scholarly journals Neuroprotective action of N-acetyl serotonin in oxidative stress-induced apoptosis through the activation of both TrkB/CREB/BDNF pathway and Akt/Nrf2/Antioxidant enzyme in neuronal cells

Redox Biology ◽  
2017 ◽  
Vol 11 ◽  
pp. 592-599 ◽  
Author(s):  
Jae-Myung Yoo ◽  
Bo Dam Lee ◽  
Dai-Eun Sok ◽  
Jin Yuel Ma ◽  
Mee Ree Kim
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzyme ◽  
Neuronal Cells ◽  
Induced Apoptosis ◽  
Neuroprotective Action ◽  
Bdnf Pathway

scholarly journals 3,3′-Diindolylmethane Promotes BDNF and Antioxidant Enzyme Formation via TrkB/Akt Pathway Activation for Neuroprotection against Oxidative Stress-Induced Apoptosis in Hippocampal Neuronal Cells

Antioxidants ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 3 ◽  
Author(s):  
Bo Dam Lee ◽  
Jae-Myung Yoo ◽  
Seong Yeon Baek ◽  
Fu Yi Li ◽  
Dai-Eun Sok ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Neurodegenerative Diseases ◽  
Antioxidant Enzyme ◽  
Neuronal Cells ◽  
Akt Pathway ◽  
Heme Oxygenase 1 ◽  
Enzyme Formation ◽  
Induced Apoptosis

3,3′-Diindolylmethane (DIM), a metabolite of indole-3-carbinol present in Brassicaceae vegetables, possesses various health-promoting effects. Nonetheless, the effect of DIM on neurodegenerative diseases has not been elucidated clearly. In this study, we hypothesized DIM may protect neuronal cells against oxidative stress-induced apoptosis by promoting the formation of brain-derived neurotrophic factor (BDNF) and antioxidant enzymes through stabilizing the activation of the tropomyosin-related kinase receptor B (TrkB) cascade and we investigated the effect of DIM on oxidative stress-mediated neurodegenerative models. DIM protected neuronal cells against oxidative stress-induced apoptosis by regulating the expression of apoptosis-related proteins in glutamate-treated HT-22 cells. Additionally, DIM improved the expression of BDNF and antioxidant enzymes, such as heme oxygenase-1, glutamate-cysteine ligase catalytic subunit, and NAD(P)H quinine oxidoreductase-1, by promoting the activation of the TrkB/protein kinase B (Akt) pathway in the cells. Consistent with in vitro studies, DIM attenuated memory impairment by protecting hippocampal neuronal cells against oxidative damage in scopolamine-treated mice. Conclusionally, DIM exerted neuroprotective and antioxidant actions through the activation of both BDNF production and antioxidant enzyme formation in accordance with the TrkB/Akt pathway in neuronal cells. Such an effect of DIM may provide information for the application of DIM in the prevention of and therapy for neurodegenerative diseases.

scholarly journals Carthamus, SalviaandStachysspecies protect neuronal cells against oxidative stress-induced apoptosis

2014 ◽  
Vol 52 (12) ◽  
pp. 1550-1557 ◽  
Author(s):  
Marjan Tavakkoli ◽  
Ramin Miri ◽  
Amir Reza Jassbi ◽  
Nasrollah Erfani ◽  
Mojtaba Asadollahi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neuronal Cells ◽  
Induced Apoptosis

Lipocalin-type prostaglandin D synthase protects against oxidative stress-induced neuronal cell death

2012 ◽  
Vol 443 (1) ◽  
pp. 75-84 ◽  
Author(s):  
Ayano Fukuhara ◽  
Mao Yamada ◽  
Ko Fujimori ◽  
Yuya Miyamoto ◽  
Toshihide Kusumoto ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Neuroblastoma Cell ◽  
Neuronal Cells ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Dependent Manner ◽  
Functional Protein ◽  
Prostaglandin D Synthase ◽  
Induced Apoptosis

