Neuroprotective effect of 5,7,3′,4′,5′-pentahydroxy dihdroflavanol-3-O-(2″-O-galloyl)-β-d-glucopyranoside, a polyphenolic compound in focal cerebral ischemia in rat

Arunadevi, R.; Lata, Suman; Bhadoria, B. K.; Ramteke, Vinod D.; Kumar, Saurabh; Sankar, P.; Kumar, Dinesh; Tandan, Surendra K.

doi:10.1016/j.ejphar.2009.09.038

Cited by 25 publications

(11 citation statements)

References 35 publications

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“…Because exogenously administered H 2 O 2 is one of the most widely used methods to induce cytotoxicity [16][17][18] , we evaluated the neuroprotective effects of sinomenine during H 2 O 2 -induced injury in PC12 cells. Pretreatment with sinomenine significantly attenuated H 2 O 2 -induced PC12 cell death, in a dose-dependent manner, at a concentration range of 0.060 to 0.600 μg/mL of the drug.…”

Section: Discussionmentioning

confidence: 99%

HPLC and LC-MS analysis of sinomenine and its application in pharmacokinetic studies in rats

Long

Chen

et al. 2010

Acta Pharmacol Sin

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Aim: To improve and validate analytical methods based on HPLC and liquid chromatography coupled to electrospray ionization tandem mass spectrometry (LC-ESI-MS/MS) for the quantitative measurement of sinomenine in rat plasma and brain tissue. Methods: The separation of analytes and the internal standard (IS), chloramphenicol, was performed on an Agilent TC-C18 column (250×4.6 mm, 5 µm). Blood samples were measured with a Surveyor photodiode array (PDA) detector at a wavelength of 263 nm. The LCQ DECA XP Plus mass spectrometer was operated in the multiple reactions monitoring mode using positive electrospray ionization, and the transition from the precursor ion (m/z 279) to the product ion (m/z 224) for sinomenine was measured in brain tissue. Results: Measurements were linear over the concentration range of 0.1-100 µg/mL for sinomenine in plasma and over the range of 0.01-5.00 µg/g for sinomenine in brain tissue. The intra-and inter-day variabilities were less than 10% of the relative standard deviation (RSD), and the extraction and recovery of sinomenine was 72.48%-80.26% from plasma and 73.75%-80.26% from brain tissue. The limit of quantification (LOQ) was 0.1 µg/mL for plasma, and 0.01 µg/g for brain tissue. Identification of sinomenine was reproducible at 0.5, 5, and 50 μg/mL in the plasma and at 0.05, 0.50, and 2.00 μg/g in brain tissue. The concentration of sinomenine measured in brain tissue after a single ip dose had a neuroprotective effect on H 2 O 2 -induced injury in PC12 cells in vitro. Conclusion: Our methods offered a sensitivity within a wide linear concentration range for sinomenine. These methods were successfully applied to evaluate sinomenine pharmacokinetics over time in rat brain tissue after a single ip dose of 30 mg/kg.

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Section: Discussionmentioning

confidence: 99%

HPLC and LC-MS analysis of sinomenine and its application in pharmacokinetic studies in rats

Long

Chen

et al. 2010

Acta Pharmacol Sin

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“…Other authors have previously reported the beneficial effects of Mediterranean diet (enriched in olive oil) for the prevention of brain and cardiovascular diseases [25,26,40]. Moreover, it was reported the improvement of brain stroke evolution with the administration of curcumin [34,35], tyrosol and hydroxytyrosol [36,38], red wine polyphenols [37], resveratrol [41], and other phenolic compounds [39]. The biological effect of the polyphenols is heterogeneous.…”

