Neferine Protects Against Brain Damage in Permanent Cerebral Ischemic Rat Associated with Autophagy Suppression and AMPK/mTOR Regulation

Sengking, Jirakhamon; Oka, Chio; Wicha, Piyawadee; Yawoot, Nuttapong; Tocharus, Jiraporn; Chaichompoo, Waraluck; Suksamrarn, Apichart; Tocharus, Chainarong

doi:10.1007/s12035-021-02554-z

Cited by 15 publications

(9 citation statements)

References 56 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The difference may stem from the different disease models, experimental animal ages, insult severity, ischemic stages, and autophagy degrees. Apparently, enhancement or inhibition of neuron autophagy may induce disease, dependent on the stages of the diseases [26]. We are interested in further investigating the molecular mechanisms underlying the action of Xe in inhibiting neuron autophagy during the process of HIBD.…”

Section: Discussionmentioning

confidence: 99%

Xenon attenuates hypoxic-ischemic brain damage by inhibiting autophagy in neonatal rats

Sun

Wei

et al. 2023

NeuroReport

View full text Add to dashboard Cite

Xenon (Xe) is an inert, colorless and odorless heavy gas and has many biological functions. However, little is known about whether and how Xe can modulate hypoxic-ischemic brain damage (HIBD) in neonatal rats. This study employed a neonatal rat model to explore the potential effect of Xe on neuron autophagy and the severity of HIBD. Neonatal Sprague–Dawley rats were subjected to HIBD, randomized and treated with Xe or mild hypothermia (at 32 °C) for 3 h. The degrees of HIBD, neuron autophagy and the neuronal functions in some neonates from each group were tested by histopathology, immunochemistry, transmission electron microscopy, western blot, open-field and Trapeze tests at 3 and 28 days post-induction of HIBD, respectively. Compared with the Sham group, hypoxic-ischemia caused larger volumes of cerebral infarction and severe brain damage, and increased autophagosome formation and Beclin-1 and microtubule-associated protein 1A/1B-light chain 3 class II (LC3-II) expression in the brain of rats, accompanied by the defect in neuronal functions. In contrast, treatment with Xe and/or hypothermia significantly reduced infarct volumes and ameliorated neurological defects in the HIBD rats, particularly for the combination of Xe and hypothermia. Xe significantly mitigated the relative levels of Beclin-1 and LC3-II expression and autophagosome formation induced by HIBD in rats. Xe acted as a neuroprotective factor against HIBD, possibly by inhibiting the hypoxia-induced neuron autophagy in rats.

show abstract

Section: Discussionmentioning

confidence: 99%

Xenon attenuates hypoxic-ischemic brain damage by inhibiting autophagy in neonatal rats

Sun

Wei

et al. 2023

NeuroReport

View full text Add to dashboard Cite

show abstract

“…Liensinine inhibits the formation of alcoholic fatty liver by improving AMPK activation and reduces palmitate acid‐induced lipid deposition in liver tissue (Liang et al, 2022). Neferine ameliorates the brain damage against permanent cerebral ischemia in rat via suppression of autophagy and regulation of AMPK/mTOR pathway (Sengking et al, 2021). Neferine, liensinine, and isoliensinine also decrease the protein expression of androgen receptor, prostate‐specific antigen, and type II 5‐α‐reductase in prostate cancer via PI3K/Akt signaling pathway (Liu et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

The anticardiac fibrosis of total alkaloids of Plumula nelumbinis by regulating circulating lipidomic profile: In vivo study

