l -Theanine attenuates cadmium-induced neurotoxicity through the inhibition of oxidative damage and tau hyperphosphorylation

Ben, Peiling; Zhang, Zhengping; Zhu, Yanyan; Xiong, Aiying; Gao, Yanhong; Mu, Jianyun; Yin, Zhimin; Luo, Lan

doi:10.1016/j.neuro.2016.09.010

Cited by 56 publications

(36 citation statements)

References 66 publications

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“…Animal experiments have also observed that cadmium contamination has a significant effect on offspring brain development and emotional responses. Has been reported a single treatment with CdCl 2 (3.75‐6 mg/kg 30 mg/L in water) caused a significant increase in apoptotic neuronal cell death in mouse cortex and hippocampus . In this study, we found that Cd inhibited the mRNA and protein expression levels of DBN, which was consistent with the results of previous studies.…”

Section: Discussionsupporting

confidence: 92%

Cadmium induces actin cytoskeleton alterations and dysfunction in Neuro‐2a cells

Song

Chen

et al. 2019

Environmental Toxicology

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Cadmium (Cd) is considered a possible etiological factor in neurodegenerative diseases. However, the exact mechanism by which Cd induces neurotoxicity is not well elucidated. In this study, Neuro-2a cells were treated with 0, 10, 20, and 40 μM cadmium chloride for 24 hours to investigate the effects of Cd on the cytoskeleton of nerve cells. MTT assay and ELISA assay were used to examine cell viability and release of lactate dehydrogenase (LDH) from cells, respectively. Results showed that Cd reduced cell viability and increased the release of LDH in a dose-dependent manner (P < 0.05). The morphology of treated cell was damaged as indicated by cell collapse and dimensionality reduction. Moreover, the axonal spines and normal features of Cd-treated neurons disappeared. We checked the ultrastructure of Neuro-2a cells and found that Cd-induced swelling, membrane damage, overflow of cytoplasm contents, and cell fragmentation. Damaged mitochondria, expanded endoplasmic reticulum, and abnormal microfilaments were found in Cd-treated cells rather than in untreated cells. Compared with the control group, the relative release of glutamate in the supernatant after Cd treatment was reduced, indicating that Cd exposure could reduce the release of glutamate by inhibiting the function of nerve-2a cells. Cd decreased the mRNA and protein expression levels of cytoskeletal proteins including DBN, SYP, and TAU, which might promote cytoskeleton alterations in Cd-treated cells. In conclusion, Cd-induced actin cytoskeleton alterations and dysfunction of cultured neurons. The results of the present study provide new insights for the investigation of Cd-induced neurotoxicity.

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Section: Discussionsupporting

confidence: 92%

Cadmium induces actin cytoskeleton alterations and dysfunction in Neuro‐2a cells

Song

Chen

et al. 2019

Environmental Toxicology

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“…We already documented that lowered antioxidant enzyme activity, including that of glutathione peroxidase (GSH-Px), catalase (CAT), and superoxide dismutase (SOD), in the brains of cadmium-intoxicated mice were counteracted by L-theanine. 15) We speculate that L-theanine reduced Ang II-induced JAK/STAT3 pathway might be due to L-theanine has antioxidant function. Further research is required to more fully explain the mechanisms of L-theanine.…”

Section: Discussionmentioning

confidence: 85%

“…Previous reports showed that it is benefit to improve relaxing, cognitive performance, hepatoprotective, neuroprotective effects against cadmium and anti-tumor. [12][13][14][15][16] Some studies have suggested that L-theanine can avert cardiovascular disease. L-Theanine administration significantly lowered the amount of 5-hydroxyindole in the brains of Wistar Kyoto (WKY) and spontaneously hypertensive rats 17) (SHRs).…”

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confidence: 99%

L-Theanine Down-Regulates the JAK/STAT3 Pathway to Attenuate the Proliferation and Migration of Vascular Smooth Muscle Cells Induced by Angiotensin II

