NGF and PI3K/Akt signaling participate in the ventral motor neuronal protection of curcumin in sciatic nerve injury rat models

Sang, Qiuling; Sun, Daju; Chen, Zonghan; Zhao, Wei

doi:10.1016/j.biopha.2018.04.116

Cited by 55 publications

(49 citation statements)

References 39 publications

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“…As a positive control for the assay we used Ac-DEVD-CHO (20 μM), an inhibitor of caspase-3 which was given 30 min before the cell damaging factor Data were normalized to vehicle-treated cells (control) and are presented as the mean ± SEM from 3 separate experiments with 2 repetitions each **P<0.01 and ***P < 0.001 vs. vehicle-treated cells ### P < 0.001 vs. H 2 O 2 -treated cells curcumin in RA-SH-SY5Y cells against 6-OHDA-evoked cell damage, which is the cell death model connected rather with apoptotic than necrotic processes that are saturated after differentiation with RA (Cheung et al 2009;No et al 2010;Park et al 2014). Our results obtained in UN-SH-SY5Y cells confirmed previous findings on neuroprotective effect of curcumin which could be mediated by its antioxidant, antiapoptotic, and anti-inflammatory mechanisms (Mhillaj et al 2019;Sang et al 2018;Uğuz et al 2016).…”

Section: Discussionsupporting

confidence: 88%

Neuroprotective Effects of Necrostatin-1 Against Oxidative Stress–Induced Cell Damage: an Involvement of Cathepsin D Inhibition

et al. 2020

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Necroptosis, a recently discovered form of non-apoptotic programmed cell death, can be implicated in many pathological conditions including neuronal cell death. Moreover, an inhibition of this process by necrostatin-1 (Nec-1) has been shown to be neuroprotective in in vitro and in vivo models of cerebral ischemia. However, the involvement of this type of cell death in oxidative stress-induced neuronal cell damage is less recognized. Therefore, we tested the effects of Nec-1, an inhibitor of necroptosis, in the model of hydrogen peroxide (H 2 O 2)-induced cell damage in human neuroblastoma SH-SY5Y and murine hippocampal HT-22 cell lines. The data showed that Nec-1 (10-40 μM) attenuated the cell death induced by H 2 O 2 in undifferentiated (UN-) and neuronal differentiated (RA-) SH-SY5Y cells with a higher efficacy in the former cell type. Moreover, Nec-1 partially reduced cell damage induced by 6-hydroxydopamine in UN-and RASH -SY5Y cells. The protective effect of Nec-1 was of similar magnitude as the effect of a caspase-3 inhibitor in both cell phenotypes and this effect were not potentiated after combined treatment. Furthermore, the non-specific apoptosis and necroptosis inhibitor curcumin augmented the beneficial effect of Nec-1 against H 2 O 2-evoked cell damage albeit only in RASH -SY5Y cells. Next, it was found that the mechanisms of neuroprotective effect of Nec-1 against H 2 O 2induced cell damage in SH-SY5Y cells involved the inhibition of lysosomal protease, cathepsin D, but not caspase-3 or calpain activities. In HT-22 cells, Nec-1 was protective in two models of oxidative stress (H 2 O 2 and glutamate) and that effect was blocked by a caspase inhibitor. Our data showed neuroprotective effects of the necroptosis inhibitor, Nec-1, against oxidative stress-induced cell damage and pointed to involvement of cathepsin D inhibition in the mechanism of its action. Moreover, a cell type-specific interplay between necroptosis and apoptosis has been demonstrated.

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Section: Discussionsupporting

confidence: 88%

Neuroprotective Effects of Necrostatin-1 Against Oxidative Stress–Induced Cell Damage: an Involvement of Cathepsin D Inhibition

et al. 2020

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“…The PI3K/AKT pathway has been documented as an essential pathway for cell survival in response to apoptosis and oxidative stress induced by a series of physiological and pathological or exogenous stimuli (53,54), while this pathway is also significantly involved in cerebral ischemia (55). To date, a number of studies have confirmed that the PI3K/AKT pathway serves an important role in the neuroprotective effects of curcumin by inhibiting apoptosis, oxidative stress and inflammation (56)(57)(58). However, there are few reports available to date on the roles of the PI3K/AKT pathway in the neuroprotective effects of curcumin against cerebral I/R injury.…”

Section: Discussionmentioning

confidence: 99%

Curcumin exerts protective effects against hypoxia‑reoxygenation injury via the enhancement of apurinic/apyrimidinic endonuclease�1 in SH‑SY5Y cells: Involvement of the PI3K/AKT pathway

Cao²,

Kang

et al. 2020

Int J Mol Med

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“…As curcumin has the capacity to reduce the inflammatory response, spinal cord expression of both NGF and c-Fos was reduced in a brachial plexus avulsion model [ 60 ]. The assumption is that the NGF measured was pro-NGF, since this is the form of NGF involved in neuronal apoptosis and death [ 78 ]. p300 and CREB-binding protein (CBP) histone acetyl transferases (HATs) mediate the expression of the other two markers, BDNF and Cox-2 [ 53 ].…”

Section: Curcumin Mechanisms Of Action and Cellular Targets In Thementioning

confidence: 99%

Key Developments in the Potential of Curcumin for the Treatment of Peripheral Neuropathies

et al. 2020

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Peripheral neuropathies (PN) can be triggered after metabolic diseases, traumatic peripheral nerve injury, genetic mutations, toxic substances, and/or inflammation. PN is a major clinical problem, affecting many patients and with few effective therapeutics. Recently, interest in natural dietary compounds, such as polyphenols, in human health has led to a great deal of research, especially in PN. Curcumin is a polyphenol extracted from the root of Curcuma longa. This molecule has long been used in Asian medicine for its anti-inflammatory, antibacterial, and antioxidant properties. However, like numerous polyphenols, curcumin has a very low bioavailability and a very fast metabolism. This review addresses multiple aspects of curcumin in PN, including bioavailability issues, new formulations, observations in animal behavioral tests, electrophysiological, histological, and molecular aspects, and clinical trials published to date. The, review covers in vitro and in vivo studies, with a special focus on the molecular mechanisms of curcumin (anti-inflammatory, antioxidant, anti-endoplasmic reticulum stress (anti-ER-stress), neuroprotection, and glial protection). This review provides for the first time an overview of curcumin in the treatment of PN. Finally, because PN are associated with numerous pathologies (e.g., cancers, diabetes, addiction, inflammatory disease...), this review is likely to interest a large audience.

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NGF and PI3K/Akt signaling participate in the ventral motor neuronal protection of curcumin in sciatic nerve injury rat models

Cited by 55 publications

References 39 publications

Neuroprotective Effects of Necrostatin-1 Against Oxidative Stress–Induced Cell Damage: an Involvement of Cathepsin D Inhibition

Neuroprotective Effects of Necrostatin-1 Against Oxidative Stress–Induced Cell Damage: an Involvement of Cathepsin D Inhibition

Curcumin exerts protective effects against hypoxia‑reoxygenation injury via the enhancement of apurinic/apyrimidinic endonuclease�1 in SH‑SY5Y cells: Involvement of the PI3K/AKT pathway

Key Developments in the Potential of Curcumin for the Treatment of Peripheral Neuropathies

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