Inhibitory effect of 18β-glycyrrhetinic acid on 12-<i>O</i>-tetradecanoyl phorbol-13-acetate-induced cutaneous oxidative stress and tumor promotion in mice

Agarwal, Megha; Iqbal, Mohammad; Athar, Mohammad

doi:10.1179/135100005x57346

Cited by 36 publications

(29 citation statements)

References 27 publications

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“…In addition, UA may inhibit skin tumor formation by inhibiting the binding of B[a]P and DMBA to epidermal DNA [19], and TPA to the epidermal membrane [108]. Further, it is well known that UA suppresses tumor promoterinduced inflammation [19,109] and ornithine decarboxylase [5,19,110], while it induces differentiation of F9 teratocarcinoma stem cells into endoderm cells [111] and M1 cells into Mb-like cells [112]. Also, UA-induced apoptosis of M4Beu melanoma cells may have some correlation to the suppression of tumorigenesis [113].…”

Section: Mutagenesis and Carcinogenesismentioning

confidence: 99%

Ursolic acid: An anti‐ and pro‐inflammatory triterpenoid

Ikeda

Murakami

Ohigashi

2008

Molecular Nutrition Food Res

379

252

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There is growing interest in the elucidation of the biological functions of triterpenoids, ubiquitously distributed throughout the plant kingdom, some of which are used as anticancer and anti-inflammatory agents in Asian countries. Ursolic acid (UA), a natural pentacyclic triterpenoid carboxylic acid, is the major component of some traditional medicine herbs and is well known to possess a wide range of biological functions, such as antioxidative, anti-inflammation, and anticancer activities, that are able to counteract endogenous and exogenous biological stimuli. In contrast to these beneficial properties, some laboratory studies have recently revealed that the effects of UA on normal cells and tissues are occasionally pro-inflammatory. Thus, UA may be designated as a double-edged sword with both positive and negative effects, and further evaluations of the effects of UA on the biological status of target cells or tissues are necessary. This review summarizes previous and current information regarding UA, and provides new insights into the underlying molecular mechanisms of its activities.

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Section: Mutagenesis and Carcinogenesismentioning

confidence: 99%

Ursolic acid: An anti‐ and pro‐inflammatory triterpenoid

Ikeda

Murakami

Ohigashi

2008

Molecular Nutrition Food Res

379

252

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“…To investigate the effectiveness of Sijunzi decoction, characterization of active components in the individual herbs and in the prescription are crucial. Ginsenoside [6], flavonoid [7] and triterpenoid [8,9] have been regarded as the active compounds in P. ginseng and G. uralensis, respectively. Different methods have been developed for the determination of the active components in the individual crude herb [6,[10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Chemical investigation on Sijunzi decoction and its two major herbs Panax ginseng and Glycyrrhiza uralensis by LC/MS/MS

Liu

Yang

Cai

2006

Journal of Pharmaceutical and Biomedical Analysis

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“…Increasing evidence indicates that glycyrrhizin (GL), a triterpenoid saponin found in Glycyrrhiza glabrata, and its hydrolyzed metabolite, 18␤-glycyrrhetinic acid (GA), reveal anti-inflammatory, anticancer, and antihepatotoxic effects (Jeong et al, 2002;Matsui et al, 2004;Agarwal et al, 2005). GL and GA have antioxidant ability and reduce oxidative damage due to carbon tetrachloride, tert-butyl hydroperoxide, or ischemia-reperfusion injury (Nagai et al, 1991;Jeong et al, 2002;Kinjo et al, 2003).…”

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confidence: 99%

Protective Effect of Glycyrrhizin on 1-Methyl-4-phenylpyridinium-Induced Mitochondrial Damage and Cell Death in Differentiated PC12 Cells

Yim¹,

Park²,

Lee³

2007

J Pharmacol Exp Ther

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Defects in mitochondrial function have been shown to participate in the induction of neuronal cell injury. The aim of the present study was to assess the preventive effect of licorice compounds glycyrrhizin and 18␤-glycyrrhetinic acid against the toxicity of parkinsonian neurotoxin 1-methyl-4-phenylpyridinium (MPP ϩ ) in relation to the mitochondria-mediated cell death process and role of oxidative stress. MPP ϩ induced the nuclear damage, the changes in the mitochondrial membrane permeability, leading to the cytochrome c release and caspase-3 activation, the formation of reactive oxygen species, and the depletion of glutathione (GSH) in differentiated PC12 cells. Glycyrrhizin up to 100 M significantly attenuated cell death and depletion of GSH due to MPP ϩ concentration-dependently. Meanwhile, 18␤-glycyrrhetinic acid showed a maximal inhibitory effect at 10 M; beyond this concentration, the inhibitory effect declined. The protective effect of licorice compounds was also detected in the rotenone-treated PC12 cells. Glycyrrhizin and 18␤-glycyrrhetinic acid prevented the MPP ϩ -induced formation of the mitochondrial permeability transition. The results show that both glycyrrhizin and a metabolite, 18␤-glycyrrhetinic acid, exhibit a depressant effect against the MPP ϩ toxicity. Glycyrrhizin and 18␤-glycyrrhetinic acid may prevent the cytotoxicity of MPP ϩ by suppressing the mitochondrial permeability transition formation. The preventive effect seems to be ascribed to the inhibitory effect on the formation of reactive oxygen species and depletion of GSH.Mitochondrial dysfunction and increased oxidative stress have been shown to be implicated in dopaminergic cell degeneration in Parkinson's disease (Jenner, 2003). In this disease, the major mitochondrial defect seems to be associated with complex I at the electron transport chain. Impairment of complex I activity leads to excess ROS formation, which causes mitochondrial dysfunction and cell death (Fleury et al., 2002;Jenner, 2003). Implication of oxidative stress in the pathogenesis and progression of Parkinson's disease is supported by the decrease in GSH content, increase in levels of lipid peroxidation products, increased production of ROS, and increase in iron content in substantia nigra (Olanow and Tatton, 1999).MPTP produces an irreversible and severe parkinsonianlike syndrome in human and nonhuman primates (Przedborski and Jackson- Lewis, 1998;Przedborski et al., 2000). The inhibition of complex I in the mitochondrial electron transport chain induced by MPP ϩ , the active metabolite of MPTP, results in impaired ATP production, loss of mitochondrial membrane potential, and formation of ROS (Cassarino et al., 1997;Schulz et al., 1997). The membrane permeability transition of mitochondria is known as a central event in the course of toxic and oxidative forms of cell injury, as well as apoptosis (Mignotte and Vayssière, 1998). Along with respiratory chain inhibition, MPP ϩ -induced neuronal cell death is suggested to be mediated by formation of the mitocho...

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Inhibitory effect of 18β-glycyrrhetinic acid on 12-O-tetradecanoyl phorbol-13-acetate-induced cutaneous oxidative stress and tumor promotion in mice

Cited by 36 publications

References 27 publications

Ursolic acid: An anti‐ and pro‐inflammatory triterpenoid

Ursolic acid: An anti‐ and pro‐inflammatory triterpenoid

Chemical investigation on Sijunzi decoction and its two major herbs Panax ginseng and Glycyrrhiza uralensis by LC/MS/MS

Protective Effect of Glycyrrhizin on 1-Methyl-4-phenylpyridinium-Induced Mitochondrial Damage and Cell Death in Differentiated PC12 Cells

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