Gastrodin Attenuates Bilateral Common Carotid Artery Occlusion-Induced Cognitive Deficits via Regulating Aβ-Related Proteins and Reducing Autophagy and Apoptosis in Rats

Liu, Bo; Gao, Jianmei; Li, Fēi; Gong, Qihai; Shi, Jingshan

doi:10.3389/fphar.2018.00405

Cited by 49 publications

(36 citation statements)

References 49 publications

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“…to be an effective agent in resisting apoptosis made by various stimulations, such as hypoxic ischaemia, 26 ethanol, 9 high glucose 27 and LPS. 28 Consistently, gastrodin exhibited anti-apoptosis effect in our experimental system.…”

Section: Lps-induced Inflammatory Injury Besides That Gastrodin Ismentioning

confidence: 99%

Retracted: Gastrodin relieves inflammation injury induced by lipopolysaccharides in MRC‐5 cells by up‐regulation of miR‐103

Qiao

Wang

et al. 2019

J Cellular Molecular Medi

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The beneficial function of gastrodin towards many inflammatory diseases has been identified. This study designed to see the influence of gastrodin in a cell model of chronic obstructive pulmonary disease (COPD). MRC‐5 cells were treated by LPS, before which gastrodin was administrated. The effects of gastrodin were evaluated by conducting CCK‐8, FITC‐PI double staining, Western blot, qRT‐PCR and ELISA. Besides this, the downstream effector and signalling were studied to decode how gastrodin exerted its function. And dual‐luciferase assay was used to detect the targeting link between miR‐103 and lipoprotein receptor‐related protein 1 (LRP1). LPS induced apoptosis and the release of MCP‐1, IL‐6 and TNF‐α in MRC‐5 cells. Pre‐treating MRC‐5 cells with gastrodin attenuated LPS‐induced cell damage. Meanwhile, p38/JNK and NF‐κB pathways induced by LPS were repressed by gastrodin. miR‐103 expression was elevated by gastrodin. Further, the protective functions of gastrodin were attenuated by miR‐103 silencing. And LRP1 was a target of miR‐103 and negatively regulated by miR‐103. The in vitro data illustrated the protective function of gastrodin in LPS‐injured MRC‐5 cells. Gastrodin exerted its function possibly by up‐regulating miR‐103 and modulating p38/JNK and NF‐κB pathways.

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Section: Lps-induced Inflammatory Injury Besides That Gastrodin Ismentioning

confidence: 99%

Retracted: Gastrodin relieves inflammation injury induced by lipopolysaccharides in MRC‐5 cells by up‐regulation of miR‐103

Qiao

Wang

et al. 2019

J Cellular Molecular Medi

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“…Recently, GAS could improve the learning and memory ability of VD rat model induced by 2VO [48]. GAS has a therapeutic effect on BCCAO-induced VD by targeting the formation of Aβ-related proteins and inhibiting autophagy and apoptosis of hippocampal neurons [49].…”

Section: Discussionmentioning

confidence: 99%

Protection effect of gastrodin on learning and memory ability in vascular dementia by promoting autophagy flux via Ca2+/CaMKII signal pathway

