Protective effects of Bacopa monnieri on ischemia-induced cognitive deficits in mice: The possible contribution of bacopaside I and underlying mechanism

Le, Xoan Thi; Pham, Hang Thi Nguyet; Nguyen, Tai Van; Nguyen, Khoi Tan; Tanaka, Ken; Fujiwara, Hironori; Matsumoto, Kinzo

doi:10.1016/j.jep.2015.01.041

Cited by 53 publications

(26 citation statements)

References 25 publications

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“…After years of investigating neuronal vulnerability to ischemic damage through different models of mimicking ischemic insults in situ , it has been emerged that the degree of neuronal damage and ultimate cell death strictly depend on severity of such modeling (e.g., a duration of lesion). Our results of a sharp neuronal loss and overwhelmed astrogliosis within destructive CA1 area by prolonged OGD (30 min duration) also argue for that, being fully consistent with previous reports of a massive cell death by OGD lasting up to an hour (Graulich et al, 2002; Rytter et al, 2003; Jung et al, 2004; Le et al, 2015) and astrogliosis (Cho et al, 2013; Honsa et al, 2014). In contrast to 30-min OGD, mild OGD (10-min duration) produced a little destruction to the hippocampal tissue, justified by a steady level of both NeuN-positive and PI-positive cells shortly after induction of mild OGD, similar to other studies (Matsuzaki et al, 1997; Lecoeur, 2002).…”

Section: Discussionsupporting

confidence: 92%

“…Over decades after the ischemic death of CA1 neurons had been established, studies were predominantly focused on a short-term CA1 neuronal death, which takes 2–3 days to become morphologically observed (Pamenter et al, 2012; Chip et al, 2013; Le et al, 2015; Secondo et al, 2015). However, much less attention has been paid toward ischemic impairments occurring later—within the time-frame of 1–3 weeks following lesion.…”

Section: Introductionmentioning

confidence: 99%

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Optimized Model of Cerebral Ischemia In situ for the Long-Lasting Assessment of Hippocampal Cell Death

Rybachuk¹,

Kopach²,

Krotov³

et al. 2017

Front. Neurosci.

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Among all the brain, the hippocampus is the most susceptible region to ischemic lesion, with the highest vulnerability of CA1 pyramidal neurons to ischemic damage. This damage may cause either prompt neuronal death (within hours) or with a delayed appearance (over days), providing a window for applying potential therapies to reduce or prevent ischemic impairments. However, the time course when ischemic damage turns to neuronal death strictly depends on experimental modeling of cerebral ischemia and, up to now, studies were predominantly focused on a short time-window—from hours to up to a few days post-lesion. Using different schemes of oxygen-glucose deprivation (OGD), the conditions taking place upon cerebral ischemia, we optimized a model of mimicking ischemic conditions in organotypical hippocampal slices for the long-lasting assessment of CA1 neuronal death (at least 3 weeks). By combining morphology and electrophysiology, we show that prolonged (30-min duration) OGD results in a massive neuronal death and overwhelmed astrogliosis within a week post-OGD whereas OGD of a shorter duration (10-min) triggered programmed CA1 neuronal death with a significant delay—within 2 weeks—accompanied with drastically impaired CA1 neuron functions. Our results provide a rationale toward optimized modeling of cerebral ischemia for reliable examination of potential treatments for brain neuroprotection, neuro-regeneration, or testing neuroprotective compounds in situ.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Optimized Model of Cerebral Ischemia In situ for the Long-Lasting Assessment of Hippocampal Cell Death

Rybachuk¹,

Kopach²,

Krotov³

et al. 2017

Front. Neurosci.

