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

Wang, Yun; Gu, Yijun; Liu, Ming; Bai, Yang; Liang, Li-Ye; Wang, Huailiang

doi:10.1155/2017/4310475

Cited by 27 publications

(27 citation statements)

References 48 publications

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“…Tertiary butylhydroquinone (TBHQ), a commonly used food antioxidant permitted by China (Health Standard GB2760.2011), is widely found in oils, biscuits, and other foods. The bodily oxidation of TBHQ can provide H+ radicals, which can stop the reaction and thus play an antioxidant role [33]. Furthermore, TBHQ induces phase II enzymes and the Nrf2 signaling pathway and shows remarkable antioxidant activity in various cell types and tissues.…”

Section: Introductionmentioning

confidence: 99%

TBHQ Attenuates Neurotoxicity Induced by Methamphetamine in the VTA through the Nrf2/HO-1 and PI3K/AKT Signaling Pathways

Meng

Zhang

Guo

et al. 2020

Oxidative Medicine and Cellular Longevity

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Methamphetamine (METH) leads to nervous system toxicity. Long-term exposure to METH results in damage to dopamine neurons in the ventral tegmental area (VTA), and depression-like behavior is a clinical symptom of this toxicity. The current study was designed to investigate whether the antioxidant tertiary butylhydroquinone (TBHQ) can alleviate neurotoxicity through both antioxidative stress and antiapoptotic signaling pathways in the VTA. Rats were randomly divided into a control group, a METH-treated group (METH group), and a METH+TBHQ-treated group (METH+TBHQ group). Intraperitoneal injections of METH at a dose of 10 mg/kg were administered to the rats in the METH and METH+TBHQ groups for one week, and METH was then administered at a dose that increased by 1 mg/kg per week until the sixth week, when the daily dosage reached 15 mg/kg. The rats in the METH+TBHQ group received 12.5 mg/kg TBHQ intragastrically. Chronic exposure to METH resulted in increased immobility times in the forced swimming test (FST) and tail suspension test (TST) and led to depression-like behavior. The production of reactive oxygen species (ROS) and apoptosis levels were increased in the VTA of animals in the METH-treated group. METH downregulated Nrf2, HO-1, PI3K, and AKT, key factors of oxidative stress, and the apoptosis signaling pathway. Moreover, METH increased the caspase-3 immunocontent. These changes were reversed by treatment with the antioxidant TBHQ. The results indicate that TBHQ can enhance Nrf2-induced antioxidative stress and PI3K-induced antiapoptotic effects, which can alleviate METH-induced ROS and apoptosis, and that the crosstalk between Nrf2 and PI3K/AKT is likely the key factor involved in the protective effect of TBHQ against METH-induced chronic nervous system toxicity.

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Section: Introductionmentioning

confidence: 99%

TBHQ Attenuates Neurotoxicity Induced by Methamphetamine in the VTA through the Nrf2/HO-1 and PI3K/AKT Signaling Pathways

Meng

Zhang

Guo

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…Exposure to METH also altered the expression of the mRNAs involved in the oxidative phosphorylation pathway (Wang et al, 2017b) in which cells use enzymes to oxidize nutrients and then to produce adenosine triphosphate. Some studies have reported that oxidative phosphorylation capacity in the mitochondria would be altered and would influence cellular function (Kim, Chin & Cho, 2017;Xia et al, 2014;Xu et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

RNA-sequencing analysis of the effect of luteolin on methamphetamine-induced hepatotoxicity in rats: a preliminary study

Qu¹,

Zhang²,

Chen³

et al. 2020

PeerJ

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In this study, RNA-sequencing (RNA-seq) was utilized to investigate the effects of luteolin on hepatotoxicity caused by methamphetamine (METH). The rats in METH group were administrated with METH (15 mg/kg, two times per day) via intraperitoneal (i.p.) injections for four consecutive days. The rats in luteolin + METH group were firstly administrated with luteolin (100 mg/kg, once a day) by oral gavage for 3 days before METH treatment. Lueolin attenuated the hepatotoxicity induced by METH via histopathological and biochemical analysis. The results of RNA-seq showed that luteolin could regulate 497 differentially expressed genes (DEGs), and the selected DEGs were mainly enriched in eight pathways, according to KEGG analysis. Furthermore, qRT-PCR was utilized to verify the results of RNA-seq. Six genes were selected as follows: liver enriched antimicrobial peptide 2 (Leap2), fatty acid synthase (Fasn), fatty acid binding protein 5 (Fabp5), patatin like phospholipase domain containing 3 (Pnpla3), myelin basic protein (Mbp) and calmodulin 3 (Calm3). Though because of the design flaws, the luteolin group has not been included, this study demonstrated that luteolin might exert hepato-protective effects from METH via modulation of oxidative phosphorylation, cytochrome P450 and certain signaling pathways.

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“…The rats in the control group were injected with an equal volume of 0.9% physiological saline solution. 23 All rats were raised in a room with controlled temperature (18-22°C) and humidity (50%-70%) and were fed with solid food and water in an alternating 12 hours light and 12 hours dark cycle. All experimental procedures involving animals were followed by the guidelines of…”

Section: Resource Center China Medical University (Certificate Numbermentioning

confidence: 99%

Resveratrol protects the integrity of alveolar epithelial barrier via SIRT1/PTEN/p‐Akt pathway in methamphetamine‐induced chronic lung injury

et al. 2020

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Objectives SIRT1 is an antioxidative factor, but its mechanism in methamphetamine (MA)‐induced lung injury remains unclear. The purpose of this study is to determine whether MA can disrupt the integrity of alveolar epithelial barrier, whether SIRT1 is involved in MA‐induced chronic lung injury and whether Resveratrol (Res) can protect the integrity of alveolar epithelial cells by regulating ROS to activate SIRT1/PTEN/p‐Akt pathway. Materials and methods The rats were randomly divided into control group and MA group. Extracted lungs were detected by Western blot, HE staining and immunohistochemistry. The alveolar epithelial cells were treated with MA or/and Res, following by Western blot, LDH leakage assay and flow cytometry. MOE is used for bio‐informatics prediction. Results Chronic exposure to MA can cause slower growth ratio of weight, increased RVI and induced lung injury including the reduced number of alveolar sacs and the thickened alveolar walls. MA‐induced apoptosis was associated with SIRT1‐related oxidative stress. Res suppressed ROS levels, activated SIRT1, negatively regulated PTEN, phosphorylated Akt, reduced LDH leakage, increased the expression of ZO‐1 and E‐cadherin and inhibited the apoptosis of alveolar epithelial cells to attenuate MA‐induced higher permeability of alveolar epithelium. Conclusions MA disrupted the integrity of alveolar epithelial barrier. Res inhibited oxidative stress and reversed MA‐induced higher permeability and apoptosis of alveolar epithelium by the activation of SIRT1/PTEN/p‐Akt pathway.

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

Cited by 27 publications

References 48 publications

TBHQ Attenuates Neurotoxicity Induced by Methamphetamine in the VTA through the Nrf2/HO-1 and PI3K/AKT Signaling Pathways

TBHQ Attenuates Neurotoxicity Induced by Methamphetamine in the VTA through the Nrf2/HO-1 and PI3K/AKT Signaling Pathways

RNA-sequencing analysis of the effect of luteolin on methamphetamine-induced hepatotoxicity in rats: a preliminary study

Resveratrol protects the integrity of alveolar epithelial barrier via SIRT1/PTEN/p‐Akt pathway in methamphetamine‐induced chronic lung injury

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