The cytoprotective role of omentin against oxidative stress-induced PC12 apoptosis

Abstract

Oxidative stress has been proven to play a critical role in the pathogenesis of neuronal injury. As a novel adipocytokine, omentin is produced by visceral adipose with insulin sensitizing effects and has been revealed to possess anti-inflammatory effects. However, the possible effect of omentin on oxidative stress remains unknown. The present study aimed to detect the potential protective effect of omentin against hydrogen peroxide (H 2 O 2 )-induced cytotoxicity of PC12 cells. The results showed that no cytotoxic effect was shown in PC12 cells co-cultured with omentin alone at a concentration of 50-1000 ng/mL. The CCK8 and TUNEL assays suggested that omentin could remarkably attenuate apoptosis induced by 100 lM H 2 O 2 . The PCR and western blotting showed that the expression levels of Bax was significantly inhibited by omentin via the upregulation of miR-128-3p at its 3 0 -UTR. Taken together, these results indicated that omentin protects PC12 cells against H 2 O 2 -induced apoptosis, and further studies need to be conducted before utilization in the clinic for the treatment of neurodegenerative diseases.

Bidirectional communication between brain and visceral white adipose tissue: Its potential impact on Alzheimer's disease

“… 65 Omentin-1 significantly suppressed the expression level of Bax and attenuated H 2 O 2 -induced neuronal apoptosis by up-regulating miR-128-3p at its 3′-UTR. 66 The increased permeability of blood-brain barrier (BBB) and decreased expression of tight junction protein were observed in vWAT-removed mice. 67 After undergoing a transient middle cerebral artery occlusion, the ischemic cerebral infarction volume, BBB permeability and intracerebral pro-inflammatory cytokines were decreased in vWAT-removed rats with preprocessed surgical operation.…”

“…Notably, the possible signaling pathways mediating the interaction between brain and vWAT are complex ( Figure 1 ). Specifically, we summarized the potential mechanisms or mediating factors mainly including autonomic nervous system, 49 , 50 , 51 , 52 , 53 , 54 , 55 , 56 , 57 neurotransmitters, 51 , 54 , 61 , 62 , 63 inflammation, 50 , 59 , 60 , 67 , 68 , 69 hormones, 52 , 54 , 65 , 66 fat metabolism 51 , 56 , 57 , 58 , 59 , 64 and glucose metabolism 53 , 54 , 57 on the basis of current studies.…”

Brain-enriched miR-128: Reduced in exosomes from Parkinson’s patient plasma, improves synaptic integrity, and prevents 6-OHDA mediated neuronal apoptosis

“…miR-128 is also extensively reported as a regulator of nonsense-mediated decay (Bruno et al, 2011;Karam and Wilkinson, 2012;Karam et al, 2013). It is worth mentioning here that although miR-128 has been predominantly reported to be neuroprotective in nature (Mao et al, 2017;Fang et al, 2019;Shi et al, 2021), it is also shown to promote neuronal degeneration under certain conditions (Adlakha and Saini, 2013;Geng et al, 2018). However, a detailed mechanistic study on the involvement of miR-128 in the apoptotic pathways of neuronal death associated with PD was still largely unexplored.…”

Exosome-derived miR-128 is decreased in Parkinson’s patient plasma that maintains synaptic integrity and protects against both intrinsic and extrinsic pathways of neuronal apoptosis in models of Parkinson’s disease

“…While on the other hand, (Zhang et al 2020)showed thatHIF-1α/microRNA-128-3p axis is neuroprotective via the Axin1-mediated Wnt/β-catenin signaling pathway in PD models. It is worth mentioning here that although miR-128 has been predominantly reported to be neuroprotective in nature (Shi et al 2021,Fang et al 2019, Mao et al 2017, Geng et al 2018, it has also shown to promote neuronal degeneration under certain conditions (Geng et al 2018),(Adlakha and Saini 2013). However, a detailed mechanistic study of the involvement of miR-128 in the apoptotic pathways leading to neuronal deathassociated with PD was still unexplored.…”