Tt¹,

Zhou²,

Yn³

et al. 2020

Preprint

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Background: Vascular dementia is a common and frequently-occurring disease in the process of human aging. Although the current treatment can delay the deterioration of the disease, it has not a great breakthrough in improving cognitive impairment. Therefore, exploring the potential key molecular targets of VD provide promising strategy for prevention and treatment. Methods: vascular dementia rats were reproduced by permanent middle cerebral artery occlusion (pMCAO) and anoxic injury of HT22 cells were induced by Cobalt Chloride (CoCl 2 , 200μM). The ability of spatial learning and memory was assessed by morris water maze (MWM) test. Histological analysis was performed by HE staining and immunohistochemical staining. The effects of gastrodin on autophagy flux and calcium signal in vascular dementia rats and HT22 cells during hypoxia injury were detected by Western blotting and immunofluorescence. Furthermore, intracellular Ca 2+ levels were quantified using a Ca 2+ quantification kit and were also measured by flow cytometric estimation of Fluo-4 AM. Results: Gastrodin significantly reversed cognitive deficits in vascular dementia rats. The results of immunohistochemical analysis and western blot confirmed that gastrodin could attenuate the levels of LC3, p62 and phosphorylated CaMKII in hippocampus of VD rats. In addition, gastrodin was similar to the early autophagic inhibitor (3-BDO) ameliorating CoCl 2 -induced autophagic flux dysfunction and p62 knockdown by siRNA also promoting autophagic flux patency, but the late autophagy inhibitor (CQ) weakened the improvement effect of gastrodin. Furthermore, gastrodin markedly inhibited CoCl 2 -induced autophagic flux dysfunction by inhibiting [Ca 2+ ] i -dependent CaMKII. Conclusion: Gastrodin is a potential promising candidate for VD by improving autophagy flux dysfunction via increasing lysosome acidification and autophagosome-lysosome fusion mediated by CaMKII-regulated suppression of p62 signaling. Keywords: Gastrodin, Vascular dementia, Neuron injury, Autophagic flux, Ca 2+ , CaMKII

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“…Morris Water Maze Test. The Morris water maze (MWM) test was carried out to evaluate the impact of ICA on the spatial learning and memory ability of mice, as described previously (Liu et al, 2018). The pool was divided into four quadrants, with a hidden platform located 1 cm below the water level in the center of the target quadrant.…”

Section: Methodsmentioning

confidence: 99%

Icariin Delays Brain Aging in Senescence-Accelerated Mouse Prone 8 (SAMP8) Model via Inhibiting Autophagy

Chen

Liu

et al. 2019

J Pharmacol Exp Ther

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Icariin (ICA), a major flavonoid extracted from the Chinese tonic herb Epimedium, exerts beneficial effects in a variety of age-dependent diseases, such as Alzheimer's disease (AD). However, the antiaging mechanisms remain unclear. The senescence-accelerated mouse-prone 8 (SAMP8) model has been used to study age-related neurodegenerative changes associated with aging and the pathogenesis of AD. Hence, the current study was designed to examine the effect of ICA on age-related cognitive decline in SAMP8 mice and explore the role of autophagy in the ICA-mediated neuroprotection. SAMP8 mice were administered with ICA starting at 5 months of age, and the treatment lasted for 3 consecutive months. Morris water maze was used to evaluate cognitive function. The senescenceassociated b-galactosidase staining was used to determine the number of senescence cells. The neuronal morphologic changes were examined via Nissl staining. The hippocampal neuronal ultrastructure was examined by transmission electron microscopy. The expression of autophagy protein was examined by Western blot. ICA-treated SAMP8 mice exhibited a robust improvement in spatial learning and memory function. Meanwhile, ICA reduced the number of senescence cells in the brains of SAMP8 mice, inhibited neuronal loss, and reversed neuronal structural changes in the hippocampi of SAMP8 mice. Moreover, ICA treatment also decreased the formation of autophagosomes in the hippocampus of SAMP8 mice, and reduced the expression of autophagy-related proteins LC3-II and p62. These results demonstrate that ICA possesses the ability to delay brain aging in SAMP8 mice, and the mechanisms are possibly mediated through the regulation of autophagy.

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Gastrodin Attenuates Bilateral Common Carotid Artery Occlusion-Induced Cognitive Deficits via Regulating Aβ-Related Proteins and Reducing Autophagy and Apoptosis in Rats

Cited by 49 publications

References 49 publications

Retracted: Gastrodin relieves inflammation injury induced by lipopolysaccharides in MRC‐5 cells by up‐regulation of miR‐103

Retracted: Gastrodin relieves inflammation injury induced by lipopolysaccharides in MRC‐5 cells by up‐regulation of miR‐103

Protection effect of gastrodin on learning and memory ability in vascular dementia by promoting autophagy flux via Ca2+/CaMKII signal pathway

Icariin Delays Brain Aging in Senescence-Accelerated Mouse Prone 8 (SAMP8) Model via Inhibiting Autophagy

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