상단 PDF Neuroprotection of AG490 in Oxidative Stress-induced Neuronal Death

Neuroprotection of AG490 in Oxidative Stress-induced Neuronal Death

Neuroprotection of AG490 in Oxidative Stress-induced Neuronal Death

스의 관계를 알아보고, 산화적 스트레스에 의해 생성된 활성산소의 조절을 관찰 하며, 미토콘드리아의 기능의 변화를 관찰하였다. AG490은 특이적인 산화제에 의 해서 인산화된 JAK2의 인산화를 억제시키고, 약물 자체가 항산화제 활성을 가지 고 있음을 알게 되었다. 약물의 구조적 특징에 의한 항산화제 활성 이외에도 AG490은 세포내의 글루타티온 (GSH)의 양을 증가시켜서 산화적 스트레스로 유 도되는 활성산소를 감소시켰다. 또한, AG490은 산화적 스트레스에 의해서 유도되 는 미토콘드리아 막전위의 감소를 막아서 신경세포의 사멸을 억제한다.
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Protective role of <i>Populus tomentiglandulosa</i> against hydrogen peroxide-induced oxidative stress in SH-SY5Y neuronal cells

Protective role of <i>Populus tomentiglandulosa</i> against hydrogen peroxide-induced oxidative stress in SH-SY5Y neuronal cells

The • OH radical scavenging activity of PT was evaluated using the method described by Chung et al. [18]. In the dark, 1400 µL of extract and four fractions from PT were mixed with 200 µL of 10 mM FeSO 4 ·7H 2 O-EDTA, 200 µL of 10 mM 2-deoxyribose solution, and 200 µL of 10 mM H 2 O 2 . The mixed solutions were incubated at 37 o C for 4 h, and then 1 mL of 1% TBA and 1 mL of 2.8% TCA were added. The mixtures were boiled for 20 min and cooled on ice. The absorbance of the mixture in a 96-well plate was read at an absorbance of 490 nm using a microplate reader. The • OH radical scavenging activity was calculated as follows:
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Protective effect of Eucommia ulmoides oliver leaves against PM<sub>2.5</sub>-induced oxidative stress in neuronal cells in vitro

Protective effect of Eucommia ulmoides oliver leaves against PM<sub>2.5</sub>-induced oxidative stress in neuronal cells in vitro

Microglial apoptosis 개선 효과 뇌에서 대식세포의 역할을 하는 microglia인 BV-2 세포는 신경 계의 면역세포로 작용하고, BV-2 세포는 외부 및 내부 자극을 통 해 활성화되어 다양한 전 염증성 사이토카인을 분비한다. 외부 및 내부 자극으로 인한 염증이 과도하게 발생하게 되면, 신경 퇴 화에 관여하는 신경 염증을 유발하게 된다(Bozic 등, 2015). 따라 서 외부 자극으로부터 염증반응을 매개하기 위해 세포막에 존재 하는 Toll-like receptor (TLR) 복합체가 활성화되고, 이는 신호 전 달에 의해 세포 증식 및 생존에 관여하는 phosphatidylinositol-3- kinase (PI3K)/Akt 경로와 세포 자살에 관여하는 c-Jun N-terminal kinases (JNK) 경로 및 nuclear factor kappa light chain enhancer of activated B cells (NF-κB) 경로 등이 조절된다(Khanna 등, 2015). 하지만 과도한 산화적 스트레스는 염증반응으로 인한 세 포 자살의 경로를 활성화시키고, 이들은 Akt, JNK, NF-κB 등을 포함하는 전사인자의 인산화를 유도한다. 또한, TNF-α, IL-1β 및 IL-6 와 같은 염증성 사이토카인을 과분비하며, caspase-3, caspase- 7 과 같은 인자의 발현을 유도해 caspase 의존성 세포 사멸을 유 발한다(Ni 등, 2015; Reuter 등, 2010). PM 2.5 는 이러한 면역계 세 포를 활성화시켜 염증반응을 매개할 수 있으며, BV-2 세포의 활 성화는 뇌 신경염증을 유도해 결과적으로 뇌 신경세포의 손상을 초래한다. 따라서 본 연구에서는 PM 2.5 를 처리한 BV-2 세포에서 세포 사멸 및 염증 반응에 관여하는 인자의 발현 수준을 확인함 으로써 EFEL이 가지는 개선 효과를 확인하였다.
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Agmatine pretreatment attenuates retinal ganglion cell death by an oxidative stress

