scholarly journals Cearoin Induces Autophagy, ERK Activation and Apoptosis via ROS Generation in SH-SY5Y Neuroblastoma Cells

Molecules ◽  
2017 ◽  
Vol 22 (2) ◽  
pp. 242 ◽  
Author(s):  
Tonking Bastola ◽  
Ren-bo An ◽  
Youn-Chul Kim ◽  
Jaehyo Kim ◽  
Jungwon Seo
2008 ◽  
Vol 19 (3) ◽  
pp. 855-864 ◽  
Author(s):  
Yoshinori Takei ◽  
Ronald Laskey

Although nerve growth factor (NGF) promotes survival of neurons, tumor necrosis factor α (TNF-α) contributes to cell death triggered by NGF depletion, through TNF-α receptor (TNFR) 1. In contrast to this effect, TNF-α can promote neural cell survival via TNF-α receptor TNFR2. Although these findings demonstrate pivotal roles of TNF-α and NGF in cell fate decisions, cross-talk between these signaling pathways has not been clarified. We find that NGF can induce TNF-α synthesis through the nuclear factor-κB transcription factor. This provides a new basis for examining the cross-talk between NGF and TNF-α. Inhibition of TNFR2 shows opposite effects on two downstream kinases of NGF, extracellular signal-regulated kinase (Erk) and Akt. It increases Erk activation by NGF, and this increased activation induces differentiation of neuroblastoma cell lines. Reciprocally, inhibition of TNFR2 decreases Akt activation by NGF. Consistent with an essential role of Akt in survival signaling, inhibition of TNF-α signaling decreases NGF-dependent survival of neurons from rat dorsal root ganglia. Thus, NGF and NGF-induced TNF-α cooperate to activate Akt, promoting survival of normal neural cells. However, the NGF-induced TNF-α suppresses Erk activation by NGF, blocking NGF-induced differentiation of neuroblastoma cells. TNFR2 signaling could be a novel target to modulate cell responses to NGF.


2013 ◽  
Vol 66 (3) ◽  
pp. 765-774 ◽  
Author(s):  
Yi-Chiang Hsu ◽  
Sue-Joan Chang ◽  
Miin-Yau Wang ◽  
Yi-Ling Chen ◽  
Tzuu-Yuan Huang

2014 ◽  
Vol 33 (5) ◽  
pp. 412-418 ◽  
Author(s):  
Eun Joo Pak ◽  
Gi Dong Son ◽  
Byung Sun Yoo

Cadmium, a highly ubiquitous heavy metal, is well known to induce neurotoxicity. However, the underlying mechanism of cadmium-mediated neurotoxicity remains unclear. We have studied cadmium inhibition of neurite outgrowth using human SH-SY5Y neuroblastoma cells induced to differentiate by all- trans-retinoic acid (RA). Cadmium, at a concentration of 3 μmol/L, had no significant effect on the viability of differentiating SH-SY5Y cells. However, the neurite outgrowth of the differentiating SH-SY5Y cells 48 hours after cadmium treatment (1-3 μmol/L cadmium) was significantly inhibited in a dose-dependent manner. Treatment of RA-stimulated differentiating SH-SY5Y cells with 1 to 3 μmol/L cadmium resulted in decreased level of cross-reactivities with 43-kDa growth-associated protein (GAP-43) in a dose-dependent manner. The reactive oxygen species (ROS) scavenger, NAC (N-acetyl-l-cysteine), recovered the expression of GAP-43 in cadmium-treated cells. The results indicate that cadmium is able to inhibit neurite outgrowth of differentiating SH-SY5Y cells and that this effect might result from ROS generation by cadmium.


Antioxidants ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 27 ◽  
Author(s):  
Weishun Tian ◽  
Jing Zhao ◽  
Jeong-Ho Lee ◽  
Md Rashedunnabi Akanda ◽  
Jeong-Hwi Cho ◽  
...  

