dl-3-n-butylphthalide protects endothelial cells against oxidative/nitrosative stress, mitochondrial damage and subsequent cell death after oxygen glucose deprivation in vitro

Li, Ling; Zhang, Bo; Tao, Youshan; Wang, Ying; Wei, Huan; Zhao, Jia; Huang, Ruxun; Pei, Zhong

doi:10.1016/j.brainres.2009.07.020

Cited by 80 publications

(46 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In our study, Oxa treatment showed a decreased activity of Mn-SOD in the brain. Many investigators have found a deviation in Mn-SOD activity in the isolated mitochondria of the brain Li et al 2009). Our result indicates that decreased Mn-SOD activity may be due to an increase in superoxide radical formation.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective activities of curcumin and quercetin with potential relevance to mitochondrial dysfunction induced by oxaliplatin

Waseem

Parvez

2015

Protoplasma

View full text Add to dashboard Cite

Peripheral neurotoxicity is one of the serious dose-limiting side effects of oxaliplatin (Oxa) when used in the treatment of malignant conditions. It is documented that it elicits major side effects specifically neurotoxicity due to oxidative stress forcing the patients to limit its clinical use in long-term treatment. Oxidative stress has been proven to be involved in Oxa-induced toxicity including neurotoxicity. The mitochondria have recently emerged as targets for anticancer drugs in various kinds of toxicity including neurotoxicity that can lead to neoplastic disease. However, there is paucity of literature involving the role of the mitochondria in mediating Oxa-induced neurotoxicity and its underlying mechanism is still debatable. The purpose of this study was to investigate the dose-dependent damage caused by Oxa on isolated brain mitochondria under in vitro conditions. The study was also designed to investigate the neuroprotective effects of nutraceuticals, curcumin (CMN), and quercetin (QR) on Oxa-induced mitochondrial oxidative stress and respiratory chain complexes in the brain of rats. Oxidative stress biomarkers, levels of nonenzymatic antioxidants, activities of enzymatic antioxidants, and mitochondrial complexes were evaluated against the neurotoxicity induced by Oxa. Pretreatment with CMN and QR significantly replenished the mitochondrial lipid peroxidation levels and protein carbonyl content induced by Oxa. CMN and QR ameliorated altered nonenzymatic and enzymatic antioxidants and complex enzymes of mitochondria. We conclude that CMN and QR, by attenuating oxidative stress as evident by mitochondrial dysfunction, hold promise as agents that can potentially reduce Oxa-induced adverse effects in the brain.

show abstract

Section: Discussionmentioning

confidence: 99%

Neuroprotective activities of curcumin and quercetin with potential relevance to mitochondrial dysfunction induced by oxaliplatin

Waseem

Parvez

2015

Protoplasma

View full text Add to dashboard Cite

show abstract

“…Some studies have reported that NBP has a diuretic effect in rats. 29,30 The urine volume of rats in group 3 (receiving 300 mg/kg hexanic extract) was significantly greater than other extract groups (methanolic and aqueous-ethanolic groups) and the spirnolactone-positive control group, as the animal cage in group 3 (300 mg/kg) was usually wet, compared to other groups (data was not shown). Thus, its diuretic effect could be one of the possible antihypertensive mechanisms of celery seeds.…”

Section: Figmentioning

confidence: 93%

Antihypertensive Effect of Celery Seed on Rat Blood Pressure in Chronic Administration

Moghadam

Imenshahidi

Mohajeri

2013

Journal of Medicinal Food

View full text Add to dashboard Cite

This study investigated the effects of different celery (Apium graveolens) seed extracts on blood pressure (BP) in normotensive and deoxycorticosterone acetate-induced hypertensive rats. The hexanic, methanolic, and aqueous-ethanolic extracts were administered intraperitoneally and their effects on BP and heart rate (HR) were evaluated in comparison with spirnolactone as a diuretic and positive control. Also, the amount of n-butylphthalide (NBP), as an antihypertensive constituent, in each extract was determined by HPLC. The results indicated that all extracts decreased BP and increased the HR in hypertensive rats, but had no effect on normotensive rats. The data showed that administration of 300 mg/kg of hexanic, methanolic, and aqueous-ethanolic (20/80, v/v) extracts of the celery seed caused 38, 24, and 23 mmHg reduction in BP and 60, 25, and 27 beats per minute increase in the HR, respectively. Also, the HPLC analysis data revealed that the content of NBP in the hexanic extract was 3.7 and 4 times greater than methanolic and aqueous-ethanolic extracts. It can be concluded that celery seed extracts have antihypertensive properties, which appears to be attributable to the actions of its active hydrophobic constitutes such as NBP and can be considered as an antihypertensive agent in chronic treatment of elevated BP.

show abstract

“…Its multiple neuroprotective effects were due to reduction of oxidative stress (6), blocking of inflammatory reactions and reduction of neuronal apoptosis (7). It had been proven that DL-NBP also exerts a protective effect on endothelial cells by suppressing the production of peroxynitrite, superoxide and nitric oxide in an acute hypoxia model (8). Notably, these protective effects were also observed in other disease models, not caused by hypoxia or ischemic injury.…”

Section: Introductionmentioning

confidence: 89%

DL-3-n-butylphthalide protects endothelial cells against advanced glycation end product-induced injury by attenuating oxidative stress and inflammation responses

Liu

Zhao

Chen

et al. 2017

Experimental and Therapeutic Medicine

View full text Add to dashboard Cite

Abstract. Endothelial dysfunction, regarded as a key step in the pathophysiological course of diabetic vascular complications, is initiated and deteriorated by advanced glycation end products (AGEs). DL-3-n-butylphthalide (DL-NBP) has been proven to have protective effects on neurons and vascular endothelial cells against ischemic and anoxic damage. The aim of the present study was to investigate whether NBP is able to attenuate AGE-induced endothelial dysfunction in vitro, and also elucidate the possible underlying mechanism. An injury model of human umbilical vein endothelial cells (HUVECs) induced by AGEs (200 µg/ml) was established. The results demonstrated that pretreatment with NBP (1-100 µM) significantly increased HUVEC viability and inhibited the apoptosis induced by AGEs. In addition, AGEs stimulated the expression levels of the receptor for AGEs protein and the downstream protein nuclear factor-κB in HUVECs, which were inhibited by pretreatment with NBP. Furthermore, it significantly reduced reactive oxygen species generation and the level of the inflammatory cytokines, intercellular cell adhesion molecule-1 and monocyte chemotactic protein-1, in HUVECs mediated by AGEs. The current findings indicated that NBP attenuated AGE-induced endothelial dysfunction by ameliorating inflammation and oxidative stress responses.

show abstract

dl-3-n-butylphthalide protects endothelial cells against oxidative/nitrosative stress, mitochondrial damage and subsequent cell death after oxygen glucose deprivation in vitro

Cited by 80 publications

References 21 publications

Neuroprotective activities of curcumin and quercetin with potential relevance to mitochondrial dysfunction induced by oxaliplatin

Neuroprotective activities of curcumin and quercetin with potential relevance to mitochondrial dysfunction induced by oxaliplatin

Antihypertensive Effect of Celery Seed on Rat Blood Pressure in Chronic Administration

DL-3-n-butylphthalide protects endothelial cells against advanced glycation end product-induced injury by attenuating oxidative stress and inflammation responses

Contact Info

Product

Resources

About