Agmatine pretreatment attenuates retinal ganglion cell death by an oxidative stress

Primary cultures of RGCs have some limitations to study RGC pathophysiology. Despite the fact that transformed rat retinal ganglion cell line (RGC-5 cell) has a number of characteristics of normal RGCs, it is mitotically active and is not exactly same as primary RGCs. It has been shown that RGC-5 cells treated by the broad-spectrum protein kinase inhibitor staurosporine are not dividing and maintain neuronal characteristics. 10-12

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Butin (7,3′,4′-trihydroxydihydroflavone) reduces oxidative stress-induced cell death via inhibition of the mitochondria-dependent apoptotic pathway

Butin (7,3′,4′-trihydroxydihydroflavone) reduces oxidative stress-induced cell death via inhibition of the mitochondria-dependent apoptotic pathway

Moreover, elevation of phospho Bcl-2 by H 2 O 2 treatment further helps to reduce its ability to bind with Bax and enhance translocation of Bax from the cytosol to mitochondria, leading to an enhanced susceptibility of the cells to apoptosis [32]. Butin significantly restored these changes induced by H 2 O 2 . These results confirmed that butin inhibited H 2 O 2 -induced apoptosis associated with regulation of Bcl-2 family proteins. Changes in caspases 9 and 3 protein expressions were evaluated for the underlying mechanisms, as cleaved caspases 9 and 3 represent downstream signals of apoptosis and the Bcl-2 protein can prevent activation of caspases during apoptosis. Butin inhibited H 2 O 2 -induced activation of caspases 9 and 3. Treatment of cells with butin showed anti-apoptotic effects in cells exposed to H 2 O 2 , as shown by apoptotic body formation, sub G 1 -hypodiploid cells levels and nuclear fragmentation.
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Protective effect of 7,8-dihydroxyflavone against oxidative stress in high glucose-damaged neuronal cells

Protective effect of 7,8-dihydroxyflavone against oxidative stress in high glucose-damaged neuronal cells

- 31 - DISCUSSION Oxidative stress plays a pivotal role in cellular injury induced by hyperglycemia. High glucose level can stimulate free radical production. Thus, a weak defense system becomes unable to counteract the enhanced ROS generation and, as a result, an imbalance occurs which leads to oxidative stress [20, 21]. In the present study, we demonstrated that 7,8-DHF dramatically inhibited high glucose-induced cell death, apoptosis, and mitochondrial dysfunction. 7,8-DHF protective effect might be attributed to its powerful antioxidant action, as evidenced by the markedly reduced ROS.
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Effects of propofol-induced autophagy against oxidative stress in human osteoblasts

Effects of propofol-induced autophagy against oxidative stress in human osteoblasts

In other studies, administration of anesthetic agents was found to result in pharmacologic preconditioning against oxidative injury [20,21]. Autophagy is a conserved cellular catabolic process that can engulf cytoplasmic components and degrade them through the lysosomal pathway, thus, they can then be recycled. Generally, autophagy is thought to be induced under stress conditions [22-24]. However, whether the induction of autophagy contributes to cell survival or cell death remains elusive. Oxidative injury is one of the most common causes of bone remodeling inhibition. Therefore, a sustainable drug is needed to identify better, safer anabolic agents with low cytotoxicity that act by either increasing osteoblast proliferation or differentiation to enhance bone formation [25]. Several lines of evidence have shown that anesthesia drugs may have a beneficial effect on bone loss and fracture outcomes [26]. On the basis of this, it was hypothesized that the antioxidant properties of propofol may protect human fetal osteoblast (hFOB) cells against oxidative injury caused by H 2 O 2 . Therefore, the aim of this study was to evaluate the protective effects of propofol- mediated autophagy activation on oxidative stress induced by H 2 O 2 treatment in the hFOB cell line.
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Protective effect of <i>Eucommia ulmoides</i> oliver leaves against PM<sub>2.5</sub>-induced oxidative stress in neuronal cells <i>in vitro</i>

