The method and effect of rapid establishment of a mild cognitive impairment model

Chen, Ting; Zhou, Qian; Xie, Dongjin; Wang, Hongzhi; Huang, Linshen; Lin, Xiaoxi; Lin, Lanying

doi:10.21037/apm-20-2026

Cited by 4 publications

(8 citation statements)

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“…In this study, an MCI rat model was established by subcutaneous injections of D-gal (1,000 mg•kg −1 •d −1 ) for 1 week, which is known to induce aging. The success rate and stability of this model were confirmed in our previous study (15). This method results in impaired cognitive function, especially in memory, without causing any behavioral abnormalities.…”

Section: Discussionsupporting

confidence: 77%

Hyperbaric oxygen therapy cognitive function in a rat model of mild cognitive impairment via ERK signaling

Lin

Zheng

et al. 2020

Ann Palliat Med

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Background: The development of novel treatment strategies to reverse or impede cognitive dysfunction associated with mild cognitive impairment (MCI) has gained attention in recent times. Meanwhile, hyperbaric oxygen (HBO) has been widely used as a neuroprotective therapy that can promote recovery of damaged neurons. The aim of this study was to investigate the effects of HBO on cognitive function in rats with MCI and to clarify the associated mechanisms. Methods:We established a D-galactose-induced MCI rat model and evaluated the role of extracellularregulated kinase (ERK) signaling in HBO therapy for cognitive function using a specific inhibitor, U0126.All Rats were randomly assigned to four groups with 12 rats per group: normal control group; D-gal model group (group MCI); D-gal + HBO group (group HBO); D-gal + HBO + U0126 group (group U0126). We evaluated cognitive function by Morris water maze and pathological changes by hematoxylin and eosin (HE) staining of hippocampal slices. Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of caspase 3, while total ERK1/2 and phospho-ERK1/2 were assessed by Western blotting.Results: Shorter escape latency was observed in the HBO group as compared to the MCI group, which was to some extent reversed by U0126. Similarly, the HBO group showed the highest number of platform crossings as compared to the MCI and U0126 groups. Pathological analysis also showed less apoptosis and better hippocampal cell morphology in the HBO group. Caspase 3 levels also differed significantly, with lowest expression in the HBO group as compared to the MCI and U0126 groups. The levels of total ERK1/2 and p-ERK1/2 were more elevated in the HBO group as compared to the MCI group.Conclusions: This study found that HBO treatment has a protective effect on early cognitive dysfunction in rats with MCI. HBO therapy may act through ERK signaling, which inhibits apoptosis and protects cognitive function.

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Section: Discussionsupporting

confidence: 77%

Hyperbaric oxygen therapy cognitive function in a rat model of mild cognitive impairment via ERK signaling

Lin

Zheng

et al. 2020

Ann Palliat Med

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“…In line with the pathological process and characteristics requirements of MCI, the previous work of this study has confirmed that the rats injected with 1,000 mg•kg −1 •d −1 d-Gal on the neck and back showed mild neuropathological changes and decreased cholinergic system function, resulting in slight oxidative damage and weakened antioxidant capacity, and mild impairment of spatial learning and memory ability. There was no change in locomotion and foraging behavior, which was consistent with the pathological process and characteristics of MCI (5).…”

Section: Rat Identificationsupporting

confidence: 77%

“…Further, oxidation resistance was abated, and minimal damage to spatial learning and memory ability was noted. No changes in the motivation and foraging behaviors were observed that would meet the requirements of the pathological process and characteristics of MCI (13).…”

Section: A B C Dmentioning

confidence: 94%

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The effects of dexmedetomidine on the cognitive function of mild cognitive impairment (MCI) rats

