大黄素对精神分裂症大鼠海马组织PI3K/Akt/mTOR信号通路的影响

doi:10.3969/j.issn.1006-6233.2024.09.06

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Abstract Objective: To investigate the impact of emodin on neurological injury and cognitive function in rats with schizophrenia (SP) by regulating the phosphatidylinositol3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway.Methods: An SP rat model was established by injecting dexamethasone (MK-801), and normal rats were used as the control group. SP rats were randomly included in the SP group, different doses (20, 40, 60mg/kg) of emodin groups, and 60mg/kg of emodin+LY294002 group. Stereotypic behavior and ataxia scoring criteria were applied to evaluate rat behavioral function. Morris water maze experiment was applied to evaluate cognitive function in rats. Reagent kits were applied to detect acetylcholinesterase (AchE) and acetylcholine (Ach) activities in brain tissue. HE was applied to detect pathological changes in hippocampal tissue. QRT-PCR was applied to detect the expression of brain-derived neurotrophic factor (BDNF) mRNA and calcium-dependent protein kinase (CaMK II) mRNA in brain tissue. Western blot was applied to detect the expression of PI3K/Akt/mTOR pathway-related proteins.Results: Compared with the control group, the number of platform crossings, Ach activity, the expression of BDNF mRNA, CaMK Ⅱ mRNA, the expression of p-PI3K/PI3K, p-Akt/Akt, and p-mTOR/mTOR were greatly reduced in the SP group, the stereotypes and ataxia scores, average avoidance latency, and AchE activity were greatly increased (P<0.05). However, after intervention with different doses of emodin, the number of platform crossings, Ach activity, the expression of BDNF mRNA, CaMK Ⅱ mRNA, the expression of p-PI3K/PI3K, p-Akt/Akt, and p-mTOR/mTOR were greatly increased, the stereotypes and ataxia scores, average avoidance latency, and AchE activity were greatly reduced, with differences between groups (P<0.05). The number of platform crossings, Ach activity, the expression of BDNF mRNA, CaMK Ⅱ mRNA, the expression of p-PI3K/PI3K, p-Akt/Akt, and p-mTOR/mTOR in 60mg/kg emodin + LY294002 group were greatly lower than 60mg/kg emodin group, the stereotypes and ataxia scores, average avoidance latency, and AchE activity were greatly increased (P<0.05).Conclusion: Emodin can improve the cognitive ability and neuroprotective function of SP rats by regulating PI3K/Akt/mTOR signaling pathway.

Key words： Emodin PI3K/Akt/mTOR signaling pathway Schizophrenia

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	WANG Dejia
	YANG Bo

Cite this article:

WANG Dejia,YANG Bo. Effect of Emodin on PI3K/Akt/Mtor Signaling Pathway in Hippocampus of Schizophrenic Rats[J]. HeBei Med, 2024, 30(9): 1446-1451.

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http://www.hbyxzzs.cn/EN/10.3969/j.issn.1006-6233.2024.09.06 OR http://www.hbyxzzs.cn/EN/Y2024/V30/I9/1446

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