Protective effect of <i>Eucommia ulmoides</i> oliver leaves against PM<sub>2.5</sub>-induced oxidative stress in neuronal cells <i>in vitro</i>

Microglial apoptosis 개선 효과 뇌에서 대식세포의 역할을 하는 microglia인 BV-2 세포는 신경 계의 면역세포로 작용하고, BV-2 세포는 외부 및 내부 자극을 통 해 활성화되어 다양한 전 염증성 사이토카인을 분비한다. 외부 및 내부 자극으로 인한 염증이 과도하게 발생하게 되면, 신경 퇴 화에 관여하는 신경 염증을 유발하게 된다(Bozic 등, 2015). 따라 서 외부 자극으로부터 염증반응을 매개하기 위해 세포막에 존재 하는 Toll-like receptor (TLR) 복합체가 활성화되고, 이는 신호 전 달에 의해 세포 증식 및 생존에 관여하는 phosphatidylinositol-3- kinase (PI3K)/Akt 경로와 세포 자살에 관여하는 c-Jun N-terminal kinases (JNK) 경로 및 nuclear factor kappa light chain enhancer of activated B cells (NF-κB) 경로 등이 조절된다(Khanna 등, 2015). 하지만 과도한 산화적 스트레스는 염증반응으로 인한 세 포 자살의 경로를 활성화시키고, 이들은 Akt, JNK, NF-κB 등을 포함하는 전사인자의 인산화를 유도한다. 또한, TNF-α, IL-1β 및 IL-6 와 같은 염증성 사이토카인을 과분비하며, caspase-3, caspase- 7 과 같은 인자의 발현을 유도해 caspase 의존성 세포 사멸을 유 발한다(Ni 등, 2015; Reuter 등, 2010). PM 2.5 는 이러한 면역계 세 포를 활성화시켜 염증반응을 매개할 수 있으며, BV-2 세포의 활 성화는 뇌 신경염증을 유도해 결과적으로 뇌 신경세포의 손상을 초래한다. 따라서 본 연구에서는 PM 2.5 를 처리한 BV-2 세포에서 세포 사멸 및 염증 반응에 관여하는 인자의 발현 수준을 확인함 으로써 EFEL이 가지는 개선 효과를 확인하였다.
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Inducible nitric oxide synthase is involved in neuronal death induced by trimethyltin in the rat hippocampus

Inducible nitric oxide synthase is involved in neuronal death induced by trimethyltin in the rat hippocampus

stress 에 의해 생성되는 nitric oxide 와 관련된 inducible nitric oxide synthase 가 높은 연관성을 갖는다고 생각된 다 . TMT 에 의한 신경세포의 사멸이 각 부위에 따라 신 호전달경로의 정도가 다를 것으로 여겨지나 , 구체적인 신호전달 경로의 차이를 규명하기 위해서 추가적인 연 구가 이루어져야 할 것이다 .

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Protective effects of red ginseng treated with gold nanoparticles against H<sub>2</sub>O<sub>2</sub>-induced oxidative stress in neuronal PC-12 cells

Protective effects of red ginseng treated with gold nanoparticles against H<sub>2</sub>O<sub>2</sub>-induced oxidative stress in neuronal PC-12 cells

현재까지 홍삼과 금재를 이용한 다양한 생리활성에 관한 연구 는 활발히 이루어지고 있음에도 불구하고, 금 나노입자 용액을 인삼에 시비하여 재배한 응용 연구는 전무하다. 따라서, 본 연구 에서는 금 나노입자 용액을 시비하여 재배한 6년근 인삼을 홍삼 으로 제조하여, 황금홍삼 열수 추출물의 총페놀 함량, 총플라보 노이드 함량 및 산화방지능을 정량적으로 분석하였다. 또한 PC- 12 신경세포를 이용하여 황금홍삼 추출물이 산화스트레스(oxidative stress) 로부터 신경세포 보호능을 평가하고, 신경전달물질인 아세 틸콜린의 가수분해에 관여하는 아세틸콜린가수분해효소(acetylcho- linesterase, AChE) 및 부틸콜린가수분해효소(butyrylcholinesterase, BChE) 의 활성 억제능을 측정함으로써 황금홍삼 추출물의 인지기 능 개선 소재로서의 가능성을 확인하고자 하였다.
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Protective effect of phloroglucinol against gamma radiation-induced oxidative stress in hair follicles

