Allicin improves endoplasmic reticulum stress-related cognitive deficits via PERK/Nrf2 antioxidative signaling pathway

Zhu, Yanhua; Li, Xianhui; Yuan, Zhe; Li, Chunyan; Tian, Rong-Bo; Jia, Weiping; Xiao, Zhu‐Ping

doi:10.1016/j.ejphar.2015.06.002

Cited by 48 publications

(33 citation statements)

References 43 publications

(38 reference statements)

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“…However, Aβ is unlikely an initiator, and more likely a mediator of AD, so Aβ-targeted interventions should not be an eventual solution to attenuating progressive aggravation toward AD. Once infectious agents have been verified as the primordial etiological cues leading to AD, the more practical medications treating AD should at least include, for example, anti-infection agents such as minocycline (El-Shimy et al, 2015; Budni et al, 2016), anti-inflammation agents such as anhydroexfoliamycin (Leirós et al, 2015) or rapamycin (Siman et al, 2015), and anti-oxidation agents such as allicin (Zhu et al, 2015). With similar importance, modulation of gut microbiota from dysbiosis to homeostasis for the early-phase prophylaxis of AD through personalized diet and prebiotic/probiotic supplementation should also be addressed (Hu et al, 2016).…”

Section: Prospectivesmentioning

confidence: 99%

Biotic/Abiotic Stress-Driven Alzheimer's Disease

Zheng

Wang

et al. 2016

Front. Cell. Neurosci.

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Section: Prospectivesmentioning

confidence: 99%

Biotic/Abiotic Stress-Driven Alzheimer's Disease

Zheng

Wang

et al. 2016

Front. Cell. Neurosci.

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“…Interestingly, olfactory neurons submitted to systemic application of tunicamycin increased NRF2 in parallel with other UPR-members such as CHOP, BIP, XBP1 [53]. These results have been extended to in vivo studies, as lateral ventricular infusion of tunicamycin in rats induced expression of PERK and NRF2 in the hippocampus accompanied by significant cognitive deficits, increased TAU phosphorylation and Aβ42 deposits [54].…”

Section: Nrf2 Participates In the Unfolded Protein Response (Upr)mentioning

confidence: 74%

Modulation of proteostasis by transcription factor NRF2 and impact in neurodegenerative diseases

2017

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Neurodegenerative diseases are linked to the accumulation of specific protein aggregates, suggesting an intimate connection between injured brain and loss of proteostasis. Proteostasis refers to all the processes by which cells control the abundance and folding of the proteome thanks to a wide network that integrates the regulation of signaling pathways, gene expression and protein degradation systems. This review attempts to summarize the most relevant findings about the transcriptional modulation of proteostasis exerted by the transcription factor NRF2 (nuclear factor (erythroid-derived 2)-like 2). NRF2 has been classically considered as the master regulator of the antioxidant cell response, although it is currently emerging as a key component of the transduction machinery to maintain proteostasis. As we will discuss, NRF2 could be envisioned as a hub that compiles emergency signals derived from misfolded protein accumulation in order to build a coordinated and perdurable transcriptional response. This is achieved by functions of NRF2 related to the control of genes involved in the maintenance of the endoplasmic reticulum physiology, the proteasome and autophagy.

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“…The Nrf2 is known as a substrate of PERK [41]. Phosphorylation of PERK can cause a conformational change of Nrf2 protein by triggering the dissociation of Keap1-Nrf2 complex, and the dissociation of Nrf2 into the nucleus upregulated expression of antioxidant genes [42]. Therefore, oxidative stress and endoplasmic reticulum stress has some certain relevance through PERK/Nrf2 pathway, which is why we choose PERK-dependent pathway of ERS.…”

Section: Discussionmentioning

confidence: 99%

“…Activation of PERK signal can induce conformational change of nuclear factor E2-related factor 2 (Nrf2), which triggers the dissociation of Kelch-like ECH-associated protein 1- (Keap1-) Nrf2 complex to adjust the oxidation-redox condition of cells [11]. Nrf2 can enhance the transcription of cytoprotective genes during oxidative stress [12].…”

Section: Introductionmentioning

confidence: 99%

TBHQ Alleviated Endoplasmic Reticulum Stress‐Apoptosis and Oxidative Stress by PERK‐Nrf2 Crosstalk in Methamphetamine‐Induced Chronic Pulmonary Toxicity

Wang

Liu

et al. 2017

Oxidative Medicine and Cellular Longevity

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Methamphetamine (MA) leads to cardiac and pulmonary toxicity expressed as increases in inflammatory responses and oxidative stress. However, some interactions may exist between oxidative stress and endoplasmic reticulum stress (ERS). The current study is designed to investigate if both oxidative stress and ERS are involved in MA-induced chronic pulmonary toxicity and if antioxidant tertiary butylhydroquinone (TBHQ) alleviated ERS-apoptosis and oxidative stress by PERK-Nrf2 crosstalk. In this study, the rats were randomly divided into control group, MA-treated group (MA), and MA plus TBHQ-treated group (MA + TBHQ). Chronic exposure to MA resulted in slower growth of weight and pulmonary toxicity of the rats by increasing the pulmonary arterial pressure, promoting the hypertrophy of right ventricle and the remodeling of pulmonary arteries. MA inhibited the Nrf2-mediated antioxidative stress by downregulation of Nrf2, GCS, and HO-1 and upregulation of SOD2. MA increased GRP78 to induce ERS. Overexpression and phosphorylation of PERK rapidly phosphorylated eIF2α, increased ATF4, CHOP, bax, caspase 3, and caspase 12, and decreased bcl-2. These changes can be reversed by antioxidant TBHQ through upregulating expression of Nrf2. The above results indicated that TBHQ can alleviate MA-induced oxidative stress which can accelerate ERS to initiate PERK-dependent apoptosis and that PERK/Nrf2 is likely to be the key crosstalk between oxidative stress and ERS in MA-induced chronic pulmonary toxicity.

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Allicin improves endoplasmic reticulum stress-related cognitive deficits via PERK/Nrf2 antioxidative signaling pathway

Cited by 48 publications

References 43 publications

Biotic/Abiotic Stress-Driven Alzheimer's Disease

Biotic/Abiotic Stress-Driven Alzheimer's Disease

Modulation of proteostasis by transcription factor NRF2 and impact in neurodegenerative diseases

TBHQ Alleviated Endoplasmic Reticulum Stress‐Apoptosis and Oxidative Stress by PERK‐Nrf2 Crosstalk in Methamphetamine‐Induced Chronic Pulmonary Toxicity

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