Article

Anti-platelet effects of bioactive compounds isolated from the bark of Rhus verniciflua Stokes

Division of Biological Sciences, Konkuk University, Sŏul, Seoul, South Korea
Journal of Ethnopharmacology (Impact Factor: 3). 07/2006; 106(1):62-9. DOI: 10.1016/j.jep.2005.12.015
Source: PubMed

ABSTRACT

It has previously been shown that EtOAc extracts of Rhus verniciflua Stokes (RVS) inhibit the platelet aggregation response. In this report, bioassay-guided fractionation using ADP-, arachidonic acid-, and collagen-induced human platelet aggregation by a whole blood aggregometer yielded the bioactive compounds isomaltol and pentagalloyl glucose from different highly effective fractions. In addition, column chromatography of fractions from RVS yielded another five compounds: butin, fisetin, sulfuretin, butein and 3,4',7,8-tetrahydroxyflavone. We investigated the effects of bioactive compounds from RVS fractions on several markers of platelet activation using receptor expression on platelet membranes, including glycoprotein IIb/IIIa (CD41), GPIIb/IIIa-like expression (PAC-1) and P-selectin (CD62), and intracelluar calcium mobilization responses by flow cytometry in healthy subjects. Dose-dependent inhibition of platelet aggregation and significantly decreased platelet activation were observed for the isomaltol- and pentagalloyl glucose-treated platelets, respectively. These results show that isomaltol and pentagalloyl glucose from the bark of Rhus verniciflua Stokes have potent anti-platelet activity and emphasize the need to further examine the mechanism of these active compounds for platelet modulation.

