Quercetin attenuates neuronal autophagy and apoptosis in rat traumatic brain injury model via activation of PI3K/Akt signaling pathway

Du, Guoliang; Zhao, Zongmao; Chen, Yonghan; Li, Zonghao; Tian, Yaohui; Liu, Zhifeng; Liu, Bin; Song, Jianqiang

doi:10.1080/01616412.2016.1240393

Cited by 56 publications

(38 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Phosphatidylinositol 3-kinase/Akt (PI3K/Akt) signaling pathway, is a significant survival pathway in neurons. 7 PI3K/Akt signaling plays a critical role in promoting neuronal survival not only in ischemic stroke, 8 but also in traumatic brain injury, 9 Parkinson's disease, 10 Alzheimer's disease, 11 intracerebral hemorrhage, 12 and SAH. 13 The neuroprotective effect of PI3K/Akt signaling has been well demonstrated in the antiapoptotic action 14 and antioxidative action, 15 but rarely in anti-inflammatory mechanism.…”

Section: Introductionmentioning

confidence: 99%

Propofol Reduces Inflammatory Brain Injury after Subarachnoid Hemorrhage: Involvement of PI3K/Akt Pathway

Zhang

Chen

et al. 2019

Journal of Stroke and Cerebrovascular Diseases

View full text Add to dashboard Cite

Background: Our previous study showed that propofol, one of the widely used anesthetic agents, can attenuate subarachnoid hemorrhage (SAH)-induced early brain injury (EBI) via inhibiting inflammatory and oxidative reaction. However, it is perplexing whether propofol attenuates inflammatory and oxidative reaction through modulating PI3K/Akt pathway. The present study investigated whether PI3K/Akt pathway is involved in propofol's anti-inflammation, antioxidation, and neuroprotection against SAH-induced EBI. Materials and methods: Adult Sprague-Dawley rats underwent SAH and received treatment with propofol or vehicle after 2 and 12 hours of SAH. LY294002 was injected intracerebroventricularly to selectively inhibit PI3K/Akt signaling. Mortality, SAH grading, neurological scores, brain water content, evans blue extravasation, myeloperoxidase, malondialdehyde, superoxide dismutase, and glutathione peroxidase were measured 24 hours after SAH. Immunoreactivity of p-Akt, t-Akt, nuclear factor-kappa B (NF-kB) p65, nuclear factor erythroid-related factor 2 (Nrf2), NAD(P)H:quinone oxidoreductase (NQO1), and cyclooxygenase-2 (COX-2) in rat brain was determined by western blot. Tumor necrosis factor-a (TNF-a) and interleukin-1b (IL-1b) in rat brain were examined by ELISA. Results: Propofol significantly reduces neurological dysfunction, BBB permeability, brain edema, inflammation, and oxidative stress, all of which were reversed by LY294002. Propofol significantly upregulates the immunoreactivity of p-Akt, Nrf2, and NQO1, all of which were abolished by LY294002. Propofol significantly downregulates the overexpression of NF-kB p65, COX-2, TNF-a, and IL-1b, all of which were inhibited by LY294002. Conclusion: These results suggest that propofol attenuates SAH-induced EBI by inhibiting inflammatory reaction and oxidative stress, which might be associated with the activation of PI3K/Akt signaling pathway.

show abstract

Section: Introductionmentioning

confidence: 99%

Propofol Reduces Inflammatory Brain Injury after Subarachnoid Hemorrhage: Involvement of PI3K/Akt Pathway

Zhang

Chen

et al. 2019

Journal of Stroke and Cerebrovascular Diseases

View full text Add to dashboard Cite

show abstract

“…TBI-induced neural death is the most prevalent cause of death in patients. Inhibition of post-injury cell death and preservation of neurons is the research focus of TBI (5). Inhibition of the cell death pathway and fundamental reduction of neuronal death is a potential treatment approach (6).…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective effect of berberine agonist against impairment of learning and memory skills in severe traumatic brain injury via Sirt1/p38 MAPK expression

