Neuroprotective effect of the ethanol extract of Artemisia capillaris on transient forebrain ischemia in mice via nicotinic cholinergic receptor

2018 ◽  
Vol 16 (6) ◽  
pp. 428-435
Author(s):  
Huiyoung Kwon ◽  
Ji Wook Jung ◽  
Young Choon Lee ◽  
Jong Hoon Ryu ◽  
Dong Hyun Kim
Keyword(s):  
Neuroprotective Effect ◽  
Ethanol Extract ◽  
Cholinergic Receptor ◽  
Forebrain Ischemia ◽  
Transient Forebrain Ischemia ◽  
Artemisia Capillaris ◽  
Nicotinic Cholinergic Receptor

scholarly journals Pycnogenol® Supplementation Attenuates Memory Deficits and Protects Hippocampal CA1 Pyramidal Neurons via Antioxidative Role in a Gerbil Model of Transient Forebrain Ischemia

Nutrients ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2477
Author(s):  
Bora Kim ◽  
Tae-Kyeong Lee ◽  
Cheol Woo Park ◽  
Dae Won Kim ◽  
Ji Hyeon Ahn ◽  
...  
Keyword(s):  
Pyramidal Neurons ◽  
Neuroprotective Effect ◽  
Ischemic Injury ◽  
Pyramidal Cells ◽  
Acid Oxidation ◽  
Forebrain Ischemia ◽  
Transient Forebrain Ischemia ◽  
Ca1 Region ◽  
Pine Tree ◽  
Before And After

Pycnogenol® (an extract of the bark of French maritime pine tree) is used for dietary supplement and known to have excellent antioxidative efficacy. However, there are few reports on neuroprotective effect of Pycnogenol® supplementation and its mechanisms against ischemic injury following transient forebrain ischemia (TFI) in gerbils. Now, we examined neuroprotective effect and its mechanisms of Pycnogenol® in the gerbils with 5-min TFI, which evokes a significant death (loss) of pyramidal cells located in the cornu ammonis (CA1) region of gerbil hippocampus from 4–5 days post-TFI. Gerbils were pretreated with 30, 40, and 50 mg/kg of Pycnogenol® once a day for 7 days before TFI surgery. Treatment with 50 mg/kg, not 30 or 40 mg/kg, of Pycnogenol® potently protected learning and memory, as well as CA1 pyramidal cells, from ischemic injury. Treatment with 50 mg/kg Pycnogenol® significantly enhanced immunoreactivity of antioxidant enzymes (superoxide dismutases and catalase) in the pyramidal cells before and after TFI induction. Furthermore, the treatment significantly reduced the generation of superoxide anion, ribonucleic acid oxidation and lipid peroxidation in the pyramidal cells. Moreover, interestingly, its neuroprotective effect was abolished by administration of sodium azide (a potent inhibitor of SODs and catalase activities). Taken together, current results clearly indicate that Pycnogenol® supplementation can prevent neurons from ischemic stroke through its potent antioxidative role.

Influence of rewarming conditions after hypothermia in gerbils with transient forebrain ischemia

1999 ◽  
Vol 91 (1) ◽  
pp. 114-120 ◽  
Author(s):  
Takehiro Nakamura ◽  
Osamu Miyamoto ◽  
Shin-Ichi Yamagami ◽  
Yoshiaki Hayashida ◽  
Toshifumi Itano ◽  
...  
Keyword(s):  
Cell Damage ◽  
Cerebral Metabolism ◽  
Neuroprotective Effect ◽  
Deep Hypothermia ◽  
Moderate Hypothermia ◽  
Forebrain Ischemia ◽  
Extracellular Glutamate ◽  
Content Type ◽  
Transient Forebrain Ischemia ◽  
Fine Print

