Paeoniflorin attenuates chronic cerebral hypoperfusion-induced learning dysfunction and brain damage in rats

Liu, Jing; Jin, Dao Zhong; Liang, Xiao; Zhu, Xing

doi:10.1016/j.brainres.2006.02.115

Cited by 83 publications

(57 citation statements)

References 35 publications

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“…4,5 Cognitive impairment has been demonstrated in animals with chronic cerebral hypoperfusion, modeling patients with vascular dementia. 21,28 Results of our experiment were in accordance with previous studies that replicated spatial memory impairment in rats with permanent Figure 3. Spatial memory evaluation using several parameters, including search error, time latency, path length (A) and swimming speed (B).…”

Section: Discussion Spatial Memory Impairment Synergistically Exacerbsupporting

confidence: 91%

“…Cell death and diffuse atrophy of the hippocampus with behavioral impairment have been reported in a rat model of transient global ischemia or chronic cerebral hypoperfusion. 21,32 On the contrary, no definite morphological change in neurons or atrophy of the hippocampus was observed in any of our experimental groups. Our results suggested that a neuronal toxic effect from the permanent occlusion of bilateral common carotid arteries, A␤ toxicity, or even a combined injury was not strong enough to induce neuronal cell death in the hippocampus.…”

contrasting

confidence: 58%

“…Neuroinflammation or demyelination with neuroinflammation has been suggested as a key pathological mechanisms of chronic cerebral hypoperfusion. [21][22][23]33 Further, microglial or astroglial activation in the hippocampus has been reported in animal models of chronic cerebral hypoperfusion or A␤ toxicity. 20,21 A rat model with a combined injury of lacunar infarction and A␤ toxicity showed increased neuroinflammation in the hippocampus.…”

Section: Mechanism Of Combined Injury From Chronic Cerebral Hypoperfumentioning

confidence: 98%

“…[21][22][23]33 Further, microglial or astroglial activation in the hippocampus has been reported in animal models of chronic cerebral hypoperfusion or A␤ toxicity. 20,21 A rat model with a combined injury of lacunar infarction and A␤ toxicity showed increased neuroinflammation in the hippocampus. 20 In our experiment, neuroinflammation was increased by the permanent occlusion of bilateral common carotid arteries and A␤ toxicity, as compared to that in sham-operated rats; however, an additional synergistic exacerbating effect was not definite in the combined injury group.…”

Section: Mechanism Of Combined Injury From Chronic Cerebral Hypoperfumentioning

confidence: 98%

“…Modeling vascular dementia in animals has been demonstrated by permanent occlusion of the bilateral common carotid arteries in rats. [21][22][23] Further, intraventricular injection of A␤ has been reported as a method for modeling of AD in rats. 24,25 In the current study, we investigated how cognitive impairment could be synergistically exacerbated in a combined injury model of chronic cerebral hypoperfusion and A␤ toxicity in rats.…”

mentioning

confidence: 99%

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Synergistic Memory Impairment Through the Interaction of Chronic Cerebral Hypoperfusion and Amlyloid Toxicity in a Rat Model

