A novel and potent biological antioxidant, Kinobeon A, from cell culture of safflower

Kanehira, Tsutomu; Takekoshi, Susumu; Nagata, Hidetaka; Matsuzaki, Kei; Kambayashi, Yasuhiro; Osamura, R. Yoshiyuki; Homma, Takao

doi:10.1016/j.lfs.2003.06.033

Cited by 31 publications

(24 citation statements)

References 20 publications

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“…The results of the present study demonstrate that safflower extract may play a protective role for renal fibrosis. Although several reports show that safflower contains active fractions which can antagonize against oxidative and inflammatory stress [Nakamura et al, 1973;Bolte et al, 2002;Kanehira et al, 2003], the functional significance of renal protection in, and mechanism of action against, renal fibrosis remain unclear. This study provides convincing evidence that the aqueous extract of safflower is a novel fibrosis antagonist that functions by suppressing TGF-b signals.…”

Section: Discussionmentioning

confidence: 99%

Safflower extract: A novel renal fibrosis antagonist that functions by suppressing autocrine TGF‐beta

Yang

Chang

Teng

et al. 2008

J of Cellular Biochemistry

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Progressive renal disease is characterized by the accumulation of extracellular matrix proteins in the renal interstitium. Hence, developing agents that antagonize fibrogenic signals is a critical issue facing researchers. The present study investigated the blood-circulation-promoting Chinese herb, safflower, on fibrosis status in NRK-49F cells, a normal rat kidney interstitial fibroblast, to evaluate the underlying signal transduction mechanism of transforming growth factor-beta (TGF-beta), a potent fibrogenic growth factor. Safflower was characterized and extracted using water. Renal fibrosis model was established both in vitro with fibroblast cells treated with beta-hydroxybutyrate and in vivo using rats undergone unilateral ureteral obstruction (UUO). Western blotting was used to examine protein expression in TGF-beta-related signal proteins such as type I and type II TGF-beta receptor, Smads2/3, pSmad2/3, Smads4, and Smads7. ELISA was used to analyze bioactive TGF-beta1 and fibronectin levels in the culture media. Safflower extract (SE) significantly inhibited beta-HB-induced fibrosis in NRK cells concomitantly with dose-dependent inhibition of the type I TGF-beta1 receptor and its down-stream signals (i.e., Smad). Moreover, SE dose-dependently enhanced inhibitory Smad7. Thus, SE can suppress renal cellular fibrosis by inhibiting the TGF-beta autocrine loop. Moreover, remarkably lower levels of tissue collagen were noted in the nephron and serum TGF-beta1 of UUO rats receiving oral SE (0.15 g/3 ml/0.25 kg/day) compared with the untreated controls. Hence, SE is a potential inhibitor of renal fibrosis. We suggest that safflower is a novel renal fibrosis antagonist that functions by down-regulating TGF-beta signals.

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Section: Discussionmentioning

confidence: 99%

Safflower extract: A novel renal fibrosis antagonist that functions by suppressing autocrine TGF‐beta

Yang

Chang

Teng

et al. 2008

J of Cellular Biochemistry

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“…These studies relied on staining for superoxide using nitroblue tetrazolium (NBT). When reduced, NBT forms a purple-brown precipitate (blue-formazan) that localizes the site of superoxide production (Maly et al, 1989;Frahry and Schopfer, 2001;Kanehira et al, 2003). When mature, whole nectaries (Stage 12) were stained for superoxide (Fig.…”

Section: Localization Of Superoxide Production To the Nectary Pores Imentioning

confidence: 99%

Tobacco Nectaries Express a Novel NADPH Oxidase Implicated in the Defense of Floral Reproductive Tissues against Microorganisms

et al. 2006

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Hydrogen peroxide produced from the nectar redox cycle was shown to be a major factor contributing to inhibition of most microbial growth in floral nectar; however, this obstacle can be overcome by the floral pathogen Erwinia amylovora. To identify the source of superoxide that leads to hydrogen peroxide accumulation in nectary tissues, nectaries were stained with nitroblue tetrazolium. Superoxide production was localized near nectary pores and inhibited by diphenylene iodonium but not by cyanide or azide, suggesting that NAD(P)H oxidase is the source of superoxide. Native PAGE assays demonstrated that NADPH (not NADH) was capable of driving the production of superoxide, diphenyleneiodonium chloride was an efficient inhibitor of this activity, but cyanide and azide did not inhibit. These results confirm that the production of superoxide was due to an NADPH oxidase. The nectary enzyme complex was distinct by migration on gels from the leaf enzyme complex. Temporal expression patterns demonstrated that the superoxide production (NADPH oxidase activity) was coordinated with nectar secretion, the expression of Nectarin I (a superoxide dismutase in nectar), and the expression of NOX1, a putative gene for a nectary NADPH oxidase that was cloned from nectaries and identified as an rbohD-like NADPH oxidase. Further, in situ hybridization studies indicated that the NADPH oxidase was expressed in the early stages of flower development although superoxide was generated at later stages (after Stage 10), implicating posttranslational regulation of the NADPH oxidase in the nectary.

