The Japanese Angelica acutiloba root and yokukansan increase hippocampal acetylcholine level, prevent apoptosis and improve memory in a rat model of repeated cerebral ischemia

Ai, Nogami-Hara; Nagao, Masaki; Takasaki, Kotaro; Egashira, Nobuaki; Fujikawa, Risako; Kubota, Kaori; Katsurabayashi, Shutaro; Hatip, Funda Bölükbaşı; Hatip‐Al‐Khatib, Izzettin; Iwasaki, Katsunori

doi:10.1016/j.jep.2017.12.025

Cited by 13 publications

(14 citation statements)

References 41 publications

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“…Furthermore, YKS increased expression of dynamin 1 in the hippocampus in those rats, suggesting that the modulation of dynamin 1 by YKS may be related to the increase in ACh release. Recently, we also showed that YKS and Angelica root increased the release of ACh in rats undergoing repeated cerebral ischemia . The increase in ACh release is thought to contribute to the positive effects of YKS on memory impairment.…”

Section: Neuropharmacological Effectsmentioning

confidence: 86%

“…Yokukansan reduced hippocampal neuronal death and inhibited the ischemia‐induced inflammatory response and DNA oxidative damage in a gerbil model of global cerebral ischemia . YKS and Angelica root prevented hippocampal apoptosis in a rat model of repeated cerebral ischemia . More recently, YKS has been reported to reduce the formation of hydroxyl radicals in cerebral ischemic injury .…”

Section: Neuropharmacological Effectsmentioning

confidence: 96%

“…YKS also reduced hippocampal neuronal death after brain ischemia via inhibition of the ischemia‐induced inflammatory response and DNA oxidative damage. YKS and Japanese Angelica root, one of the constituent herbs of YKS, improved the memory deficits, increased the release of ACh, and prevented hippocampal apoptosis in a rat model of repeated cerebral ischemia . Moreover, YKS has been reported to ameliorate learning deficits in the Tg2576 mouse model of AD and in senescence‐accelerated mouse prone‐8 (SAMP8) mice as assessed using the Morris water‐maze test.…”

Section: Behavioral Effectsmentioning

confidence: 99%

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Pharmacological effects of yokukansan on behavioral and psychological symptoms of dementia

Egashira

Iwasaki

2019

Traditional & Kampo Medicine

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Background Cognitive dysfunction is often accompanied by behavioral and psychological symptoms of dementia (BPSD) in patients with Alzheimer's disease and other forms of senile dementia. BPSD include agitation, aggression, and hallucinations. BPSD have a serious effect on the quality of life of dementia patients and their caregivers, but effective drug therapy for BPSD has not been identified as yet. Typical and atypical antipsychotics that are used for the treatment of BPSD are known to cause a variety of extrapyramidal adverse events. Yokukansan (YKS, Yi‐gan san in Chinese) is a Japanese traditional herbal (kampo) medicine that is used to alleviate night‐crying and irritation in children, as well as to treat neurosis and insomnia. It is currently also used to treat BPSD. Methods In this review, we summarize the pharmacological effects of YKS in the context of BPSD. Conclusion YKS is expected to be useful in treating and/or preventing BPSD.

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Section: Neuropharmacological Effectsmentioning

confidence: 86%

Section: Neuropharmacological Effectsmentioning

confidence: 96%

Section: Behavioral Effectsmentioning

confidence: 99%

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Pharmacological effects of yokukansan on behavioral and psychological symptoms of dementia

Egashira

Iwasaki

2019

Traditional & Kampo Medicine

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“…e present study expanded our previous research and investigated the potential neuroprotective mechanisms of GTPs concerning endogenous antioxidation and ER stress. e imbalance of oxidation and antioxidation is a direct reason for deficits of neurological functions and high mortality during CIRI [24,25]. GTPs possess higher antioxidant activity than vitamin E and vitamin C [26,27].…”

Section: Discussionmentioning

confidence: 99%

Green Tea Polyphenols Modulated Cerebral SOD Expression and Endoplasmic Reticulum Stress in Cardiac Arrest/Cardiopulmonary Resuscitation Rats