Shi

Yang

et al. 2022

Journal of Food Biochemistry

View full text Add to dashboard Cite

Plumula nelumbinis has great medicinal potential as a herbal tea and traditional drug in China. This study was aimed to evaluate the anticardiac fibrosis of the total alkaloids of P. nelumbinis (TAP). TAP at 50 mg/kg/day significantly ameliorated isoproterenolinduced cardiac fibrosis in mice (p < .05). The circulating lipidomics study revealed that TAP improved the lipid metabolism dysfunction in cardiac fibrosis. Meanwhile, TAP suppressed the lipid accumulation, decreased MDA level (p < .01) in heart, and increased FFA level (p < .01). Furthermore, integrating lipidomics, chemical profiles and pharmacology network analysis found that AMPK and PI3K/Akt signaling pathways were the potential targeted pathway by TAP to regulate lipid metabolism dysfunction including glycerophospholipid metabolism. Above all, TAP provided a potential anticardiac fibrosis effect partly through regulation of lipid profiles. Practical applications1. The total alkaloids of Plumula nelumbinis (TAP) suppressed ISO-induced cardiac fibrosis in mice.2. Network pharmacology analysis and experiments revealed that TAP-regulated AMPK and PI3K/Akt signaling pathway to improve lipid metabolism disorder in cardiac fibrosis.3. This study provides evidence to the therapeutic potential of TAP in the treatment of ISO-induced cardiac fibrosis and could be a drug candidate for prevention and treatment of cardiac fibrosis.

show abstract

“…Neurological deficits in the mice were assessed with the following five-point scale at 24 h after surgery according to previous reports [ 32 , 33 ]: 0, no observable deficit; 1, inability to extend the contralateral forepaw; 2, circling from the contralateral to affected side; 3, falling to the contralateral side of infarct; 4, depressed level of consciousness or no spontaneous activity.…”

Section: Methodsmentioning

confidence: 99%

Eriocalyxin B alleviated ischemic cerebral injury by limiting microglia-mediated excessive neuroinflammation in mice

Chen,

Zhang,

Zhao

et al. 2024

Exp. Anim.

View full text Add to dashboard Cite

Excessive neuroinflammation mediated by microglia has a detrimental effect on the progression of ischemic stroke. Eriocalyxin B (EriB) was found with a neuroprotective effect in mice with Parkinson’s disease via the suppression of microglial overactivation. This study aimed to investigate the roles of EriB in permanent middle cerebral artery occlusion (pMCAO) mice. The pMCAO was induced in the internal carotid artery of the mice by the intraluminal filament method, and EriB (10 mg/kg) was administered immediately after surgery by intraperitoneal injection. The behavior score, 2,3,5-triphenyltetrazole chloride staining, Nissl staining, TUNEL, immunohistochemistry, immunofluorescence, PCR, ELISA, and immunoblotting revealed that EriB administration reduced brain infarct and neuron death and ameliorated neuroinflammation and microglia overactivation in pMCAO mice, manifested by alterations of TUNEL-positive cell numbers, ionized calcium binding adaptor molecule 1 (Iba-1)-positive cell numbers, and expression of tumor necrosis factor-α, interleukin 6, IL-1β, inducible nitric oxide synthase, and arginase 1. In addition, EriB suppressed ischemia-induced activation of nuclear factor kappa B (NF-κB) signaling in the brain penumbra, suggesting the involvement of NF-κB in EriB function. In conclusion, EriB exerted anti-inflammatory effects in ischemia stroke by regulating the NF-κB signaling pathway, and this may provide insights into the neuroprotective effect of EriB in the treatment of ischemic stroke.

show abstract

Neferine Protects Against Brain Damage in Permanent Cerebral Ischemic Rat Associated with Autophagy Suppression and AMPK/mTOR Regulation

Cited by 15 publications

References 56 publications

Xenon attenuates hypoxic-ischemic brain damage by inhibiting autophagy in neonatal rats

Xenon attenuates hypoxic-ischemic brain damage by inhibiting autophagy in neonatal rats

The anticardiac fibrosis of total alkaloids of Plumula nelumbinis by regulating circulating lipidomic profile: In vivo study

Eriocalyxin B alleviated ischemic cerebral injury by limiting microglia-mediated excessive neuroinflammation in mice

Contact Info

Product

Resources

About