Object. Recently, several studies have demonstrated that hypothermia has a beneficial effect on clinical outcome; however, it is difficult to determine the appropriate rewarming conditions in clinical use. The purpose of the present study was to examine the influence of rewarming conditions in gerbils with transient forebrain ischemia.Methods. Ischemia was induced in the gerbils by a 5-minute bilateral common carotid artery occlusion, after which the animals were immediately subjected to moderate or deep hypothermia. After moderate hypothermia (30.5°C for 4 hours) the animals were rewarmed over standard, fast, or slow time periods. After deep hypothermia (24°C for 2 hours) the animals were rewarmed in a standard, fast, slow, or stepwise manner. Cerebral blood flow (CBF), extracellular glutamate, and lactate were monitored. Hippocampal CA1 cell damage was assessed 7 days after induction of ischemia.In animals treated with moderate hypothermia, the rewarming rate had no influence on the number of surviving neurons. However, fast rewarming from deep hypothermia (to 37°C for 30 minutes) failed to provide the neuroprotective effect of hypothermia. Furthermore, this group showed a poor recovery of CBF (p < 0.01) and, consequently, an increase in extracellular glutamate (p < 0.01) and lactate (p < 0.01) in the hippocampus.Conclusions. The results of this study indicate a transient uncoupling of CBF and cerebral metabolism during fast rewarming from deep hypothermia, whereas slow and stepwise rewarming periods were found to be useful for protection against uncoupling of CBF and cerebral metabolism during rewarming.

scholarly journals Neuroprotective Effect of Sodium Orthovanadate on Delayed Neuronal Death after Transient Forebrain Ischemia in Gerbil Hippocampus

2001 ◽  
Vol 21 (11) ◽  
pp. 1268-1280 ◽  
Author(s):  
Takayuki Kawano ◽  
Kohji Fukunaga ◽  
Yusuke Takeuchi ◽  
Motohiro Morioka ◽  
Shigetoshi Yano ◽  
...  
Keyword(s):  
Neuronal Death ◽  
Neuroprotective Effect ◽  
Delayed Neuronal Death ◽  
Intraventricular Injection ◽  
Mongolian Gerbils ◽  
Sodium Orthovanadate ◽  
Forebrain Ischemia ◽  
Neuroprotective Effects ◽  
Transient Forebrain Ischemia ◽  
Ca1 Region

In transient forebrain ischemia, sodium orthovanadate as well as insulinlike growth factor-1 (IGF-1) rescued cells from delayed neuronal death in the hippocampal CA1 region. Adult Mongolian gerbils were subjected to 5-minute forebrain ischemia. Immunoblotting analysis with anti–phospho-Akt/PKB (Akt) antibody showed that phosphorylation of Akt at serine-473 (Akt-Ser-473) in the CA1 region decreased immediately after reperfusion, and in turn transiently increased 6 hours after reperfusion. The decreased phosphorylation of Akt-Ser-473 was not observed in the CA3 region. The authors then tested effects of intraventricular injection of orthovanadate and IGF-1, which are known to activate Akt. Treatment with orthovanadate or IGF-1 30 minutes before ischemia blocked delayed neuronal death in the CA1 region. The neuroprotective effects of orthovanadate and IGF-1 were associated with preventing decreased Akt-Ser-473 phosphorylation in the CA1 region observed immediately after reperfusion. Immunohistochemical studies with the anti–phospho-Akt-Ser-473 antibody also demonstrated that Akt was predominantly in the nucleus and was moderately activated in the cell bodies and dendrites of pyramidal neurons after orthovanadate treatment. The orthovanadate treatment also prevented the decrease in phosphorylation of mitogen-activated protein kinase (MAPK). Pretreatment with combined blockade of phosphatidylinositol 3-kinase and MAPK pathways totally abolished the orthovanadate-induced neuroprotective effect. These results suggest that the activation of both Akt and MAPK activities underlie the neuroprotective effects of orthovanadate on the delayed neuronal death in the CA1 region after transient forebrain ischemia.

scholarly journals Stimulation of β2-Adrenoceptors Inhibits Apoptosis in Rat Brain after Transient Forebrain Ischemia

