Gastrodin as a multi-target protective compound reverses learning memory deficits and AD-like pathology in APP/PS1 transgenic mice

Yue-Qin, Zeng; Gu, Juan-Hua; Chen, Liang; Zhang, Taotao; Zhou, Xin‐Fu

doi:10.1016/j.jff.2020.104324

Cited by 16 publications

(18 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The results of animal behavior experiments in Figures 1B–G suggested that we successfully constructed AD model mice with Dgal, and Done and Gas at doses of 90 and 210 mg/kg, respectively, could improve the memory of AD mice. Our results are consistent with those of other studies ( Obrenovich et al, 2020 ; Zeng et al, 2021 )…”

Section: Discussionsupporting

confidence: 94%

Gastrodin From Gastrodia elata Enhances Cognitive Function and Neuroprotection of AD Mice via the Regulation of Gut Microbiota Composition and Inhibition of Neuron Inflammation

Fasina

Wang

et al. 2022

Front. Pharmacol.

View full text Add to dashboard Cite

Gastrodin (Gas) is known to exhibit neuroprotective effects in Alzheimer’s disease (AD). However, the detailed mechanism of action is still unclear. In the present study, we focused on the microbiome–gut–brain axis to investigate the mechanism of action of Gas using a D-galactose (Dgal)–induced AD model. Gas reversed the memory dysfunction of Dgal-administered mice. Neurons in the cerebral cortex and hippocampus were reduced in the Dgal-administered group, and the decrease of neurons was suppressed in 90 and 210 mg/kg Gas treatment groups. 16S rRNA sequence analysis was carried out to explore the composition of gut microbiota in fecal samples of mice. Gas treatment had a positive correlation with Firmicutes and had a negative correlation with Cyanobacteria, Proteobacteria, and Deferribaceters. Importantly, the LPS and proinflammatory cytokines in the brain increased in Dgal-administered mice, but these parameters recovered to normal levels after oral administration of Gas. To determine whether the microbiota–gut–brain axis is involved in the neuroprotective effect of Gas, the mice were given antibiotic cocktail before and during the trial period to decrease the gut microbiota of mice. The antibiotic cocktail partially eliminated the neuroprotective effect of Gas by changing the gut microbiome composition. These results indicated that Gas improves the memory of the AD mouse model via partly targeting the microbiota–gut–brain axis and mitigating neuron inflammation.

show abstract

Section: Discussionsupporting

confidence: 94%

Gastrodin From Gastrodia elata Enhances Cognitive Function and Neuroprotection of AD Mice via the Regulation of Gut Microbiota Composition and Inhibition of Neuron Inflammation

Fasina

Wang

et al. 2022

Front. Pharmacol.

View full text Add to dashboard Cite

show abstract

“…Long-term gastrodin management inhibits the polymerization and decomposition of oligarchic A β , prevents its induced cellular neurotoxicity, reduces the level of A β plaques and high pTau, and alleviates oxidative stress in APP/PS1 transgenic mice [ 75 ] ( Figure 3 ). Excessive autophagy can be inhibited by lowering the levels of Beclin-1, LC3-II, and P62 in both neuronal cells and astrocytes [ 76 , 77 ]. In addition, the P38 MAPK signaling pathway is also involved in this process [ 34 ].…”

Section: Resultsmentioning

confidence: 99%

Gastrodin and Vascular Dementia: Advances and Current Perspectives

Deng

Chen

Meng

et al. 2022

Evidence-Based Complementary and Alternative Medicine

View full text Add to dashboard Cite

Gastrodia elata, a traditional Chinese medicine, has been widely used since ancient times to treat diseases such as dizziness, epilepsy, stroke, and memory loss. Gastrodin, one of the active components of Gastrodia elata, has been used in the treatment of migraine, epilepsy, Parkinson’s disease, dementia, and depression in recent years. It can improve cognitive function and related neuropsychiatric symptoms through various effects and is considered as a promising treatment for dementia. Vascular dementia is a kind of severe cognitive impairment syndrome caused by vascular factors, and it is the dementia syndrome with the largest number of patients besides Alzheimer’s disease. Although there is still a lack of evidence-based explorations, the paper reviewed the mechanism and methods of gastrodin in the treatment of vascular dementia, providing a reference for clinical therapy.

