Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and represents the most common form of senile dementia. Autophagy and mitophagy are cellular processes that play a key role in the aggregation of β-amyloid (Aβ) and tau phosphorylation. As a consequence, impairment of these processes leads to the progression of AD. Thus, interest is growing in the search for new natural compounds, such as Moringin (MOR), with neuroprotective, anti-amyloidogenic, antioxidative, and anti-inflammatory properties that could be used for AD prevention. However, MOR appears to be poorly soluble and stable in water. To increase its solubility MOR was conjugated with α-cyclodextrin (MOR/α-CD). In this work, it was evaluated if MOR/α-CD pretreatment was able to exert neuroprotective effects in an AD in vitro model through the evaluation of the transcriptional profile by next-generation sequencing (NGS). To induce the AD model, retinoic acid-differentiated SH-SY5Y cells were exposed to Aβ1-42. The MOR/α-CD pretreatment reduced the expression of the genes which encode proteins involved in senescence, autophagy, and mitophagy processes. Additionally, MOR/α-CD was able to induce neuronal remodeling modulating the axon guidance, principally downregulating the Slit/Robo signaling pathway. Noteworthy, MOR/α-CD, modulating these important pathways, may induce neuronal protection against Aβ1-42 toxicity as demonstrated also by the reduction of cleaved caspase 3. These data indicated that MOR/α-CD could attenuate the progression of the disease and promote neuronal repair

Silvestro, S.; Chiricosta, L.; Gugliandolo, A.; Iori, R.; Rollin, P.; Perenzoni, D.; Mattivi, F.; Bramanti, P.; Mazzon, E. (2021). The Moringin/α-CD pretreatment induces neuroprotection in an in vitro model of Alzheimer’s disease: a transcriptomic study. CURRENT ISSUES IN MOLECULAR BIOLOGY, 43 (1): 197-214. doi: 10.3390/cimb43010017 handle: http://hdl.handle.net/10449/68573

The Moringin/α-CD pretreatment induces neuroprotection in an in vitro model of Alzheimer’s disease: a transcriptomic study

Iori, Renato;Perenzoni, Daniele;Mattivi, Fulvio;
2021

Abstract

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and represents the most common form of senile dementia. Autophagy and mitophagy are cellular processes that play a key role in the aggregation of β-amyloid (Aβ) and tau phosphorylation. As a consequence, impairment of these processes leads to the progression of AD. Thus, interest is growing in the search for new natural compounds, such as Moringin (MOR), with neuroprotective, anti-amyloidogenic, antioxidative, and anti-inflammatory properties that could be used for AD prevention. However, MOR appears to be poorly soluble and stable in water. To increase its solubility MOR was conjugated with α-cyclodextrin (MOR/α-CD). In this work, it was evaluated if MOR/α-CD pretreatment was able to exert neuroprotective effects in an AD in vitro model through the evaluation of the transcriptional profile by next-generation sequencing (NGS). To induce the AD model, retinoic acid-differentiated SH-SY5Y cells were exposed to Aβ1-42. The MOR/α-CD pretreatment reduced the expression of the genes which encode proteins involved in senescence, autophagy, and mitophagy processes. Additionally, MOR/α-CD was able to induce neuronal remodeling modulating the axon guidance, principally downregulating the Slit/Robo signaling pathway. Noteworthy, MOR/α-CD, modulating these important pathways, may induce neuronal protection against Aβ1-42 toxicity as demonstrated also by the reduction of cleaved caspase 3. These data indicated that MOR/α-CD could attenuate the progression of the disease and promote neuronal repair
Settore CHIM/08 - CHIMICA FARMACEUTICA
Silvestro, S.; Chiricosta, L.; Gugliandolo, A.; Iori, R.; Rollin, P.; Perenzoni, D.; Mattivi, F.; Bramanti, P.; Mazzon, E. (2021). The Moringin/α-CD pretreatment induces neuroprotection in an in vitro model of Alzheimer’s disease: a transcriptomic study. CURRENT ISSUES IN MOLECULAR BIOLOGY, 43 (1): 197-214. doi: 10.3390/cimb43010017 handle: http://hdl.handle.net/10449/68573
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