Choi

Lee²,

Han³

et al. 2011

Stroke

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Background and Purpose-Vascular pathology and Alzheimer disease (AD) pathology have been shown to coexist in the brains of dementia patients. We investigated how cognitive impairment could be exacerbated in a rat model of combined injury through the interaction of chronic cerebral hypoperfusion and amyloid beta (A␤) toxicity. Methods-In Wistar rats, chronic cerebral hypoperfusion was modeled by permanent occlusion of bilateral common carotid arteries (BCCAo). Further, AD pathology was modeled by bilateral intracerebroventricular A␤ (A␤ toxicity) using a nonphysiological A␤ peptide (A␤ 25 to 35). The experimental animals were divided into 4 groups, including sham, single injury (A␤ toxicity or BCCAo), and combined injury (BCCAo-A␤ toxicity) groups (nϭ7 per group) . Cerebral blood flow and metabolism were measured using small animal positron emission tomography. A Morris water maze task, novel object location and recognition tests, and histological investigation, including neuronal cell death, apoptosis, neuroinflammation, and AD-related pathology, were performed. Results-Spatial memory impairment was synergistically exacerbated in the BCCAo-A␤ toxicity group as compared to the BCCAo or A␤ toxicity groups (PϽ0.05). Compared to the sham group, neuroinflammation with microglial or astroglial activation was increased both in multiple white matter lesions and the hippocampus in other experimental groups. AD-related pathology was enhanced in the BCCAo-A␤ toxicity group compared to the A␤ toxicity group. Conclusion-Our experimental results support a clinical hypothesis of the deleterious interaction between chronic cerebralhypoperfusion and A␤ toxicity. Chronic cerebral hypoperfusion-induced perturbation in the equilibrium of AD-related pathology may exacerbate cognitive impairment in a rat model of combined injury. (Stroke. 2011;42:2595-2604.)Key Words: Alzheimer disease Ⅲ amyloid beta Ⅲ chronic cerebral hypoperfusion Ⅲ Morris water maze Ⅲ vascular dementia A lzheimer disease (AD) and vascular dementia are the most common causes of cognitive decline in the aging population. 1 Accumulation of insoluble amyloid beta (A␤) in the brain has been identified as the major culprit for the cognitive impairment observed in AD patients. 2 Because senile plaques composed of the A␤ peptide have been found in the brains of AD patients, 2 extensive research has focused on the amyloid hypothesis to explain AD pathology.A hypothesis emphasizing the interaction between AD and vascular pathologies has recently emerged. [3][4][5] The Nun study and other clinico-pathological studies 6 -8 have revealed that patients with AD exhibit concomitant vascular lesions in the brain. Further, epidemiological studies have shown that the major risk factors for AD mostly coincide with those for vascular dementia. 4 The Rotterdam study, 9 a large population-based prospective study, reported an increased prevalence of atherosclerosis in patients either with AD or Received March 11, 2011; accepted March 31, 2011 A converging hypothesis involving chronic ...

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Section: Discussion Spatial Memory Impairment Synergistically Exacerbsupporting

confidence: 91%

contrasting

confidence: 58%

Section: Mechanism Of Combined Injury From Chronic Cerebral Hypoperfumentioning

confidence: 98%

Section: Mechanism Of Combined Injury From Chronic Cerebral Hypoperfumentioning

confidence: 98%

mentioning

confidence: 99%

See 3 more Smart Citations

Synergistic Memory Impairment Through the Interaction of Chronic Cerebral Hypoperfusion and Amlyloid Toxicity in a Rat Model

Choi

Lee²,

Han³

et al. 2011

Stroke

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Hemodynamic changes and neuronal damage detected by 9.4 T MRI in rats with chronic cerebral ischemia and cognitive impairment

Sun

Chen

et al. 2022

Brain and Behavior

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Introduction:The bilateral common carotid artery occlusion (BCCAO) rat model is an ideal animal model for simulating the pathology of chronic brain hypoperfusion in humans. However, dynamic changes in neuronal activity, cellular edema, and neuronal structural integrity in vivo after BCCAO have rarely been reported. The purpose of this study is to use a 9.4 T MRI to explore the pathophysiological mechanisms of vascular dementia. Materials and Methods:Twelve Sprague-Dawley (SD) rats were randomly divided into two groups: the sham group and the model group (n = 6 for each group). Rats were subjected to MRI using T2*WI, diffusion tensor imaging (DTI), and DWI sequences by MRI at the following six time points: presurgery and 6 h, 3 days, 7 days, 21 days, and 28 days postsurgery. Then, the T2*, fractional anisotropy (FA), and average apparent diffusion coefficient (ADC) values were measured in the bilateral cortices and hippocampi. After MRI scanning, all rats in both groups were subjected to the Y-maze test, novel object recognition test, and open-field test to assess their learning, memory, cognition, and locomotor activity. Results:The T2*, FA, and ADC values in the cerebral cortex and hippocampus decreased sharply at 6 h after BCCAO in the model group compared with those of the sham group. By Day 28, the T2* and ADC values gradually increased to close to those in the sham group, but the FA values changed little, and the rats in the model group hadThis is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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Phytochemical and Biological Studies of Paeoniaceae

Peng

Yao-chun³

et al. 2010

Chemistry & Biodiversity

120

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Paeoniflorin attenuates chronic cerebral hypoperfusion-induced learning dysfunction and brain damage in rats

Cited by 83 publications

References 35 publications

Synergistic Memory Impairment Through the Interaction of Chronic Cerebral Hypoperfusion and Amlyloid Toxicity in a Rat Model

Synergistic Memory Impairment Through the Interaction of Chronic Cerebral Hypoperfusion and Amlyloid Toxicity in a Rat Model

Hemodynamic changes and neuronal damage detected by 9.4 T MRI in rats with chronic cerebral ischemia and cognitive impairment

Phytochemical and Biological Studies of Paeoniaceae

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