Wang

Zhang

2018

Mol Med Report

View full text Add to dashboard Cite

Berberine has multiple clinical applications, including the treatment of tumors, diabetes, cardiovascular diseases, hyperlipidemia, inflammation, bacterial and viral infections, cerebral ischemic injuries, mental diseases, Alzheimer's disease and osteoporosis. In the present study, the neuroprotective effect of berberine agonist rescue learning and memory in severe traumatic brain injury (TBI), and the possible mechanism underlying these observations was explored. The protective effect of berberine agonist significantly recovered learning and memory skills, attenuated brain edema and inhibited matrix metalloproteinase‑3 and ‑9 protein expression in mice with severe TBI. Berberine agonist significantly reduced inflammation, oxidative stress and apoptosis levels in mice with severe TBI. Berberine agonist promoted choline acetyltransferase activity and inhibited the activity of acetylcholinesterase. Collectively, results of the present study revealed that the neuroprotective effect of berberine agonist rescues learning and memory skills in severe TBI.

show abstract

“…1) is a kind of flavonoid antioxidant substance, present in a variety of plants such as apples, green tea, onions, grape skins and so on. The red wine also contains a lot, and it is not easily soluble in water (13). It is regarded to have protective effect on cardiovascular and respiratory systems.…”

Section: Introductionmentioning

confidence: 99%

Quercetin prevents alcohol‑induced liver injury through targeting of PI3K/Akt/nuclear factor‑κB and STAT3 signaling pathway

2017

View full text Add to dashboard Cite

Abstract. Quercetin is a type of flavonoid compound, which has potent antioxidant and anti-inflammatory activities, capable of treating a variety of diseases including neurodegenerative diseases, tumors, diabetes and obesity. The present study selected alcohol-induced liver injury model mice and aimed at studying the protective role of quercetin in preventing alcohol-induced liver injury. In alcohol-induced liver injury mice treated with quercetin, it was demonstrated that levels of aspartate transaminase, alanine transaminase, total bilirubin and triglyceride were reduced. In addition to this, the activities of the antioxidant enzymes superoxide dismutase and glutathione peroxidase were increased, malondialdehyde was inhibited, and interleukin (IL)-1β, IL-6, IL-10 and inducible nitric oxide synthase were suppressed. Quercetin additionally suppressed the protein expression levels of B-cell lymphoma (Bcl)-2, Bcl-2 associated X apoptosis regulator, Caspase-3, poly ADP-ribose polymerase, and signal transducer and activator of transcription (STAT) 3 phosphorylation, nuclear factor (NF)-κB and protein kinase B (Akt) phosphorylation levels in alcohol-induced liver injured mice. These results suggested that the protective role of quercetin prevents alcohol-induced liver injury through the phosphoinositide 3-kinase/Akt/NF-κB and STAT3 pathway.

show abstract

Quercetin attenuates neuronal autophagy and apoptosis in rat traumatic brain injury model via activation of PI3K/Akt signaling pathway

Abstract: In conclusion, our observations indicate that post-injury treatment with quercetin could inhibit neuronal autophagy and apoptosis in the hippocampus in a rat model of TBI. The neuroprotective effects of quercetin may be related to modulation of PI3K/Akt signaling pathway.

Cited by 56 publications

References 33 publications

Propofol Reduces Inflammatory Brain Injury after Subarachnoid Hemorrhage: Involvement of PI3K/Akt Pathway

Propofol Reduces Inflammatory Brain Injury after Subarachnoid Hemorrhage: Involvement of PI3K/Akt Pathway

Neuroprotective effect of berberine agonist against impairment of learning and memory skills in severe traumatic brain injury via Sirt1/p38 MAPK expression

Quercetin prevents alcohol‑induced liver injury through targeting of PI3K/Akt/nuclear factor‑κB and STAT3 signaling pathway

Contact Info

Product

Resources

About