1998 ◽  
Vol 18 (9) ◽  
pp. 1032-1039 ◽  
Author(s):  
Yuan Zhu ◽  
Carsten Culmsee ◽  
Irina Semkova ◽  
Josef Krieglstein
Keyword(s):  
Neuronal Damage ◽  
Neuroprotective Effect ◽  
Global Ischemia ◽  
Neuroprotective Activity ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tunel Staining ◽  
Forebrain Ischemia ◽  
Transient Forebrain Ischemia ◽  
Dna Laddering

We have previously demonstrated that the neuroprotective effect of the β2-adrenoceptor agonist clenbuterol in vitro and in vivo was most likely mediated by an increased nerve growth factor (NGF) expression. In the present study, we examined whether clenbuterol was capable of inhibiting apoptosis caused by ischemia. Transient forebrain ischemia was performed in male Wistar rats (300 to 350 g) by clamping both common carotid arteries and reducing the blood pressure to 40 mm Hg for 10 minutes. Clenbuterol(0.1, 0.5, and 1.0 mg/kg intraperitoneally) was administered 3 hours before ischemia or immediately after ischemia. The brains were removed for histologic evaluation 7 days after ischemia. The time course of DNA fragmentation was determined 1, 2, 3 and 4 days after ischemia. Staining with terminal deoxynucleotidyl transferase(TdT)-mediated dUTP nick end-labeling (TUNEL) was used for further analysis of DNA fragments in situ 3 days after ischemia. The NGF protein was assayed by enzyme-linked immunosorbent assay. Ten-minute forebrain ischemia damaged 80% to 90% of the neurons in the hippocampal CA1 region evaluated 7 days after ischemia. Pretreatment with clenbuterol (0.5 and 1.0 mg/kg) reduced the neuronal damage by 18.1% ( P< 0.01) and 13.1% ( P < 0.05), respectively. The neuroprotective effect also was found when clenbuterol (0.5 mg/kg) was administered immediately after ischemia ( P < 0.05). The DNA laddering appeared in striatum 1 day and in hippocampus 2 days after ischemia and peaked on the third day in both regions. The DNA laddering was nearly abolished in the hippocampus and partially blocked in striatum and cortex by 0.5 mg/kg clenbuterol. These results were confirmed by TUNEL staining. Clenbuterol (0.5 mg/kg intraperitoneally) elevated the NGF protein level by 33% ( P < 0.05) in the hippocampus and 41% ( P < 0.05) in the cortex 6 hours after ischemia. Three days after ischemia, the NGF levels in these regions were no longer different between the clenbuterol-treated and control groups. This study clearly demonstrates that clenbuterol possesses a neuroprotective activity and a marked capacity to inhibit DNA degradation after global ischemia. The results suggest that clenbuterol increases NGF expression during the first hours after global ischemia and thereby protects neurons against apoptotic damage.

Neuroprotective effect of mivazerol, an alpha2-agonist, after transient forebrain ischemia in rats*

2005 ◽  
Vol 49 (8) ◽  
pp. 1117-1123 ◽  
Author(s):  
T. Kimura ◽  
M. Sato ◽  
T. Nishikawa ◽  
M. Tanaka ◽  
Y. Tobe ◽  
...  
Keyword(s):  
Neuroprotective Effect ◽  
Forebrain Ischemia ◽  
Transient Forebrain Ischemia

scholarly journals Intraventricular Administration of Insulin and IGF-1 in Transient Forebrain Ischemia

1994 ◽  
Vol 14 (2) ◽  
pp. 237-242 ◽  
Author(s):  
C. Z. Zhu ◽  
R. N. Auer
Keyword(s):  
Growth Factor ◽  
Insulin Action ◽  
Neuroprotective Effect ◽  
Direct Interaction ◽  
High Dose ◽  
Hippocampal Damage ◽  
Intraventricular Administration ◽  
Forebrain Ischemia ◽  
Transient Forebrain Ischemia ◽  
Glucose Levels