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“…This test was conducted as previously described (Le et al, 2015;Yamada et al, 2011;Xu et al, 2015) with minor modifications. Briefly, each mouse was first habituated to the test arena (W 25 Â L 35Â H 40 cm) for 10 min/day for 3 days.…”

Section: Behavior Testing Analysismentioning

confidence: 99%

Hypothermia-induced ischemic tolerance is associated with Drp1 inhibition in cerebral ischemia-reperfusion injury of mice

et al. 2016

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“…Our findings suggested that treatments with BM are beneficial for dementia and other neurodegenerative disorders. 10) This idea was further supported by our previous studies using in vivo and in vitro models of cerebral ischemia. In an in vivo study using a transient two vessel occlusion mouse model (T2VO), we found that the standardized BME containing 21.8% bacoside A and 11.0% bacopaside I attenuated transient cerebral ischemia-induced cognitive deficits.…”

Section: Introductionmentioning

confidence: 64%

“…The present results provide further support to our idea that BME is beneficial for the treatment of cognitive dysfunctions caused by various insults related to cerebral ischemia and Alzheimer's disease, which lead to neuronal damage/degeneration. 10,11) We previously demonstrated that BME ameliorated OBX-induced cognitive impairments in mice and that this effect was attributable to several mechanisms, such as the inhibition of acetylcholinesterase activity, enhanced synaptic plasticity-related signaling in the hippocampus, and the prevention of OBX-induced medial septal cholinergic neurons projecting to the hippocampus. 10) On the other hand, evidence indicates that TMT-induced cognitive deficits are also mediated by dysfunctional central cholinergic systems 23) as well as neurosignaling systems including BDNF and cAMP response element-binding protein (CREB) in the hippocampus.…”

Section: Discussionmentioning

confidence: 99%

<i>Bacopa monnieri</i> (L.) Ameliorates Cognitive Deficits Caused in a Trimethyltin-Induced Neurotoxicity Model Mice

Pham

Phan²,

Tran

et al. 2019

Biological & Pharmaceutical Bulletin

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We previously demonstrated that Bacopa monnier (L.) WETTST. extract (BME) ameliorated cognitive dysfunction in animal models of dementia by enhancing synaptic plasticity-related signaling in the hippocampus and protecting cholinergic neurons in the medial septum. To further clarify the pharmacological features and availability of BME as a novel anti-dementia agent, we investigated whether BME affects neuronal repair using a mouse model of trimethyltin (TMT)-induced neuronal loss/self-repair in the hippocampus. Mice pretreated with TMT (2.8 mg/kg, intraperitoneally (i.p.)) on day 0 were given BME (50 mg/kg, per os (p.o.)) once daily for 15-30 d. Cognitive performance of the animals was elucidated twice by the object location test and modified Y maze test on days 17-20 (Phase I) and days 32-35 (Phase II) or by the passive avoidance test on Phase II. TMT impaired hippocampus-dependent spatial working memory and amygdala-dependent fear-motivated memory. The administration of BME significantly prevented TMT-induced cognitive deficits. The protective effects of BME on the spatial memory deficits were confirmed by Nissl staining of hippocampal tissues and propidium iodide staining of organotypic hippocampal slice cultures. Immunohistochemical studies conducted on days 17 and 32 revealed that thirty days of treatment with BME increased the number of 5-bromo-2′-deoxyuridine (BrdU)-immunopositive cells in the dentate gyrus region of TMT-treated mice, whereas fifteen days of treatment with BME had no effect. These results suggest that BME ameliorates TMT-induced cognition dysfunction mainly via protecting the hippocampal neurons from TMT-induced hippocampal lesions and partly via promoting neuroregeneration in the dentate gyrus regions.

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Protective effects of Bacopa monnieri on ischemia-induced cognitive deficits in mice: The possible contribution of bacopaside I and underlying mechanism

Cited by 53 publications

References 25 publications

Optimized Model of Cerebral Ischemia In situ for the Long-Lasting Assessment of Hippocampal Cell Death

Optimized Model of Cerebral Ischemia In situ for the Long-Lasting Assessment of Hippocampal Cell Death

Hypothermia-induced ischemic tolerance is associated with Drp1 inhibition in cerebral ischemia-reperfusion injury of mice

<i>Bacopa monnieri</i> (L.) Ameliorates Cognitive Deficits Caused in a Trimethyltin-Induced Neurotoxicity Model Mice

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