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

Wu, Lei; Cao, Jiang; Kang, Ying; Dai, Yaji; Fang, Wei; Huang, Peng

doi:10.3892/ijmm.2020.4483

Cited by 21 publications

(31 citation statements)

References 59 publications

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Section: Antioxidant Ingredients In the Dietmentioning

confidence: 99%

“…Research has shown that curcumin is a hormetic agent that stabilizes Nrf2 and enhances the expression of HO-1 [ 185 , 186 ]. Furthermore, curcumin upregulates the antiapoptotic Bcl-2 protein and downregulates the proapoptotic proteins, Bax and caspase-3 [ 187 ]. The oxidative stress biomarkers, including MDA (malondialdehyde), SOD, and GSH, are upregulated (SOD, GSH) or downregulated (MDA) by curcumin [ 188 ].…”

Section: Antioxidant Ingredients In the Dietmentioning

confidence: 99%

“…For example, curcumin and resveratrol can phosphorylate Nrf2 through the PI3K/Akt signaling pathway. Phosphorylated Nrf2 translocates into the nucleus and binds to ARE/sMaf, promoting the transcription of ARE-driven genes and thereby alleviating oxidative stress-mediated damage [ 187 , 191 , 194 ]. Similarly, dietary components can also activate AMPK, CK2, PKC, ERK, and p38 signaling pathways to cause Nrf2 phosphorylation and nuclear translocation, thus promoting the transcription of antioxidant genes [ 141 , 204 , 206 , 208 ].…”

Section: Antioxidant Ingredients In the Dietmentioning

confidence: 99%

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The Keap1-Nrf2 System: A Mediator between Oxidative Stress and Aging

Chao

Xiao

2021

Oxidative Medicine and Cellular Longevity

190

136

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Oxidative stress, a term that describes the imbalance between oxidants and antioxidants, leads to the disruption of redox signals and causes molecular damage. Increased oxidative stress from diverse sources has been implicated in most senescence-related diseases and in aging itself. The Kelch-like ECH-associated protein 1- (Keap1-) nuclear factor-erythroid 2-related factor 2 (Nrf2) system can be used to monitor oxidative stress; Keap1-Nrf2 is closely associated with aging and controls the transcription of multiple antioxidant enzymes. Simultaneously, Keap1-Nrf2 signaling is also modulated by a more complex regulatory network, including phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt), protein kinase C, and mitogen-activated protein kinase. This review presents more information on aging-related molecular mechanisms involving Keap1-Nrf2. Furthermore, we highlight several major signals involved in Nrf2 unbinding from Keap1, including cysteine modification of Keap1 and phosphorylation of Nrf2, PI3K/Akt/glycogen synthase kinase 3β, sequestosome 1, Bach1, and c-Myc. Additionally, we discuss the direct interaction between Keap1-Nrf2 and the mammalian target of rapamycin pathway. In summary, we focus on recent progress in research on the Keap1-Nrf2 system involving oxidative stress and aging, providing an empirical basis for the development of antiaging drugs.

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Section: Antioxidant Ingredients In the Dietmentioning

confidence: 99%

Section: Antioxidant Ingredients In the Dietmentioning

confidence: 99%

Section: Antioxidant Ingredients In the Dietmentioning

confidence: 99%

See 1 more Smart Citation

The Keap1-Nrf2 System: A Mediator between Oxidative Stress and Aging

Chao

Xiao

2021

Oxidative Medicine and Cellular Longevity

190

136

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“… 25 Wu et al indicated that curcumin could attenuate OGD/R-induced injury in SH-SY5Y cells via increasing the levels of SOD and GSH. 26 In this study, we found that physcion could reduce OGD/R-induced oxidative stress in SH-SY5Y cells, as shown by the decreased generations of ROS and MDA, and the increased activities of GSH and SOD. These data suggested that physcion could protect SH-SY5Y cells against OGD/R-induced oxidative stress.…”

Section: Discussionmentioning

confidence: 60%

Physcion Protects Rats Against Cerebral Ischemia-Reperfusion Injury via Inhibition of TLR4/NF-kB Signaling Pathway

