Yongjie Zhou, Hui Li
Abstract
Maosheng Fang, Hong Qian, Kuan Zeng, Meng Ye, Yongjie Zhou, Hui Li
Abstract
Objective To investigate the antagonistic effect of ω-3PUFAs on cognitive impairment in MK-801-induced schizophrenia (SZ) rats and its mechanism. Methods Rat model of schizophrenia was induced by MK-801. Morris water maze was used to detect the change of cognitive function in rats. The number of neonatal neurons in hippocampus was detected by Brdu staining. CREB, p-CREB, BDNF, TrkB and p-TrkB levels were detected by Weston Blot. Results MK-801 induced schizophrenia-like cognitive impairment (the escape latency in the water maze test was (6.51±3.10)s for Ctr group, (15.27±6.20)s for Mod group; acrossing times was (4.63±1.06) times for Ctr group, (2.00±1.15) times for Mod group), reduced the number of neonatal neurons in hippocampus (the relative level of neonatal neuron number per unit area, Mod/Ctr was 0.656±0.066) and impaired the CREB/BDNF/TrkB pathway (the relative level of gray value, Mod/Ctr: CREB was 0.393±0.065, p-CREB was 0.591±0.015, BDNF was 0.716±0.115, TrkB was 0.787±0.029, p-TrkB was 0.586±0.013). ω-3PUFAs improved the CREB/BDNF/TrkB pathway activity by increasing CREB and TrKB level and their phosphorylation (the relative level of gray value, Pre/Ctr: CREB was 1.139±0.111, p-CREB was 0.845±0.243, BDNF was 0.864±0.133, TrkB was 0.916±0.022, p-TrkB was 0.952±0.047), and then recovered the number of neonatal neurons in hippocampus (the relative level of neonatal neuron number per unit area, Pre/ Ctr was 1.183±0.101), thereby reduced the cognitive dysfunction in schizophrenia rats(the escape latency in the water maze was (7.44±4.55)s for Pre; acrossing times was (3.86±1.68) times for Pre). Conclusion ω-3PUFAs can relieve the MK-801-induced schizophrenia-like cognitive impairment. Key words: Schizophrenia; MK-801; ω-3PUFAs; Cognition impairment
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Objective To investigate the antagonistic effect of ω-3PUFAs on cognitive impairment in MK-801-induced schizophrenia (SZ) rats and its mechanism. Methods Rat model of schizophrenia was induced by MK-801. Morris water maze was used to detect the change of cognitive function in rats. The number of neonatal neurons in hippocampus was detected by Brdu staining. CREB, p-CREB, BDNF, TrkB and p-TrkB levels were detected by Weston Blot. Results MK-801 induced schizophrenia-like cognitive impairment (the escape latency in the water maze test was (6.51±3.10)s for Ctr group, (15.27±6.20)s for Mod group; acrossing times was (4.63±1.06) times for Ctr group, (2.00±1.15) times for Mod group), reduced the number of neonatal neurons in hippocampus (the relative level of neonatal neuron number per unit area, Mod/Ctr was 0.656±0.066) and impaired the CREB/BDNF/TrkB pathway (the relative level of gray value, Mod/Ctr: CREB was 0.393±0.065, p-CREB was 0.591±0.015, BDNF was 0.716±0.115, TrkB was 0.787±0.029, p-TrkB was 0.586±0.013). ω-3PUFAs improved the CREB/BDNF/TrkB pathway activity by increasing CREB and TrKB level and their phosphorylation (the relative level of gray value, Pre/Ctr: CREB was 1.139±0.111, p-CREB was 0.845±0.243, BDNF was 0.864±0.133, TrkB was 0.916±0.022, p-TrkB was 0.952±0.047), and then recovered the number of neonatal neurons in hippocampus (the relative level of neonatal neuron number per unit area, Pre/ Ctr was 1.183±0.101), thereby reduced the cognitive dysfunction in schizophrenia rats(the escape latency in the water maze was (7.44±4.55)s for Pre; acrossing times was (3.86±1.68) times for Pre). Conclusion ω-3PUFAs can relieve the MK-801-induced schizophrenia-like cognitive impairment. Key words: Schizophrenia; MK-801; ω-3PUFAs; Cognition impairment
Key concepts: CREB, Tropomyosin receptor kinase B, Internal medicine, Hippocampus, Endocrinology, Morris water navigation task, Medicine, Neurotrophic factors