Qin

Chen

et al. 2020

BioMed Research International

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Background. Reducing cerebral ischemia-reperfusion injury is crucial for improving survival and neurologic outcomes after cardiac arrest/cardiopulmonary resuscitation (CA/CPR). The purpose of this study is to investigate the neuroprotective effects of green tea polyphenols (GTPs) concern with the modulation of endogenous antioxidation and endoplasmic reticulum stress. Methods. After subjecting to CA/CPR, rats were randomized into the saline group (NS, n = 40) and the GTPs group (GTPs, n = 40). Each group was blindly located into four subgroups according to four time points (12 h, 24 h, 48 h, and 72 h). Other rats without experiencing CA/CPR severed as the Sham group (Sham, n = 10). Brain tissue samples were harvested at relative time points. The expressions of superoxide dismutase 1 (SOD1), superoxide dismutase 2 (SOD2), caspase-3, and C/EBP-homologous protein (CHOP) were detected by immunofluorescence, dead neurons were assayed by TUNEL staining, and the expressions of caspase-12 and glucose-regulated proteins 78 kDa (GRP78) were evaluated by western blotting, respectively. Results. Comparing with that in NS group, GTPs increased the expression of SOD1 and SOD2 at 12 h, 24 h, 48 h, 72 h, and the expression of GRP78 at 24 h and 48 h (p<0.05) butdecreased caspase-12, CHOP, caspase-3 level, and apoptotic number of neurons (p<0.05) after restoration of spontaneous circulation (ROSC). Conclusion. GTPs exert neuroprotective effects via mechanisms that may be related to the enhancement of endogenous antioxidant capacity and inhibition of endoplasmic reticulum stress in CA/CPR rat models.

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“…The pathogenesis of IRI involves a complex sequence of physiological events, including documented inflammatory cascade, excitotoxicity, oxidative stress, deficiencies in nerve growth factor, and presence of apoptosis [ 6 – 8 ]. Accumulating evidence suggests that neuronal apoptosis represents a prominent form of cell death which leads to declines in neurological functions during IRI [ 9 , 10 ]. Because intact neurons are the basis of normal nerve function, inhibition of neuronal apoptosis contributes to the recovery of neurological function and effectively improves the long-term prognosis of patients.…”

Section: Introductionmentioning

confidence: 99%

Protective Effects of Oleuropein Against Cerebral Ischemia/Reperfusion by Inhibiting Neuronal Apoptosis

Zhang

Liu

2018

Med Sci Monit

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BackgroundIn this study, we investigated the potential neuroprotective effect of oleuropein (OLE) on apoptotic changes via modulating Akt/glycogen synthase kinase 3 beta (Akt/GSK-3β) signaling in a rat model of cerebral ischemia/reperfusion injury (IRI).Material/MethodsSprague-Dawley male rats (12 weeks, n=200) were randomly assigned to 5 groups: sham group, vehicle (IRI+ vehicle) group, OLE (IRI+OLE) group, OLE+LY294002 (IRI+OLE+LY294002) group, and LY294002(IRI+LY294002) group. The rats were subjected to cerebral ischemia/reperfusion injury (IRI) model and treated once daily for 5 days with vehicle and OLE (100 mg/kg via intraperitoneal injection) after IRI injury. LY294002 (0.3 mg/kg) was intraperitoneally injected once at 30 min after IRI injury. Brain edema, neurological deficit, rotarod latencies, and Morris water maze (MWM) performance were evaluated after IRI. The number of dead cells were assayed by TUNEL staining. Western blot was used to detect the expression of Bcl-2, Bax, cleaved caspase-3 (CC3), neurotrophic factors, and the phosphorylation levels of Akt and GSK-3β.ResultsCompared with the vehicle group, brain water content, neurological deficits, rotarod latencies, and escape latency following IRI were reduced in the OLE group. Cell apoptosis and reduced neurotrophic factor caused by IRI was also attenuated by OLE. Furthermore, increased p-Akt and decreased p-GSK-3β were caused by OLE, which were associated with decrease of Bax/Bcl-2 ratio and the suppression of Caspase-3 activity after IRI. Importantly, all the beneficial effects of OLE in the vehicle group were abrogated by PI3K inhibitor LY294002.ConclusionsCerebral ischemia was protected by OLE via suppressing apoptosis through the Akt/GSK-3β pathway and upregulating neurotrophic factor after IRI.

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The Japanese Angelica acutiloba root and yokukansan increase hippocampal acetylcholine level, prevent apoptosis and improve memory in a rat model of repeated cerebral ischemia

Cited by 13 publications

References 41 publications

Pharmacological effects of yokukansan on behavioral and psychological symptoms of dementia

Pharmacological effects of yokukansan on behavioral and psychological symptoms of dementia

Green Tea Polyphenols Modulated Cerebral SOD Expression and Endoplasmic Reticulum Stress in Cardiac Arrest/Cardiopulmonary Resuscitation Rats

Protective Effects of Oleuropein Against Cerebral Ischemia/Reperfusion by Inhibiting Neuronal Apoptosis

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