Protective effect of bromocriptine against BH4-induced Cath.a cell death involving up-regulation of antioxidant enzymes

Lim, Ju Hee; Kim, Sa Suk; Boo, Doo Hyun; No, Haja; Kang, Bok Yun; Kim, Eun-Mee; Hwang, Onyou; Choi, Hyun Jin

doi:10.1016/j.neulet.2008.12.056

Cited by 22 publications

(13 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Activation of PI3K and its downstream effector Akt has also been shown to suppress apoptosis and promote cell survival [25–27]. It has been shown that activation of PI3K leads to the phosphorylation and activation of Akt, which promotes cell survival by enhancing the expression of anti-apoptotic proteins and inhibiting the activity of pro-apoptotic proteins [28,29].…”

Section: Resultsmentioning

confidence: 99%

Myricetin Protects Cells against Oxidative Stress-Induced Apoptosis via Regulation of PI3K/Akt and MAPK Signaling Pathways

Kang

Wang

Zhang

et al. 2010

IJMS

104

View full text Add to dashboard Cite

Recently, we demonstrated that myricetin exhibits cytoprotective effects against H2O2-induced cell damage via its antioxidant properties. In the present study, myricetin was found to inhibit H2O2-induced apoptosis in Chinese hamster lung fibroblast (V79-4) cells, as shown by decreased apoptotic bodies, nuclear fragmentation, sub-G1 cell population, and disruption of mitochondrial membrane potential (Δψm), which are increased in H2O2-treated cells. Western blot data showed that in H2O2-treated cells, myricetin increased the level of Bcl-2, which is an anti-apoptotic factor, and decreased the levels of Bax, active caspase-9 and -3, which are pro-apoptotic factors. And myricetin inhibited release of cytochrome c from mitochondria to cytosol in H2O2-treated cells. Myricetin-induced survival correlated with Akt activity, and the rescue of cells by myricetin treatment against H2O2-induced apoptosis was inhibited by the specific PI3K (phosphoinositol-3-kinase) inhibitor. Myricetin-mediated survival also inhibited the activation of p38 mitogen activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK), which are members of MAPK. Our studies suggest that myricetin prevents oxidative stress-induced apoptosis via regulation of PI3K/Akt and MAPK signaling pathways.

show abstract

Section: Resultsmentioning

confidence: 99%

Myricetin Protects Cells against Oxidative Stress-Induced Apoptosis via Regulation of PI3K/Akt and MAPK Signaling Pathways

Kang

Wang

Zhang

et al. 2010

IJMS

104

View full text Add to dashboard Cite

show abstract

“…In this publication, bromocriptine was loaded into CS nanoparticles, resulting in particles with a mean size of 161.3 ± 4.7 nm, and a zeta potential of +40.3 ± 2.7 mV. Bromocriptine acts as a protector of dopaminergic cells and is therefore a well-known drug in Parkinson’s disease [119]. Bromocriptine was labeled with technetium, a radio-active substance, to measure the distribution.…”

Section: Improvement Of the Nose-to-brain Pathway Through Formulatmentioning

confidence: 99%

Formulations for Intranasal Delivery of Pharmacological Agents to Combat Brain Disease: A New Opportunity to Tackle GBM?

Woensel

Wauthoz

Rosière

et al. 2013

Cancers

136

View full text Add to dashboard Cite

Despite recent advances in tumor imaging and chemoradiotherapy, the median overall survival of patients diagnosed with glioblastoma multiforme does not exceed 15 months. Infiltration of glioma cells into the brain parenchyma, and the blood-brain barrier are important hurdles to further increase the efficacy of classic therapeutic tools. Local administration methods of therapeutic agents, such as convection enhanced delivery and intracerebral injections, are often associated with adverse events. The intranasal pathway has been proposed as a non-invasive alternative route to deliver therapeutics to the brain. This route will bypass the blood-brain barrier and limit systemic side effects. Upon presentation at the nasal cavity, pharmacological agents reach the brain via the olfactory and trigeminal nerves. Recently, formulations have been developed to further enhance this nose-to-brain transport, mainly with the use of nanoparticles. In this review, the focus will be on formulations of pharmacological agents, which increase the nasal permeation of hydrophilic agents to the brain, improve delivery at a constant and slow release rate, protect therapeutics from degradation along the pathway, increase mucoadhesion, and facilitate overall nasal transport. A mounting body of evidence is accumulating that the underexplored intranasal delivery route might represent a major breakthrough to combat glioblastoma.

show abstract

“…BRC has also been reported to have antioxidant effects, inhibit free radical formation and scavenge free radicals and retard apoptosis, which is probably accelerated in PD [14,15]. BRC is available in tablet and capsule dosage form (2.5 --20 mg/day, in divided doses), and these dosage forms exhibit low bioavailability (6%) due to extensive first-pass metabolism and non-targeted delivery results in side effects such as GI side effects, headache and dizziness [16].…”

Section: Introductionmentioning

confidence: 99%

Optimised nanoformulation of bromocriptine for direct nose-to-brain delivery: biodistribution, pharmacokinetic and dopamine estimation by ultra-HPLC/mass spectrometry method

Shadab

Haque

Fazil

et al. 2014

Expert Opinion on Drug Delivery

View full text Add to dashboard Cite

show abstract

Protective effect of bromocriptine against BH4-induced Cath.a cell death involving up-regulation of antioxidant enzymes

Cited by 22 publications

References 34 publications

Myricetin Protects Cells against Oxidative Stress-Induced Apoptosis via Regulation of PI3K/Akt and MAPK Signaling Pathways

Myricetin Protects Cells against Oxidative Stress-Induced Apoptosis via Regulation of PI3K/Akt and MAPK Signaling Pathways

Formulations for Intranasal Delivery of Pharmacological Agents to Combat Brain Disease: A New Opportunity to Tackle GBM?

Optimised nanoformulation of bromocriptine for direct nose-to-brain delivery: biodistribution, pharmacokinetic and dopamine estimation by ultra-HPLC/mass spectrometry method

Contact Info

Product

Resources

About