show abstract

“…Gastrodin treatment also attenuated glutamate‐induced iron dysregulation in HT‐22 cells (Jiang, Cheng, et al, 2020) by increasing ferroportin and decreasing iron levels. Several mechanistic studies also demonstrated its neuroprotective activity against Aβ 42 ‐induced neurotoxicity in SH‐SY5Y cells (Zeng et al, 2021; Zhang et al, 2016) and transgenic AD mouse models, including Tg2576 (Zhang et al, 2016) and APP/PS1 (Zeng et al, 2021) by alleviating oxidative stress, neuroinflammation and AD‐like pathology.…”

Section: Iron and Ferroptosis As Therapeutic Targets For Admentioning

confidence: 98%

“…While curcumin shows potential effect in pre-clinical investigations, current clinical evidence is not positive, with one significant limitation being the low bioavailability of curcumin (Ringman et al, 2012;Voulgaropoulou et al, 2019). Some other polyphenols with the ability to penetrate the BBB, such as gastrodin (Zeng et al, 2021) and baicalein/5,6,7trihydroxyflavone (Wei et al, 2014), demonstrated antiferroptotic activity in cell culture models . Gastrodin protected against H 2 O 2 -and glutamate-induced ferroptotic lethality , possibly via up-regulation of Nrf2, haeme oxygenase (HO)-1, glutathione and GPX4 and downregulation of MDA levels in vitro.…”

Section: Polyphenolsmentioning

confidence: 99%

“…Some other polyphenols with the ability to penetrate the BBB, such as gastrodin (Zeng et al, 2021) and baicalein/5,6,7‐trihydroxyflavone (Wei et al, 2014), demonstrated anti‐ferroptotic activity in cell culture models (Jiang, Cheng, et al, 2020; Li, Li, et al, 2019). Gastrodin protected against H 2 O 2 ‐ and glutamate‐induced ferroptotic lethality (Jiang, Cheng, et al, 2020; Jiang, Chu, et al, 2020), possibly via up‐regulation of Nrf2, haeme oxygenase (HO)‐1, glutathione and GPX4 and down‐regulation of MDA levels in vitro.…”

Section: Iron and Ferroptosis As Therapeutic Targets For Admentioning

confidence: 99%

See 1 more Smart Citation

Ferroptosis as a mechanism of neurodegeneration in Alzheimer's disease

Jakaria

Belaidi

Bush

et al. 2021

Journal of Neurochemistry

125

View full text Add to dashboard Cite

Alzheimer's disease (AD) is the most prevalent form of dementia, with complex pathophysiology that is not fully understood. While β‐amyloid plaque and neurofibrillary tangles define the pathology of the disease, the mechanism of neurodegeneration is uncertain. Ferroptosis is an iron‐mediated programmed cell death mechanism characterised by phospholipid peroxidation that has been observed in clinical AD samples. This review will outline the growing molecular and clinical evidence implicating ferroptosis in the pathogenesis of AD, with implications for disease‐modifying therapies.

show abstract

Gastrodin as a multi-target protective compound reverses learning memory deficits and AD-like pathology in APP/PS1 transgenic mice

Cited by 16 publications

References 34 publications

Gastrodin From Gastrodia elata Enhances Cognitive Function and Neuroprotection of AD Mice via the Regulation of Gut Microbiota Composition and Inhibition of Neuron Inflammation

Gastrodin From Gastrodia elata Enhances Cognitive Function and Neuroprotection of AD Mice via the Regulation of Gut Microbiota Composition and Inhibition of Neuron Inflammation

Gastrodin and Vascular Dementia: Advances and Current Perspectives

Ferroptosis as a mechanism of neurodegeneration in Alzheimer's disease

Contact Info

Product

Resources

About