Velvet Antler Methanol Extracts Ameliorate Parkinson’s Disease by Inhibiting Oxidative Stress and Neuroinflammation: From <i>C. elegans</i> to Mice

Liu, Ying; Li, Hongyuan; Li, Yunfei; Yang, Min; Wang, Xiaohui; Peng, Yinghua

doi:10.1155/2021/8864395

Cited by 11 publications

(11 citation statements)

References 47 publications

(28 reference statements)

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“…Zhang et al (19) proposed that ε-viniferin could enhance SIRT3-mediated forkhead box O3 (FOXO3) deacetylation, increase ATP production, decrease ROS production and alleviate mitochondrial depolarization, thus inhibiting rotenone-induced neuronal cell apoptosis. Oxidative stress injury and mitochondrial dysfunction caused by abnormal aggregation of Aβ, α-synuclein, or Huntington's disease in different target neurons can result in severe neuron loss (20)(21)(22), which is the common pathogenesis of different neurodegenerative diseases. SIRT3 promotes the survival of target neurons, such as dopaminergic or cholinergic neurons (23).…”

Section: Sirt3 Expression Alleviates Microglia Activation-induced Dop...mentioning

confidence: 99%

SIRT3 expression alleviates microglia activation‑induced dopaminergic neuron injury through the mitochondrial pathway

et al. 2022

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The mitochondrial protein sirtuin 3 (SIRT3) can counteract cell damage caused by oxidative stress and inflammation, and contribute to cell survival primarily by improving mitochondrial function. However, the effects of SIRT3 in dopaminergic neuronal cells (DACs) remain unclear. In our previous studies, microglia activation-associated cytotoxicity was observed to promote the apoptosis of DACs, along with the decrease of SIRT3 expression. The aim of the present study was to explore the potential neuroprotective effect of SIRT3 expression against dopaminergic neuron injury caused by microglia activation, and clarify its possible mechanisms. SIRT3 overexpression in DACs reduced the production of intracellular reactive oxygen species (ROS), cell apoptosis rate, mitochondrial membrane potential (ΔΨm) depolarization, opening of mitochondrial permeability transition pore (mPTP) and cyclophilin D (CypD) protein level, and promoted cell cycle progression. However, SIRT3 siRNA-mediated knockdown further aggravated microglia activation-mediated cytotoxicity, including ROS accumulation, increased cell apoptosis and mPTP opening, elevated the CypD level, enhanced mitochondrial ΔΨm depolarization, concomitant to cell cycle arrest at G 0 /G 1 phase. The mechanisms of SIRT3 mitigated microglia activation-induced DAC dysfunction, which included decreased mPTP opening and Bax/Bcl-2 ratio, inhibition of mitochondrial cytochrome c release to the cytoplasm, reduced caspase-3/9 activity, increased LC3II/LC3I and beclin-1 protein expression levels, and decreased nucleotide-binding oligomerization domain, leucine rich repeat and pyrin domain-containing protein 3 (NLRP3), caspase-1, IL-1β and IL-18 protein expression. In conclusion, these results indicated that SIRT3 expression attenuated cell damage caused by microglia activation through the mitochondrial apoptosis pathway in DACs. The mitophagy-NLRP3 inflammasome pathway may also be associated with this neuroprotection. These findings may provide new intervention targets for the survival of dopaminergic neurons and the prevention and treatment of Parkinson's disease.

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Section: Sirt3 Expression Alleviates Microglia Activation-induced Dop...mentioning

confidence: 99%

SIRT3 expression alleviates microglia activation‑induced dopaminergic neuron injury through the mitochondrial pathway

et al. 2022

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“…Neuroinflammation and oxidative stress are manifested in various neurological diseases [ 16 – 18 ]. As one of the pattern recognition receptors, the nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome is a supramolecular complex composed of NLRP3, apoptosis-associated speck-like protein (ASC), and caspase-1, which are indispensable for the body's innate immunity against microbial infection [ 19 ].…”

Section: Introductionmentioning

confidence: 99%

Thioredoxin-Interacting Protein (TXNIP) Knockdown Protects against Sepsis-Induced Brain Injury and Cognitive Decline in Mice by Suppressing Oxidative Stress and Neuroinflammation

Zhang

Xing

Liu

et al. 2022

Oxidative Medicine and Cellular Longevity

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Sepsis-associated encephalopathy (SAE) is linked to increased morbidity and mortality rates in patients with sepsis. Increased cytokine production and neuronal apoptosis are implicated in the pathogenesis of the SAE. Neuroinflammation plays a major role in sepsis-induced brain injury. Thioredoxin-interacting protein (TXNIP), an inhibitor of thioredoxin, is associated with oxidative stress and inflammation. However, whether the TXNIP is involved in the sepsis-induced brain injury and the underlying mechanism is yet to be elucidated. Therefore, the present study was aimed at elucidating the effects of TXNIP knockdown on sepsis-induced brain injury and cognitive decline in mice. Lipopolysaccharide (LPS) was injected intraperitoneally to induce sepsis brain injury in mice. The virus-carrying control or TXNIP shRNA was injected into the lateral ventricle of the brain 4 weeks before the LPS treatment. The histological changes in the hippocampal tissues, encephaledema, and cognitive function were detected, respectively. Also, the 7-day survival rate was recorded. Furthermore, the alterations in microglial activity, oxidative response, proinflammatory factors, apoptosis, protein levels (TXNIP and NLRP3 inflammasome), and apoptosis were examined in the hippocampal tissues. The results demonstrated that the TXNIP and NLRP3 inflammasome expression levels were increased at 6, 12, and 24 h post-LPS injection. TXNIP knockdown dramatically ameliorated the 7-day survival rate, cognitive decline, brain damage, neuronal apoptosis, and the brain water content, inhibited the activation of microglia, downregulated the NLRP3/caspase-1 signaling pathway, and reduced the oxidative stress and the neuroinflammatory cytokine levels at 24 h post-LPS injection. These results suggested a crucial effect of TXNIP knockdown on the mechanism of brain injury and cognitive decline in sepsis mice via suppressing oxidative stress and neuroinflammation. Thus, TXNIP might be a potential therapeutic target for SAE patients.

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“…Several studies have been conducted using molecular techniques and cellular and animal models to confirm the pharmacological effects of these components. Deer antler has great potential in treating many diseases such as bone injuries [ 4 ], neurodegenerative diseases [ 5 ], tumors [ 6 ], and inflammatory conditions [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

Health Effects of Peptides Extracted from Deer Antler

Xia

Liu²,

Jiao

et al. 2022

Nutrients

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Deer antler is widely used as a nutraceutical in Asian countries. In the past decades, deer antler peptides (DAPs) have received considerable attention because of their various biological properties such as antioxidant, anti-inflammatory, anti-bone damage, anti-neurological disease, anti-tumor and immunomodulatory properties. This review describes the production methods of DAPs and the recent progress of research on DAPs, focusing on the physiological functions and their regulatory mechanisms.

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Velvet Antler Methanol Extracts Ameliorate Parkinson’s Disease by Inhibiting Oxidative Stress and Neuroinflammation: From C. elegans to Mice

Cited by 11 publications

References 47 publications

SIRT3 expression alleviates microglia activation‑induced dopaminergic neuron injury through the mitochondrial pathway

SIRT3 expression alleviates microglia activation‑induced dopaminergic neuron injury through the mitochondrial pathway

Thioredoxin-Interacting Protein (TXNIP) Knockdown Protects against Sepsis-Induced Brain Injury and Cognitive Decline in Mice by Suppressing Oxidative Stress and Neuroinflammation

Health Effects of Peptides Extracted from Deer Antler

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