Oxidative stress plays a vital role in neurodegenerative diseases. Cornus officinalis (CC) has a wide range of pharmacological activities (e.g., antioxidant, neuroprotective, and anti-inflammatory). The present study was undertaken to elucidate the neuroprotective mechanism of CC and fermented CC (FCC) on stress and H2O2-induced oxidative stress damage in rats and SH-SY5Y cells. A dose of 100 mg/kg CC or FCC was orally administered to rats 1 h prior to immobilization 2 h per day for 14 days. CC, especially FCC administration decreased immobility time in forced swim test (FST), effectively alleviated the oxidative stress, and remarkably decreased corticosterone, β-endorphin and increased serotonin levels, respectively. In cells, CC and FCC significantly inhibited reactive oxygen species (ROS) generation, lactate dehydrogenase (LDH) release and significantly increased the genes expression of antioxidant and neuronal markers, such as superoxide dismutase (SOD), catalase (CAT), and brain-derived neurotrophic factor (BDNF). Moreover, the pro-apoptotic factor Bax and anti-apoptotic factor Bcl-2 (Bax/Bcl-2) ratio was regulated by CC and FCC pretreatment. Both in rats and cells, CC and FCC downregulated mitogen-activated protein kinase (MAPK) phosphorylation. Taken together, these results demonstrated that CC and particularly FCC ameliorated oxidative stress and may be used on the neuroprotection.


Pharmaceutics ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 1203
Author(s):  
Do Kyung Kim ◽  
Won Jong Rhee

Oxidative stress is implicated in many diseases, including cardiovascular and neurodegenerative diseases. Because an increased level of oxidative stress causes apoptosis, it is necessary to inhibit cellular responses to oxidative stress. In this study, Carex, a nanovesicle from carrot, was isolated and investigated as a novel biomaterial with antioxidative function in cardiomyoblasts and neuroblastoma cells. A high concentration of nanovesicles was purified from carrots, using size-exclusion chromatography in combination with ultrafiltration. The characterization of Carex demonstrated that it had properties similar to those of extracellular vesicles. Carex showed low cytotoxicity in both H9C2 cardiomyoblasts and SH-SY5Y neuroblastoma cells, when a high level of Carex was delivered to the cells. Carex was further investigated for its antioxidative and apoptotic effects, and it significantly inhibited ROS generation and apoptosis in vitro in myocardial infarction and Parkinson’s disease models. Carex inhibited the reduction of antioxidative molecule expression, including Nrf-2, HO-1, and NQO-1, in both models. Considering its antioxidative function and high production yield, Carex is a potential drug candidate for the treatment of myocardial infarction as well as Parkinson’s disease. Thus, the results demonstrated in this study will contribute to an exploration of a novel drug, using nanovesicles from plants, including carrots.


Nanomaterials ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 977
Author(s):  
Silvana Alfei ◽  
Barbara Marengo ◽  
Giulia Elda Valenti ◽  
Cinzia Domenicotti

Drug resistance is a multifactorial phenomenon that limits the action of antibiotics and chemotherapeutics. Therefore, it is essential to develop new therapeutic strategies capable of inducing cytotoxic effects circumventing chemoresistance. In this regard, the employment of natural and synthetic cationic peptides and polymers has given satisfactory results both in microbiology, as antibacterial agents, but also in the oncological field, resulting in effective treatment against several tumors, including neuroblastoma (NB). To this end, two polystyrene-based copolymers (P5, P7), containing primary ammonium groups, were herein synthetized and tested on etoposide-sensitive (HTLA-230) and etoposide-resistant (HTLA-ER) NB cells. Both copolymers were water-soluble and showed a positive surface charge due to nitrogen atoms, which resulted in protonation in the whole physiological pH range. Furthermore, P5 and P7 exhibited stability in solution, excellent buffer capacity, and nanosized particles, and they were able to reduce NB cell viability in a concentration-dependent way. Interestingly, a significant increase in reactive oxygen species (ROS) production was observed in both NB cell populations treated with P5 or P7, establishing for both copolymers an unequivocal correlation between cytotoxicity and ROS generation. Therefore, P5 and P7 could be promising template macromolecules for the development of new chemotherapeutic agents able to fight NB chemoresistance.


2019 ◽  
Vol 1861 (8) ◽  
pp. 1446-1457 ◽  
Author(s):  
Caterina Merla ◽  
Micaela Liberti ◽  
Claudia Consales ◽  
Agnese Denzi ◽  
Francesca Apollonio ◽  
...  

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