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“…The cytoprotective effects of antioxidants against DOX is usually associated with the inhibition of lipid peroxidation, regardless of the type and structure of antioxidant. 16,[42][43][44][45] Although the active antioxidants in PU extract have not been identified, its suppression of lipid peroxide formation warrants further investigation.…”

Section: )mentioning

confidence: 99%

“…[12][13][14][15][16] Among traditional herbs, Phyllanthus spp. (Euphorbiaceae) has been used in Aryuvedic medicine for more than 2000 years and in Thai folk medicine for the treatment of many diseases, such as diarrhea, hepatitis, diabetes, abdominal pain, and kidney disease.…”

mentioning

confidence: 99%

Antioxidative and Cardioprotective Effects of Phyllanthus urinaria L. on Doxorubicin-Induced Cardiotoxicity

Chularojmontri

Wattanapitayakul

Herunsalee

et al. 2005

Biological & Pharmaceutical Bulletin

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Doxorubicin (DOX) is an effective and broadly used agent to treat a variety of malignacies, such as leukemias, breast and ovarian cancer, and Hodgkin and non-Hodgkin lymphoma. The major limitation of clinical use is the development of cardiotoxicity. The adverse effects are dose dependent and can vary from transient electrocardiographic abnormalities to cardiomyopathy and heart failure. Recent studies have suggested that the mechanism of DOX-induced cardiotoxicity involves the generation of reactive oxygen species (ROS), especially superoxide anion and hydrogen peroxide.1-3) The main cellular damage caused by ROS includes lipid peroxidation, protein cross-linking, and DNA fragmentation. These may lead to cardiac dysfunction, apoptosis, and development of cardiomyopathy. 4-7)Although protection or alleviation of DOX toxicity can be achieved by administration of antioxidant vitamins such as ascorbic acid and vitamin E, their cardioprotective effects remain controversial. [8][9][10] It is well established that there is no universal "best" antioxidant. For example, ascorbic acid efficiently protects against lipid damage but not against protein damage.11) Thus alternative naturally occurring antioxidants may potentially be candidates for antioxidant therapy.It has been shown in many studies that traditionally used plant extracts protect against oxidative damage caused by a wide array of insults including DOX.12-16) Among traditional herbs, Phyllanthus spp. (Euphorbiaceae) has been used in Aryuvedic medicine for more than 2000 years and in Thai folk medicine for the treatment of many diseases, such as diarrhea, hepatitis, diabetes, abdominal pain, and kidney disease. 17,18) The antioxidant effects of plant species in the genus Phyllanthus have been reported. For example, Phyllanthus amarus (synonym: Phyllanthus niruri) reduced oxidative damage from radiation 19) and protected against hepatotoxicity induced by CCl 4 . 20) Phyllanthus emblica protected rat hearts from oxidative stress induced by ischemic-reperfusion injury.21) Phyllanthus urinaria L. is another medicinal plant that has attracted research attention in the treatment of several diseases. Substantial progress in determining its phytochemical and pharmacologic properties has been made. Several potential antioxidant compounds (e.g., polyphenols, lignans, flavonoids, gallic acid, ellagic acid, etc.) have been isolated from this plant. [22][23][24][25][26] However, to the best of our knowledge, there has been no report on the potential antioxidant effects of Phyllanthus urinaria. Therefore the purpose of this study was to investigate the antioxidant effects of Phyllanthus urinaria for the protection of cardiac cells from DOX cardiotoxicity. Cardiac toxicity is a major adverse effect caused by doxorubicin (DOX) therapy. Many recent studies have shown that DOX toxicity involves generation of reactive oxygen species (ROS). Although protection or alleviation of DOX toxicity can be achieved by administration of antioxidant vitamins such as ascorbic acid and vitamin ...

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A novel and potent biological antioxidant, Kinobeon A, from cell culture of safflower

Cited by 31 publications

References 20 publications

Safflower extract: A novel renal fibrosis antagonist that functions by suppressing autocrine TGF‐beta

Safflower extract: A novel renal fibrosis antagonist that functions by suppressing autocrine TGF‐beta

Tobacco Nectaries Express a Novel NADPH Oxidase Implicated in the Defense of Floral Reproductive Tissues against Microorganisms

Antioxidative and Cardioprotective Effects of Phyllanthus urinaria L. on Doxorubicin-Induced Cardiotoxicity

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