Section: Discussionmentioning

confidence: 96%

“…Fatty acids may modulate inflammatory response [27,28], modify the antioxidant status of many tissues [29,30,31], and regulate ceramide generation [32]. In addition, several studies confirmed that other components of dietary fats such as polyphenols play an important role in the prevention of stroke and cardiovascular illnesses or they attenuate the detrimental effects caused by ischemia [33][34][35][36][37][38][39][40][41]. (2) the inflammatory response (prostaglandin and citokine production), (3) activity of phospholipase A2 and nitric oxide synthetase isoforms, (4) production of ceramide, and (5) activation of cellular death cascades (caspase-3 and milli-and micro-calpains) in order to contribute with experimental evidence that supports nutritional recommendation for the prevention of damages produced by brain stroke.…”

Section: Introductionmentioning

confidence: 97%

Dietary fats significantly influence the survival of penumbral neurons in a rat model of chronic ischemic by modifying lipid mediators, inflammatory biomarkers, NOS production, and redox-dependent apoptotic signals

et al. 2015

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“…MMP-9 downregulation by resveratrol was also observed in an in vitro model of neuronal ischemic injury [109]. 5,7,3′,4′,5′-pentahydroxy dihdroflavanol-3- O -(2″- O galloyl)- beta- d -glucopyranoside (AP1), a polyphenolic compound isolated from Anogeissus pendula Edgew (an arid forest tree), was effective in reducing apoptotic cells in rat brain following transient focal cerebral ischemia [110]. The effect of TSG in protecting rat brain from MCAO is by increasing the anti-apoptotic Bcl-2 proteins [102].…”

Section: Protective Role Of Polyphenols In Neuronal Ischemic Injurymentioning

confidence: 99%

“…[88] reported a protective effect of green tea polyphenol EGCG against neuronal damage and brain edema after unilateral cerebral ischemia in gerbils. AP1, a polyphenolic compound, also reduced brain edema in rats after transient focal ischemia [110]. We recently reported the protective effects of polyphenols from green tea [112] as well as cinnamon [113] on glial swelling in cultures following ischemia-like injury [138].…”

Section: Role Of Polyphenols In Attenuating Oxidative Stress and Mmentioning

confidence: 99%

Effect of Polyphenols on Oxidative Stress and Mitochondrial Dysfunction in Neuronal Death and Brain Edema in Cerebral Ischemia

Panickar

Anderson

2011

IJMS

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Polyphenols are natural substances with variable phenolic structures and are elevated in vegetables, fruits, grains, bark, roots, tea, and wine. There are over 8000 polyphenolic structures identified in plants, but edible plants contain only several hundred polyphenolic structures. In addition to their well-known antioxidant effects, select polyphenols also have insulin-potentiating, anti-inflammatory, anti-carcinogenic, anti-viral, anti-ulcer, and anti-apoptotic properties. One important consequence of ischemia is neuronal death and oxidative stress plays a key role in neuronal viability. In addition, neuronal death may be initiated by the activation of mitochondria-associated cell death pathways. Another consequence of ischemia that is possibly mediated by oxidative stress and mitochondrial dysfunction is glial swelling, a component of cytotoxic brain edema. The purpose of this article is to review the current literature on the contribution of oxidative stress and mitochondrial dysfunction to neuronal death, cell swelling, and brain edema in ischemia. A review of currently known mechanisms underlying neuronal death and edema/cell swelling will be undertaken and the potential of dietary polyphenols to reduce such neural damage will be critically reviewed.

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Neuroprotective effect of 5,7,3′,4′,5′-pentahydroxy dihdroflavanol-3-O-(2″-O-galloyl)-β-d-glucopyranoside, a polyphenolic compound in focal cerebral ischemia in rat

Cited by 25 publications

References 35 publications

HPLC and LC-MS analysis of sinomenine and its application in pharmacokinetic studies in rats

HPLC and LC-MS analysis of sinomenine and its application in pharmacokinetic studies in rats

Dietary fats significantly influence the survival of penumbral neurons in a rat model of chronic ischemic by modifying lipid mediators, inflammatory biomarkers, NOS production, and redox-dependent apoptotic signals

Effect of Polyphenols on Oxidative Stress and Mitochondrial Dysfunction in Neuronal Death and Brain Edema in Cerebral Ischemia

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