Protective effect of phloroglucinol against gamma radiation-induced oxidative stress in hair follicles

Departments of 1 Advanced Convergence Technology & Science, 2 Veterinary Medicine, 3 Marine Life Sciences, 4 Civil and Enviromental Engineering, and 5 Nuclear and Energy Engineering, Jeju National University, Jeju 64243, Korea (Received: January 22, 2016; Revised: March 13, 2016; Accepted: March 18, 2016) Abstract : When exposed to gamma-rays, hair follicular cells immediately go through apoptosis, which hampers their rapid differentiation essential for the regeneration of hair. Phloroglucinol (PG) is a phenolic compound of Ecklonia cava, brown algae abundant in Jeju island, Korea. Containing plentiful polyphenols, PG is known for its instructive effects by inhibiting apoptosis, scavenging oxygen radicals, and protecting cells against oxidative stress. In this study, we demonstrate that PG rescues radiosensitive hair follicular cells from gamma radiation-induced apoptosis and DNA damage. To identify protective capacity of PG on hair follicles, we irradiated with 8.5 Gy (1.5 Gy/min) of gamma- rays to the whole body of C57BL/6 mice at day 6 after depilation with or without PG. In mice exposed to radiation, the expression of proapoptotic molecule p53 was downregulated in the skin of PG treated group. On immunohistochemical observation of the skin, PG inhibited the immunoreactivity of p53 and cleaved caspase-3. PG treatment protected hair follicular cells from cell death due to gamma-radiation. Our results suggest that PG presents radioprotective effects by inhibiting apoptosis of radiosensitive hair follicular cells and can protect hair follicular cells from gamma-ray induced damage.
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Protective effect of ethanolic extract of antler-shaped Ganoderma lingzhi against oxidative stress in PC12 neuronal cell line

Protective effect of ethanolic extract of antler-shaped Ganoderma lingzhi against oxidative stress in PC12 neuronal cell line

Hyung Don Kim, Eun Young Lee, Jeong-Yong Park, Kyung Hye Seo, Kang-Hyo Lee, Jehun Choi, Jae-Gu Han, Jae-Han Cho*, and Seung Eun Lee* Department of Herbal Crop Research, NIHHS, RDA, Eumseong, Chungbuk 27709, Korea. ABSTRACT: This study was carried out to identify medicinal mushrooms with protective effects against oxidative stress in PC12 neuronal cell line, followed by evaluation of their antioxidant property. Extracts of medicinal mushrooms, including Ganoderma lucidum extract (GLE), antler-shaped Ganoderma lingzhi extract (AGLE), Hericium erinaceus extract (HEE), and Sanghuangporus baumii extract (SBE), were screened for cytotoxicity using MTT assay. None of the extracts up to 10 µg/ml concentration affected cell viability. These extracts were further checked for their protective effect against oxidative stress-induced reactive oxygen species (ROS) production. Exposure to 50 µM H 2 O 2 induced ROS generation in PC12 cells, which was inhibited only by treatment with AGLE. In addition, inhibition of H 2 O 2 -induced ROS generation by AGLE was found to be in a dose-dependent manner (2.5, 5, and 10 µg/ml). Microscopic examination of DCF fluorescence for detection of ROS showed a similar pattern.
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A study on neuroprotective effects of methyl lucidone on glutamate-induced neuronal cell death in HT-22 neurons

A study on neuroprotective effects of methyl lucidone on glutamate-induced neuronal cell death in HT-22 neurons

