dl -3- n -butylphthalide suppresses PDGF-BB-stimulated vascular smooth muscle cells proliferation via induction of autophagy

Hu, Haijuan; Liu, Bin; Zuo, Ya-Bei; Liu, Demin; Xie, Ruiqin; Cui, Wei

doi:10.1016/j.lfs.2016.03.010

Cited by 11 publications

(8 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…From the primary screen (Qosa et al, 2016), we identified several hit compounds from which the following compounds were selected for further characterization due to available studies reporting their potential neuroprotective effects (Table 1) (Lim et al, 1997; Fernández-Tomé et al, 1999; Wirtz-Brugger and Giovanni, 2000; Mangialasche et al, 2012; Pena-Ortega et al, 2012; Hu et al, 2016). These compounds are 8-bromoguanosine 3,5-cyclic monophosphate sodium salt (BrG), JW74, 1,10-phenanthroline monohydrate (Phen), SB216763 (SB2) and α-tocopherol (Tph).…”

Section: Methodsmentioning

confidence: 99%

“…Among these hits, five investigational compounds reported to have a neuroprotective effect and/or affect pathways associated with AD were selected for further evaluation in the current study. These hit compounds are 8-bromoguanosine 3,5-cyclic monophosphate sodium salt (Fernández-Tomé et al, 1999; Wirtz-Brugger and Giovanni, 2000), JW74 (Hu et al, 2016), 1,10-phenanthroline monohydrate (Lim et al, 1997), SB216763 (Pena-Ortega et al, 2012), and α-tocopherol (Mangialasche et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Characterization of Hit Compounds Identified from High-throughput Screening for their Effect on Blood–brain Barrier Integrity and Amyloid-β Clearance: In Vitro and In Vivo Studies

et al. 2018

View full text Add to dashboard Cite

In Alzheimer's disease (AD) the blood-brain barrier (BBB) is compromised, thus therapeutic targeting of the BBB to enhance its integrity and function could be a unique approach to treat, slow or hold the progression of AD. Recently, we have developed an in vitro high-throughput screening assay to screen for compounds that increase the integrity of a cell-based BBB model. Results from primary screen identified multiple hit compounds that enhanced the monolayer integrity. Herein, further characterization of selected hit compounds, namely 8-bromoguanosine cyclic monophosphate, JW74, 1,10-phenanthroline monohydrate, SB216763 and α-tocopherol was performed. Compounds were subjected to concentration-dependent studies to determine their EC50 and potency to enhance the cell-based model integrity by the Lucifer Yellow permeability and amyloid-beta (Aβ) transport across the monolayer. The compounds demonstrated different EC50s to enhance the monolayer integrity ranging from 0.4 to 12.8 µM, and different effect on enhancing Aβ transport with highest transport observed for α-tocopherol (2.2-fold increase). Such effects were associated with increased levels of tight junction proteins such as claudin-5 and/or ZO-1, and Aβ major transport proteins LRP1 and P-glycoprotein. In vivo studies for α-tocopherol were performed in AD mouse model; consistent with the in vitro results α-tocopherol significantly increased BBB integrity measured by IgG extravasation, and reduced brain Aβ levels. In conclusion, findings support our developed cell-based BBB model as a functional predictive in vivo tool to select hit compounds, and suggest that enhancing BBB tightness and function has the potential to reduce Aβ pathology associated with AD.

show abstract

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Characterization of Hit Compounds Identified from High-throughput Screening for their Effect on Blood–brain Barrier Integrity and Amyloid-β Clearance: In Vitro and In Vivo Studies

et al. 2018

View full text Add to dashboard Cite

show abstract

“…The results showed several common neuroprotective mechanisms ranging from reduction of oxidative stress to prevention of apoptosis to induction of autophagy through suppression of the β -catenin signaling pathway [72] to promotion of angiogenesis. The converging points of NBP antioxidative [71], antiapoptotic, and proangiogenic effects on those conditions are believed to be through reduction of caspase-3 activity, upregulation of vascular endothelial growth factor (VEGF) expression, and elimination of ROS production [70, 73–75].…”

Section: Nbp and Other Conditionsmentioning

confidence: 99%

A Review of Recent Advances in Neuroprotective Potential of 3-N-Butylphthalide and Its Derivatives