Dong

Wang

Song

et al. 2021

DDDT

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Background Ischemic stroke (IS) is characterized by the rapid loss of brain function due to ischemia. Physcion has been found to have a neuroprotective effect against cerebral ischemia-reperfusion (I/R) injury. However, the mechanism by which physcion regulates cerebral I/R injury remains largely unknown. Methods An oxygen-glucose deprivation/reperfusion (OGD/R) model in SH-SY5Y cells and a rat cerebral ischemia-reperfusion (I/R) model were established, respectively. CCK-8 and flow cytometry assays were used to detect the viability and apoptosis of SH-SY5Y cells. Moreover, enzyme-linked immunosorbent assay (ELISA) was used to measure the levels of SOD, MDA, GSH-Px, TNF-α, IL-1β, IL-6 and IL-10 in the supernatant of SH-SY5Y cells. Meanwhile, Western blot assay was used to detect the expressions of TLR4, p-p65 and p-IκB in SH-SY5Y cells and I/R rats. Results In this study, physcion treatment significantly rescued OGD/R-induced neuronal injury. In addition, physcion decreased inflammatory response in SH-SY5Y cells after OGD/R insult, as shown by the decreased levels of the pro-inflammatory factors TNF-α, IL-1β, IL-6 and IL-10. Moreover, physcion attenuated the oxidative stress in OGD/R-treated SY-SY5Y cells, as evidenced by the increased SOD and GSH levels and the decreased ROS and MDA levels. Meanwhile, physcion significantly reduced cerebral infarction, attenuated neuronal injury and apoptosis in I/R rats. Furthermore, physcion markedly decreased the expressions of TLR4, p-NF-κB p65 and p-IκB in the brain tissues of rats subjected to I/R and in SH-SY5Y cells exposed to OGD/R. Conclusion In conclusion, our study indicated that physcion protected neuron cells against I/R injury in vitro and in vivo by inhibition of the TLR4/NF-kB pathway; thus, physcion might serve as a promising therapeutic candidate for IS.

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“…These studies con rm our hypotheses regarding the anti-in ammatory effect of the components of JH-CX-DG formula. Wu et al [21] demonstrated that JH can exert bene cial effects on ischemic cerebral injury by upregulating the caspase3 and Bcl-2 expression, downregulating the Bax expression, and promoting PI3K/AKT pathway activation. Hurley et al [22] showed that JH also resulted in a dose-dependent increase in hippocampal BDNF and protected the brain nerves.…”

Section: Discussionmentioning

confidence: 99%

System Pharmacological Mechanism and Compatibility Laws of Jianghuang from Traditional Chinese Medicine In Blood-Regulating Formulae

Liu¹,

Wang

2020

Preprint

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Background: Jianghuang (JH) is a popular ingredient in blood-regulating traditional Chinese Medicine (TCM) that could be effective for the treatment of various diseases. We demonstrate the compatibility laws and system pharmacological mechanisms of the key formula containing JH by leveraging data mining of bioinformatics databases.Material/Methods: The compatibility laws of blood-regulating formulae containing JH from the Chinese Traditional Medicine Formula Dictionary were analyzed using a generalized rule induction (GRI) algorithm implemented. The putative target gene and miRNA were retrieved via a combination of the Arrowsmith knowledge discovery tool and FunRich 3.1.3. System pharmacological mechanisms are traced by their protein-protein interaction (PPI) network, and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis was conducted using Uniprot, the Human Protein Atlas (HPA), STRING 11.0, and KOBAS 3.0.Results: We found that the JH-CX-DG formula (Ligusticum chuanxiong-Angelica sinensis) could represent a key formula containing JH in blood-regulating TCM formulae. The JH-CX-DG formula was observed to directly target AKT, TLR4, caspase-3, PI3K, mTOR, p38 MAPK, VEGF, iNOS, Nrf2, BDNF, NF-κB, Bcl-2, and Bax 13 targets and regulate targets through 13 miRNA. The PPI network and KEGG pathway enrichment analysis showed that the JH-CX-DG formula possess potential pharmacological effects including anti-inflammatory, improving microcirculation, and anti-tumor through the regulation of multiple pathways including PI3K/Akt, MAPK, Toll-like receptor, T cell receptor, EGFR, VEGFR, Apoptosis, HIF-1 (p < 0.05).Conclusion: The JH-CX-DG formula can exert beneficial pharmacological effects through multi-target and multi-pathway interactions. It can be effectively administered for the treatment of inflammatory diseases, microcirculation disorders, cardiovascular disease, and cancer. We found a new effective drug formula through analyzing the compatibility law and systemic pharmacological mechanism of JH. Our study provides a theoretical basis and directions for subsequent research on the JH-CX-DG formula.

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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

Cited by 21 publications

References 59 publications

The Keap1-Nrf2 System: A Mediator between Oxidative Stress and Aging

The Keap1-Nrf2 System: A Mediator between Oxidative Stress and Aging

Physcion Protects Rats Against Cerebral Ischemia-Reperfusion Injury via Inhibition of TLR4/NF-kB Signaling Pathway

System Pharmacological Mechanism and Compatibility Laws of Jianghuang from Traditional Chinese Medicine In Blood-Regulating Formulae

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