22 ӀV. DISCUSSION The excessive intracellular ROS causes various diseases by damaging cellular components, such as DNA, lipids and proteins. In CNS, the high level of ROS results in neuronal cell death, which contributes to neurodegenerative diseases. Oxidative glutamate toxicity has been described in primary neuronal cell cultures (Murphy et al., 1989; Oka et al., 1993), neuronal cell line (Davis and Maher, 1994; Miyamoto et al., 1989) and tissue slices (Vornov and Coyle, 1991). Here I used the mouse hippocampal cell line, HT-22, because it is a commonly used cell line for oxidative glutamate toxicity. The high level of extracellular glutamate suppresses cystine uptake through the inhibition of glutamate/cystine antiporter, which induces oxidative stress and neuronal cell death. In this process, HO-1 as antioxidant enzyme is one of candidates to reduce oxidative stress. The present study investigated whether MLC could inhibit oxidative glutamate toxicity.
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LDHB deficiency ameliorates ischemic neuronal cell death

LDHB deficiency ameliorates ischemic neuronal cell death

And then, further study is needed to confirm why PcomA size is increased in LDHB deficiency under ischemic condition and how PcomA size is regulated. Metabolic adaptation also is in close connection with ischemic cell death (Michelle et al., 2009). LDHB is most important enzyme for energy metabolism of neuronal cells, according to astrocyte-to-neuron lactate-shuttle theory. Therefore, LDHB deficiency may induce metabolic adaptation, such as increased capillary surface area that results in increased oxygen delivery, decreased energy demand and increased energy production efficiency, and this metabolic adaptation might contribute to resistance of neuronal cells to cell death under ischemic stress. LDHB deficiency mice also may be involved in the ischemic precondition which is resistance to the loss of blood supply and oxygen. To confirm whether ischemic precondition is induced by LDHB deficiency, further studies are needed.
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JNK/FOXO-mediated neuronal expression of fly homologue of peroxiredoxin II reduces oxidative stress and extends life span

JNK/FOXO-mediated neuronal expression of fly homologue of peroxiredoxin II reduces oxidative stress and extends life span

Activation of c-Jun N-terminal kinase (JNK) signaling in neurons increases stress resistance and extends life span, in part through FOXO-mediated transcription in Drosophila. However, the JNK/ FOXO target genes are unknown. Here, we identified Jafrac1, a Drosophila homolog of human Peroxiredoxin II (hPrxII), as a downstream effecter of JNK/FOXO signaling in neurons that enhances stress resistance and extends life span. We found that Jafrac1 was expressed in the adult brain and induced by para- quat, a reactive oxygen species-generating chemical. RNA inter- ference-mediated neuronal knockdown of Jafrac1 enhanced, while neuronal overexpression of Jafrac1 and hPrxII sup- pressed, paraquat-induced lethality in flies. Neuronal expres- sion of Jafrac1 also significantly reduced ROS levels, restored mitochondrial function, and attenuated JNK activation caused by paraquat. Activation of JNK/FOXO signaling in neurons increased the Jafrac1 expression level under both normal and oxidative stressed conditions. Moreover, neuronal knockdown of Jafrac1 shortened, while overexpression of Jafrac1 and hPrxII extended, the life span in flies. These results support the hypoth- esis that JNK/FOXO signaling extends life span via amelioration of oxidative damage and mitochondrial dysfunction in neurons.
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Calcium overload is essential for the acceleration of staurosporine-induced cell death following neuronal differentiation in PC12 cells.

Calcium overload is essential for the acceleration of staurosporine-induced cell death following neuronal differentiation in PC12 cells.

Differentiation of neuronal cells has been shown to ac- celerate stress-induced cell death, but the underlying mechanisms are not completely understood. Here, we find that early and sustained increase in cytosolic ([Ca 2+ ] c ) and mitochondrial Ca 2+ levels ([Ca 2+ ] m ) is es- sential for the increased sensitivity to staurosporine- induced cell death following neuronal differentiation in PC12 cells. Consistently, pretreatment of differ- entiated PC12 cells with the intracellular Ca 2+ -chelator EGTA-AM diminished staurosporine-induced PARP cleavage and cell death. Furthermore, Ca 2+ overload and enhanced vulnerability to staurosporine in differ- entiated cells were prevented by Bcl-X L overexpr- ession. Our data reveal a new regulatory role for differ- entiation-dependent alteration of Ca 2+ signaling in cell death in response to staurosporine.
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Angiotensin II potentiates zinc-induced cortical neuronal death by acting on angiotensin II type 2 receptor