Abdoulaye

Guo

2016

BioMed Research International

View full text Add to dashboard Cite

The research of alternative treatment for ischemic stroke and degenerative diseases has always been a priority in neurology. 3-N-Butylphthalide (NBP), a family of compounds initially isolated from the seeds of Apium graveolens Linn., has shown significant neuroprotective effects. Previous extensive studies have demonstrated that NBP promotes a better poststroke outcome and exerts a multitargeted action on several mechanisms, from oxidative stress to mitochondrial dysfunction to apoptosis to inflammation. Additionally, recent findings on several neurological disorders have shown that NBP's beneficial effects extend beyond the management of stroke. However, despite the increasing number of studies toward a better understanding and the rapid advances made in therapeutic options, to date, dl-3-N-butylphthalide, a synthetic variation of l-3-N-butylphthalide, remains the only clinically approved anti-ischemic agent in China, stressing the difficulties for a viable and effective transition from experimental to clinical practice. Events indicate that NBP, due to its multitargeted effect and the adaptability of its basic structure, can be an important game changer and a precursor to a whole new therapeutic approach to several neurological conditions. The present review discusses recent advances pertaining to the neuroprotective mechanisms of NBP-derived compounds and the possibility of their clinical implementation in the management of various neurological conditions.

show abstract

“…In the context of our findings, it appears that upregulation of autophagy occurs in the presence of overexpression of TUG1, giving rise to the greater functional activity of EPCs. Recent pieces of evidence indicate that overexpression of miR-29c-3p inhibited autophagy in ovarian cancer [ 47 ], and DL-3-nbutylphthalide protected vascular smooth muscle cells from PDGF-BB-stimulated proliferation by inducing autophagy through suppression of the β-catenin signaling pathway [ 48 ]. In our study, we speculate that miR-29c-3p/PDGF-BB/Wnt signaling pathway may involve in the autophagy in EPCs under high glucose treatment, but it needs to be further explored in the following research.…”

Section: Discussionmentioning

confidence: 99%

TUG1 enhances high glucose-impaired endothelial progenitor cell function via miR-29c-3p/PDGF-BB/Wnt signaling

Zhi

Han

et al. 2020

Stem Cell Res Ther

View full text Add to dashboard Cite

Background Diabetes is associated with the dysfunction of endothelial progenitor cells (EPCs), characterized as impaired angiogenesis, a phenomenon thought to be involved in the development of diabetic foot. lncRNA plays an essential role in microvascular dysfunction and signaling pathways in patients with diabetes. lncRNA taurine upregulated gene 1 (TUG1) participates in angiogenesis in various cells. However, the mechanisms of TUG1 activity in EPCs have not been elucidated. Methods We isolated and then characterized EPCs from the peripheral blood of mice using immunofluorescence and flow cytometry. Western blot detected the wnt/β-catenin pathway in high glucose-treated EPCs. Bioinformatics analysis predicted a putative binding site for TUG1 on miR-29c-3p. The interactions among TUG1, platelet-derived growth factor-BB (PDGF-BB), and miR-29c-3p were analyzed by luciferase assays. In vivo, diabetic mouse ischemic limb was treated with normal saline or TUG1 overexpression lentiviruses. Results We found that EPC migration, invasion, and tube formation declined after treatment with high glucose, but improved with TUG1 overexpression. Mechanically, wnt/β-catenin pathway and autophagy were involved in the function of TUG1 overexpression in high glucose-treated EPCs. Moreover, TUG1 regulates the PDGF-BB/wnt pathway and function of high glucose-treated EPCs via miR-29c-3p. In vivo, injection of TUG1 lentivirus in a diabetic mouse ischemic limb model stimulated angiogenesis. Conclusions Our findings suggest that TUG1 restores high glucose-treated EPC function by regulating miR-29c-3p/PDGF-BB/Wnt signaling.

show abstract

dl -3- n -butylphthalide suppresses PDGF-BB-stimulated vascular smooth muscle cells proliferation via induction of autophagy

Cited by 11 publications

References 31 publications

Characterization of Hit Compounds Identified from High-throughput Screening for their Effect on Blood–brain Barrier Integrity and Amyloid-β Clearance: In Vitro and In Vivo Studies

Characterization of Hit Compounds Identified from High-throughput Screening for their Effect on Blood–brain Barrier Integrity and Amyloid-β Clearance: In Vitro and In Vivo Studies

A Review of Recent Advances in Neuroprotective Potential of 3-N-Butylphthalide and Its Derivatives

TUG1 enhances high glucose-impaired endothelial progenitor cell function via miR-29c-3p/PDGF-BB/Wnt signaling

Contact Info

Product

Resources

About