Zhou¹,

Xie²,

Chen³

et al. 2022

Ann Transl Med

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Background: The study sought to investigate the effects of dexmedetomidine (DEX) on cognitive function after anesthesia and to examine its actual mechanism.Methods: A total of 48 rats were injected with d-galactose (D-gal) 1,000 mg•kg −1 •d −1 and normal saline at the neck and back for 1 week to establish rats with mild cognitive impairment (MCI) and conduct behavioral tests. Sevoflurane was inhaled and DEX was pumped into each group respectively. Morris water maze (MWM) test was conducted 24 hours later. The inflammatory factors interleukin (IL)-1, interleukin (IL)-6, and a tumor necrosis factor (TNF)-α in brain homogenate were quantitatively measured by enzymelinked immunosorbent assay (ELISA) on the next day. The apoptosis of hippocampal cells was observed by hematoxylin-eosin staining (HE staining). Results:In relation to the model establishment, we found that there was no significant difference in body weight and swimming speed before and after modeling. There was no statistically significant difference in the escape latency between Groups A, B, C, and D before modeling. After modeling, there was no statistical difference in the escape latency between Groups A, B, and C, but the difference was statistically significant when compared to Group D (P<0.05). In relation to the DEX intervention, we found that compared to Group C, MWM test performance in Groups A and B was considerably worse longer escape latencies and fewer platform crossings within 90 seconds), and were more significant in Group A. Compared with Group D, the levels of inflammatory cytokines of the brain homogenates were elevated, and this elevation was highest in Group A, followed by Group B; the pathological changes were consistent with changes in behavioral tests.In Group A, there were obvious disorders of glial cell arrangement, apoptosis and deletion. There was no significant change in Group D. And the changes of vertebral cells in Group B and Group C were slight, with orderly arrangement and intact cell structure.Conclusions: DEX inhibits the apoptosis of hippocampal cells and reduces the cognitive dysfunction of rats with MCI induced by D-gal via the inhibition of the release of inflammatory cytokines.

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Section: Discussionmentioning

confidence: 94%

The Effects of Dexmedetomidine on the Cognitive Function of Mild Cognitive Impairment (MCI) Rats

Zhou¹,

Xie²,

Chen³

et al. 2021

Preprint

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Background: The study sought to investigate the effects of dexmedetomidine on cognitive function after anesthesia and to examine its actual mechanism. Methods: A total of 48 rats were randomly divided into model Groups A, B, C, or D. Rats in Groups A, B, and C received a hypodermic injection of D-gal with a concentration of 1,000 mg·kg−1·d−1 respectively for 1 week. Group D received the same volume of saline. The Morris water maze (MWM) test was performed within 6 days of the injection. After the behavior test, Group A received an inhalation dose of 2% sevoflurane. Group B received an inhalation dose of 2% sevoflurane and an intraoperative infusion of dexmedetomidine with a concentration of 10 μg·kg−1·h−1. Group C served as the control group and received no treatment. Group D received an inhalation dose of 2% sevoflurane. Results: In relation to the model establishment, we found that there was no significant difference in body weight and swimming speed before and after modeling. There was no statistically significant difference in the escape latency between Groups A, B, C, and D before modeling. After modeling, there was no statistical difference in the escape latency between Groups A, B, and C, but the difference was statistically significant when compared to Group D (P<0.05). In relation to the dexmedetomidine intervention, we found that compared to Group C, MWM test performance in Group A and B was considerably worse (longer escape latencies and fewer platform crossings within 90 seconds), and were more significant in Group A. .Compared with Group D, the levels of IL-1, IL-6, and TNF-α of the brain homogenates were elevated, and this elevation was highest in Group A, followed by Group B; The pathological changes were consistent with changes in behavioral tests. In group A, there were obvious disorders of glial cell arrangement, apoptosis and deletion. There was no significant change in group D. And the changes of vertebral cells in group B and group C were slight, with orderly arrangement and intact cell structure.Conclusions: Dexmedetomidine inhibits the apoptosis of hippocampal cells and reduces the cognitive dysfunction of rats with MCI induced by D-galactose via the inhibition of the release of inflammatory cytokines.

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The method and effect of rapid establishment of a mild cognitive impairment model

Cited by 4 publications

References 11 publications

Hyperbaric oxygen therapy cognitive function in a rat model of mild cognitive impairment via ERK signaling

Hyperbaric oxygen therapy cognitive function in a rat model of mild cognitive impairment via ERK signaling

The effects of dexmedetomidine on the cognitive function of mild cognitive impairment (MCI) rats

The Effects of Dexmedetomidine on the Cognitive Function of Mild Cognitive Impairment (MCI) Rats

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