L-PGDS [lipocalin-type PGD (prostaglandin D) synthase] is a dual-functional protein, acting as a PGD2-producing enzyme and a lipid transporter. L-PGDS is a member of the lipocalin superfamily and can bind a wide variety of lipophilic molecules. In the present study we demonstrate the protective effect of L-PGDS on H2O2-induced apoptosis in neuroblastoma cell line SH-SY5Y. L-PGDS expression was increased in H2O2-treated neuronal cells, and the L-PGDS level was highly associated with H2O2-induced apoptosis, indicating that L-PGDS protected the neuronal cells against H2O2-mediated cell death. A cell viability assay revealed that L-PGDS protected against H2O2-induced cell death in a concentration-dependent manner. Furthermore, the titration of free thiols in H2O2-treated L-PGDS revealed that H2O2 reacted with the thiol of Cys65 of L-PGDS. The MALDI–TOF (matrix-assisted laser-desorption ionization–time-of-flight)-MS spectrum of H2O2-treated L-PGDS showed a 32 Da increase in the mass relative to that of the untreated protein, showing that the thiol was oxidized to sulfinic acid. The binding affinities of oxidized L-PGDS for lipophilic molecules were comparable with those of untreated L-PGDS. Taken together, these results demonstrate that L-PGDS protected against neuronal cell death by scavenging reactive oxygen species without losing its ligand-binding function. The novel function of L-PGDS could be useful for the suppression of oxidative stress-mediated neurodegenerative diseases.

Tubuloside B fromCistanche salsaRescues the PC12 Neuronal Cells from 1-Methyl-4-phenylpyridinium Ion-Induced Apoptosis and Oxidative Stress

Planta Medica ◽  
2002 ◽  
Vol 68 (11) ◽  
pp. 966-970 ◽  
Author(s):  
Guoqing Sheng ◽  
Xiaoping Pu ◽  
Li Lei ◽  
Pengfei Tu ◽  
Changling Li
Keyword(s):  
Oxidative Stress ◽  
Neuronal Cells ◽  
Induced Apoptosis ◽  
And Oxidative Stress

scholarly journals Neuroprotective Effects of Coreopsis lanceolata Flower Extract against Oxidative Stress-Induced Apoptosis in Neuronal Cells and Mice

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 951
Author(s):  
Hyung Don Kim ◽  
Ji Yeon Lee ◽  
Jeong-Yong Park ◽  
Dong Hwi Kim ◽  
Min Hye Kang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Pc12 Cells ◽  
Caspase 3 ◽  
Antioxidant Activities ◽  
Neuronal Cells ◽  
Water Extract ◽  
Protective Effects ◽  
Neuroprotective Effects ◽  
Induced Apoptosis

(1) Background: Coreopsis lanceolata L. is a perennial plant of the family Asteraceae, and its flower is known to contain flavonoids with various bioactivities. We evaluated the effect of Coreopsis lanceolata L. flower (CLF) extracts on H2O2-induced oxidative stress (OS) in neuronal cells and mouse neurons. (2) Methods: The flowering part of CL was used as CLF1 (70% ethanol extract) and CLF2 (water extract), and 10 types of phenolic compounds were quantified using high-performance liquid chromatography. To evaluate the neuroprotective effects of CLF, the antioxidant activities of the extracts were measured, and the expression levels of antioxidant enzymes and proteins related to OS-induced apoptosis in neuronal cells and mouse neurons treated with the extracts were investigated. (3) Results: In the in vitro study, CLF ameliorated H2O2-induced oxidative stress and induced the expression of antioxidant enzymes in PC12 cells. Furthermore, CLF1 enhanced the expression of the Bcl-xL protein but reduced the expression of Bax and the cleavage of caspase-3. In the same manner, CLF1 showed neuroprotective effects against OS in vivo. Pretreatment with CLF1 (200 mg/kg) increased the Bcl-2 protein and decreased Bax compared with the 1-methyl-4-phenylpyridinium ion (MPP+)-treated C57BL/6 mice model group. Our results suggest that the protective effects of CLF1 on MPP+-induced apoptosis may be due to its anti-apoptotic activity, through regulating the expression of the Bcl-2 family. (4) Conclusions: CLF1 exerts neuroprotective effects against OS-induced apoptosis in PC12 cells in a Parkinson’s disease model mouse. This effect may be attributable to the upregulation of Bcl-2 protein expression, downregulation of Bax expression, and inhibition of caspase-3 activation. These data indicate that CLF may provide therapeutic value for the treatment of progressive neurodegenerative diseases.

scholarly journals Neuroprotective Effect of Carotenoid-Rich Enteromorpha prolifera Extract via TrkB/Akt Pathway against Oxidative Stress in Hippocampal Neuronal Cells