Angiotensin II potentiates zinc-induced cortical neuronal death by acting on angiotensin II type 2 receptor

Because zinc toxicity occurs largely through oxidative stress, the levels of superoxides in zinc-treated neurons were assessed by DCF fluorescence microscopy. Combined treatment with zinc and angiotensin II substantially increased the levels of superoxides in neurons compared to those induced by zinc alone. This increase in oxidative stress by angiotensin II was completely blocked by the addition of PD123319. Finally, since zinc-induced oxidative stress may be caused by induction and/or activation of NADPH oxidase, the activation status of Rac and the level of the NADPH oxidase subunit p67 phox were measured. Angiotensin II markedly increased Rac activity and the levels of p67 phox in zinc-treated neurons and astrocytes in a PD123319-dependent manner.
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Mechanism of ethanol-induced purkinje cell death in developing rat cerebellum: Its Implication in apoptosis and oxidative damage

Mechanism of ethanol-induced purkinje cell death in developing rat cerebellum: Its Implication in apoptosis and oxidative damage

The ability of oxidative stress to provoke necrotic cell death as a résu1ï of massive cellular damages associated t 。 1ipid peroxidation18) and a1teration of proteins20) and nucleic acids19) have been well docwnented for a long time. ROS has been a1so know 끼 to act as signalling molecu1es in apoptotic pathway. For example , some anti-oxidants can inhibit activation of caspase and subsequent steps leading to apoptotic cell death17l. 1n the present study , 8-0HdG imnnmoreactivity in cells of Purkinje cell layer was observed for a longer time unti1 24 h 따 'ter ethanol administration , at which time point the active caspase-3 and -9 immunoreactivities were gone by. This longer duration of 8 OHdG immunoreactivity may reflect the persistent production of ROS leve1s in response to ethanol exposure , since it has been demonstrated 낭 lat ROS levels in the extract of whole cerebellum remains elevated by 24 h after ethano1 administration24l. Therefore , it is plausible that the 1ater increase of ROS levels may convert the apoptotic pathway of p1 미 r 매매 e cell death into necrotic pathway ,which may also reflect the absence of DNA fragmentation in TUNEL staining
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Hepatocyte protection and antioxidant effect of Citri Unshius Pericarpium against cadmium-induced oxidative stress

Hepatocyte protection and antioxidant effect of Citri Unshius Pericarpium against cadmium-induced oxidative stress

Methods : Component analysis of Citri Unshius Pericarpium was analyzed by UPLC with C 18 column. Cell viability was determined by MTT assay. The enzyme activity of superoxide dismutase (SOD) and the level of reactive oxygen species (ROS) and reduced glutathione (GSH) were analyzed using commercially available kits. Results : Cadmium caused severe HepG2 cell death. Cadmium also increased ROS production, consistent with depletion of GSH and inhibition of the SOD enzyme. However, CEE treatment reduced cell death and relieved oxidative stress caused by cadmium toxicity. CEE lowered ROS levels and improved depletion of GSH levels. CEE also enhanced the enzymatic activity of SOD. In component analysis, hesperidin was the most abundant of the five marker compounds (Narigenin, Narigin, Narirutin, Hesperidin and Hesperidin), which assumes that hesperidin partially contributed to the antioxidant activity of CEE.
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Phytoceramide shows neuroprotection and ameliorates scopolamine-induced memory impairment

Phytoceramide shows neuroprotection and ameliorates scopolamine-induced memory impairment

In immature hippocampal neurons, ceramide plays bipotential roles in cell survival and dendrite outgrowth in a dose-dependent manner [18]. It was also found that ceramide prevents cell death of motoneurons cultures through inhibition of oxidative signals [19]. These results suggest that the cellular level of ceramide is critical for regulation of neuronal survival and differentiation. In our results PCER inhibited the glutamate-induced neurotoxicity in cultured neuronal cells, while PSO did not show the neuroprotective effect with same dose of PCER in the cultured neuronal cells. There are some structural differences between PCER and PSO. Phytosphingosine is structurally similar to sphingosine, except that PSO has a hydroxyl group at C-4 of the sphingoid long-chain base instead of the trans double bond between C-4 and C-5.
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