A beneficial effect of insulin in reducing cerebral ischemic damage has been recently demonstrated, and a direct central mechanism of insulin action in cerebral ischemia has been proposed. To test the hypothesis that one of the neuroprotective mechanisms of insulin action involves a direct interaction with CNS tissue via a growth factor effect, a continuous intraventricular infusion of two doses of insulin and of insulin-like growth factor 1 (IGF-1) was given to fed Wistar rats subjected to 10 min, 15 s of transient forebrain ischemia. Quantitative neuropathology after 1-week survival showed that low-dose insulin (7 IU/rat/day; n = 10) reduced selective necrosis in the striatum (p = 0.015) and one level of the hippocampus (p = 0.023) as compared with animals infused with phosphate-buffered saline (200 μl/rat/day; n = 8). IGF-1 (50 μg/rat/day; n = 8) significantly ameliorated hippocampal damage in four of the six hippocampal levels (p < 0.05). High-dose insulin infusion (23 IU/rat/day; n = 8) produced a robust reduction in cortical (p = 0.0108), striatal (p = 0.003), and hippocampal (p < 0.05) necrosis at all coronal levels. However, this high-dose insulin reduced the blood sugar significantly (p < 0.01), from 11.8 to 7.8 m M, probably by virtue of centrally administered insulin reaching the periphery. We conclude that insulin and IGF-1 offer a moderate, centrally mediated, neuroprotective effect, likely mediated at least in part via a growth factor mechanism. In addition, we confirm our earlier findings that higher doses of insulin, accompanied by lowering of peripheral blood glucose levels even within the physiologic range, yield the greatest protective effect.

scholarly journals Pre-Treatment with Laminarin Protects Hippocampal CA1 Pyramidal Neurons and Attenuates Reactive Gliosis Following Transient Forebrain Ischemia in Gerbils

Marine Drugs ◽  
2020 ◽  
Vol 18 (1) ◽  
pp. 52 ◽  
Author(s):  
Tae-Kyeong Lee ◽  
Ji Hyeon Ahn ◽  
Cheol Woo Park ◽  
Bora Kim ◽  
Young Eun Park ◽  
...  
Keyword(s):  
Calcium Binding ◽  
Neuroprotective Effect ◽  
Ischemia Reperfusion ◽  
Brown Seaweed ◽  
Reactive Gliosis ◽  
Cresyl Violet ◽  
Forebrain Ischemia ◽  
Transient Forebrain Ischemia ◽  
Hippocampal Ca1 ◽  
Fluoro Jade B

Transient brain ischemia triggers selective neuronal death/loss, especially in vulnerable regions of the brain including the hippocampus. Laminarin, a polysaccharide originating from brown seaweed, has various pharmaceutical properties including an antioxidant function. To the best of our knowledge, few studies have been conducted on the protective effects of laminarin against ischemic injury induced by ischemic insults. In this study, we histopathologically investigated the neuroprotective effects of laminarin in the Cornu Ammonis 1 (CA1) field of the hippocampus, which is very vulnerable to ischemia-reperfusion injury, following transient forebrain ischemia (TFI) for five minutes in gerbils. The neuroprotective effect was examined by cresyl violet staining, Fluoro-Jade B histofluorescence staining and immunohistochemistry for neuronal-specific nuclear protein. Additionally, to study gliosis (glial changes), we performed immunohistochemistry for glial fibrillary acidic protein to examine astrocytes, and ionized calcium-binding adaptor molecule 1 to examine microglia. Furthermore, we examined alterations in pro-inflammatory M1 microglia by using double immunofluorescence. Pretreatment with 10 mg/kg laminarin failed to protect neurons in the hippocampal CA1 field and did not attenuate reactive gliosis in the field following TFI. In contrast, pretreatment with 50 or 100 mg/kg laminarin protected neurons, attenuated reactive gliosis and reduced pro-inflammatory M1 microglia in the CA1 field following TFI. Based on these results, we firmly propose that 50 mg/kg laminarin can be strategically applied to develop a preventative against injuries following cerebral ischemic insults.

Sign in / Sign up

Export Citation Format

Share Document