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    • "In addition to the activities discussed above, Rhus verniciflua Stokes exhibited numerous other activities by in vitro studies. For example, in one study, Rhus verniciflua Stokes showed dose-dependent inhibitory activity towards adenosine diphosphate- (ADP-), collagen-, and arachidonic acid- (AA-) induced aggregation of human platelets [37]. In another study, total extract from Rhus verniciflua Stokes showed Aldo-keto reductase family 1 B10 (AKR1B10), which may be responsible for detoxification of reactive aldehydes, inhibitory activity [38]. "
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    ABSTRACT: Despite the fact that numerous researches were performed on prevention and treatment of inflammation related diseases, the overall incidence has not changed remarkably. This requires new approaches to overcome inflammation mediated diseases, and thus traditional medicine could be an efficacious source for prevention and treatment of these diseases. In this review, we discuss the contribution of traditional medicine, especially Rhus verniciflua Stokes, to modern medicine against diverse inflammation mediated diseases. Traditionally, this remedy has been used in Eastern Asia for the treatment of gastric problems, hepatic disorders, infectious diseases, and blood disorders. Modern science has provided the scientific basis for the use of Rhus verniciflua Stokes against such disorders and diseases. Various chemical constituents have been identified from this plant, including phenolic acid, and flavonoids. Cell-based studies have exhibited the potential of this as antibacterial, antioxidant, neuroprotective, anti-inflammatory, growth inhibitory, and anticancer activities. Enormous animal studies have shown the potential of this against proinflammatory diseases, neurodegenerative diseases, diabetes, liver diseases, and chemical insults. At the molecular level, this medicinal plant has been shown to modulate diverse cell-signaling pathways. In clinical studies, Rhus verniciflua Stokes has shown efficacy against various cancer patients such as colorectal, gastric, hepatic, renal, pancreatic, and pulmonary cancers. Thus, this remedy is now exhibiting activities in the clinic.
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    • "Sulfuretin is a major flavonoid isolated from the stem bark of Albizzia julibrissin and heartwood of Rhus verniciflua (Jung et al., 2003; Kim et al., 2010). It has been used to reduce oxidative stress, platelet aggregation, anti-inflammatory activities, and mutagenesis (Jeon et al., 2006; Lee et al., 2002; Park et al., 2004; Song et al., 2010b). Thus, this compound is thought to provide health benefits by decreasing the risk of various diseases, particularly certain cancers, diabetes, and rheumatoid arthritis (Choi et al., 2003; Jang et al., 2003; Kim et al., 2009; Song et al., 2010b). "
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    ABSTRACT: Sulfuretin, a potent anti-oxidant, has been thought to provide health benefits by decreasing the risk of oxidative stress-related diseases. In this study, we investigated the mechanisms of sulfuretin protection of neuronal cells from cell death induced by the Parkinson's disease (PD)-related neurotoxin 6-hydroxydopamine (6-OHDA). We examined whether sulfuretin acts as an anti-oxidant to reduce oxidative stress and mitochondrial-mediated apoptotic cascade events in 6-OHDA-induced neurotoxicity in SH-SY5Y cells. We also investigated whether sulfuretin specifically acts by inhibiting phosphorylation of mitogen-activated protein kinase (MAPK), phosphatidylinositol 3-kinase (PI3K)/Akt, and glycogen synthase kinase-3beta (GSK-3β) as well as activation of the nuclear factor-κappa B (NF-κB) pathway. Sulfuretin significantly inhibited neuronal cell death, neurotoxicity, apoptosis, and reactive oxygen species (ROS) production. Sulfuretin also strikingly attenuated 6-OHDA-induced mitochondrial dysfunction. Moreover, sulfuretin significantly attenuated 6-OHDA-induced phosphorylation of c-Jun N-terminal kinase (JNK), p38, extracellular signal-regulated kinase 1/2 (ERK 1/2) MAPKs, PI3K/Akt, and GSK-3β. Eventually, sulfuretin inhibited 6-OHDA-induced NF-κB translocation to the nucleus induced by 6-OHDA. The results of the current study provide the first evidence that sulfuretin protects SH-SY5Y cells against 6-OHDA-induced neuronal cell death, possibly through inhibition of phosphorylation of MAPK, PI3K/Akt, and GSK-3β, which leads to mitochondrial protection, NF-κB modulations and subsequent suppression of apoptosis via ROS-dependent pathways. Thus, we conclude that sulfuretin may have a potential role for neuroprotection and, therefore, may be used as a therapeutic agent for PD.
    Full-text · Article · May 2014 · Neurochemistry International
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    • "Sulfuretin is a major flavonoid isolated from the stem bark of Albizzia julibrissin and heartwood of Rhus verniciflua (Jung et al., 2003; Kim et al., 2010). It has been used to reduce oxidative stress, platelet aggregation, anti-inflammatory activities, and mutagenesis (Jeon et al., 2006; Lee et al., 2002; Park et al., 2004; Song et al., 2010b). Thus, this compound is thought to provide health benefits by decreasing the risk of various diseases, particularly certain cancers, diabetes, and rheumatoid arthritis (Choi et al., 2003; Jang et al., 2003; Kim et al., 2009; Song et al., 2010b). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Sulfuretin, a potent anti-oxidant, has been thought to provide health benefits by decreasing the risk of oxidative stress-related diseases. In this study, we investigated the mechanisms of sulfuretin protection of neuronal cells from cell death induced by the Parkinson’s disease (PD)-related neurotoxin 6-hydroxydopamine (6-OHDA). We examined whether sulfuretin acts as an anti-oxidant to reduce oxidative stress and mitochondrial-mediated apoptotic cascade events in 6-OHDA-induced neurotoxicity in SH-SY5Y cells. We also investigated whether sulfuretin specifically acts by inhibiting phosphorylation of mitogen-activated protein kinase (MAPK), phosphatidylinositol 3-kinase (PI3K)/Akt, and glycogen synthase kinase-3beta (GSK-3β) as well as activation of the nuclear factor-κappa B (NF-κB) pathway. Sulfuretin significantly inhibited neuronal cell death, neurotoxicity, apoptosis, and reactive oxygen species (ROS) production. Sulfuretin also strikingly attenuated 6-OHDA-induced mitochondrial dysfunction. Moreover, sulfuretin significantly attenuated 6-OHDA-induced phosphorylation of c-Jun N-terminal kinase (JNK), p38, extracellular signal-regulated kinase 1/2 (ERK 1/2) MAPKs, PI3K/Akt, and GSK-3β. Eventually, sulfuretin inhibited 6-OHDA-induced NF-κB translocation to the nucleus induced by 6-OHDA. The results of the current study provide the first evidence that sulfuretin protects SH-SY5Y cells against 6-OHDA-induced neuronal cell death, possibly through inhibition of phosphorylation of MAPK, PI3K/Akt, and GSK-3β, which leads to mitochondrial protection, NF-κB modulations and subsequent suppression of apoptosis via ROS-dependent pathways. Thus, we conclude that sulfuretin may have a potential role for neuroprotection and, therefore, may be used as a therapeutic agent for PD.
    Full-text · Article · Jan 2014 · Neurochemistry International
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