Ben

et al. 2018

Biological & Pharmaceutical Bulletin

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L-Theanine, a green tea amino acid derivative, has cardiovascular qualities. The focus of the current evaluation was to examine the suppression of L-theanine on cultured vascular smooth muscle cell (VSMC) proliferation and migration that is prompted by angiotensin II (Ang II). The VSMCs were treated with noncytotoxic concentrations of L-theanine and then stimulated with Ang II. The CCK-8 and Transwell chamber assays were monitored on the proliferation and migration rate, respectively. We discovered that L-theanine (50 and 100 µM) significantly halted Ang II-induced VSMC proliferation and migration. This was joined by a decline in the amount of cyclin D1. An additional discovery was that L-theanine lowered the proportion of S-phase cells, whereas the number of G1/G0-phase cells in Ang II-stimulated VSMCs was elevated, based on flow cytometry. Western blotting analyses indicated that L-theanine had no impact on extracellularsignal-regulated kinase 1/2 (ERK1/2) activation prompted by Ang II. Nevertheless, L-theanine significantly lowered Ang II-prompted phosphorylation of Janus kinase 2 (JAK2), c-Src tyrosine kinase, and signal transducer and activators of transcription 3 (STAT3). The outcomes revealed that L-theanine subdued the Ang II-prompted proliferation and migration of VSMC, partly via the obstruction of the JAK/STAT3 pathway instead of via just the ERK pathway. Key words L-theanine; vascular smooth muscle cell; proliferation; signal transducer and activator of transcription 3 (STAT3); Janus kinase 2 (JAK2); angiotensin II Angiotensin II (Ang II), a main result of the renin-angiotensin-aldosterone system (RAAS), acts on vascular smooth muscle cells (VSMCs) and induces microartery contraction. VSMCs were chronic exposed to Ang II resulting in cell proliferation, hypertrophy and aging. 1) Abnormal proliferation of VSMCs makes vascular remodeling a pivotal process in the pathogenesis of hypertension. In addition, it is the structural foundation of the decline of hypertension. 2) Looking for drugs that can both inhibit blood pressure and inhibit proliferation of VSMCs is an important strategy to prevent hypertensive diseases. Ang II connects to Ang II type 1 (AT1) receptors and signals via small guanosine 5′-triphosphate (GTP)-binding proteins, including the Rho family, Ras family and Rac family, which control VSMC gene expression, proliferation, migration, and cytoskeletal reorganization. 3) Ang II prompts the mitogen-activated protein kinase (MAPK) pathway, such as the p42/p44 extracellular signal-related kinases (ERK1/2),

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“…Both studies concluded that the soil, water and the phosphate ores present in the industrial slag heaps in this region showed highly elevated levels of the heavy metals chromium, nickel and cadmium. The chronic exposure to Cr, Ni and Cd is toxic for humans and has been associated with different neurodegenerative diseases, including tauopathies such as Alzheimer's disease [19][20][21][22] . However, little is known about the mechanisms by which these three heavy metals induce PSP pathogenesis and tau accumulation.…”

Section: Resultsmentioning

confidence: 99%

Heavy metals contaminating the environment of a progressive supranuclear palsy cluster induce tau accumulation and cell death in cultured neurons

Alquézar

Felix

McCandlish

et al. 2020

Sci Rep

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l -Theanine attenuates cadmium-induced neurotoxicity through the inhibition of oxidative damage and tau hyperphosphorylation

Cited by 56 publications

References 66 publications

Cadmium induces actin cytoskeleton alterations and dysfunction in Neuro‐2a cells

Cadmium induces actin cytoskeleton alterations and dysfunction in Neuro‐2a cells

L-Theanine Down-Regulates the JAK/STAT3 Pathway to Attenuate the Proliferation and Migration of Vascular Smooth Muscle Cells Induced by Angiotensin II

Heavy metals contaminating the environment of a progressive supranuclear palsy cluster induce tau accumulation and cell death in cultured neurons

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