Marine Drugs ◽  
2020 ◽  
Vol 18 (7) ◽  
pp. 372 ◽  
Author(s):  
Seung Yeon Baek ◽  
Mee Ree Kim
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Neuroprotective Effect ◽  
Neuronal Cells ◽  
Food Supplement ◽  
Akt Pathway ◽  
Heme Oxygenase 1 ◽  
Neuroprotective Effects ◽  
Glutamate Cysteine Ligase ◽  
Induced Apoptosis

In this study, we found that E. prolifera extract (EAEP) exhibits neuroprotective effects in oxidative stress-induced neuronal cells. EAEP improved cell viability as well as attenuated the formation of intracellular reactive oxygen species (ROS) and apoptotic bodies in glutamate-treated hippocampal neuronal cells (HT-22). Furthermore, EAEP improved the expression of brain-derived neurotrophic factor (BDNF) and antioxidant enzymes such as heme oxygenase-1 (HO-1), NAD(P)H quinine oxidoreductase-1 (NQO-1), and glutamate–cysteine ligase catalytic subunit (GCLC) via the tropomyosin-related kinase receptor B/ protein kinase B (TrkB/Akt) signaling pathway. In contrast, the pre-incubation of K252a, a TrkB inhibitor, or MK-2206, an Akt-selective inhibitor, ameliorated the neuroprotective effects of EAEP in oxidative stress-induced neuronal cells. These results suggest that EAEP protects neuronal cells against oxidative stress-induced apoptosis by upregulating the expression of BDNF and antioxidant enzymes via the activation of the TrkB/Akt pathway. In conclusion, such an effect of EAEP, which is rich in carotenoid-derived compounds, may justify its application as a food supplement in the prevention and treatment of neurodegenerative disorders.

scholarly journals Acetaldehyde Induces Neurotoxicity In Vitro via Oxidative Stress- and Ca2+ Imbalance-Mediated Endoplasmic Reticulum Stress

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Jiahui Cui ◽  
Yang Liu ◽  
Xing Chang ◽  
Wenfeng Gou ◽  
Xuejiao Zhou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Early Stage ◽  
Neuronal Cells ◽  
Toxic Metabolite ◽  
Related Protein ◽  
Ht22 Cells ◽  
Induced Apoptosis

Excessive drinking can damage brain tissue and cause cognitive dysfunction. Studies have found that the early stage of neurodegenerative disease is closely related to heavy drinking. Acetaldehyde (ADE) is the main toxic metabolite of alcohol. However, the exact mechanisms of ADE-induced neurotoxicity are not fully clear. In this article, we studied the cytotoxic effect of ADE in HT22 cells and primary cultured cortical neuronal cells. We found that ADE exhibited cytotoxicities against HT22 cells and primary cultured cortical neuronal cells in dose-dependent manners. Furthermore, ADE induced apoptosis of HT22 cells by upregulating the expression of caspase family proapoptotic proteins. Moreover, ADE treatment could significantly increase the intracellular Ca2+ and reactive oxygen species (ROS) levels and activate endoplasmic reticulum stress (ERS) in HT22 cells. ADE upregulated ERS-related CHOP expression dose-dependently in primary cultured cortical neuronal cells. In addition, inhibition of ROS with antioxidant N-acetyl-L-cysteine (NAC) reduced the accumulation of ROS and reversed ADE-induced increase of ERS-related protein and apoptosis-related protein levels. Mitigation of ERS with ERS inhibitor 4-PBA obviously suppressed ADE-induced apoptosis and the expression of ERS-related proteins. Therefore, ADE induces neurotoxicity of HT22 cells via oxidative stress- and Ca2+ imbalance-mediated ERS.

Cocoa flavonoids up-regulate antioxidant enzyme activity via the ERK1/2 pathway to protect against oxidative stress-induced apoptosis in HepG2 cells☆

2010 ◽  
Vol 21 (3) ◽  
pp. 196-205 ◽  
Author(s):  
María Ángeles Martín ◽  
Ana Belén Granado Serrano ◽  
Sonia Ramos ◽  
María Izquierdo Pulido ◽  
Laura Bravo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Enzyme Activity ◽  
Antioxidant Enzyme ◽  
Hepg2 Cells ◽  
Antioxidant Enzyme Activity ◽  
Induced Apoptosis
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