Atractylenolide I and atractylenolide III inhibit Lipopolysaccharide‐induced TNF‐<i>α</i> and NO production in macrophages

Li, Cuiqin; He, Langchong; Jin, Ju-qing

doi:10.1002/ptr.2040

Cited by 123 publications

(87 citation statements)

References 23 publications

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“…ARA actually contains three types of atractylenolides (I, II, and III), 23) although AIII is the most abundant. 13) AIII has been reported to possess various biological activities, which include the inhibition of lipopolysaccharide-induced inflammatory responses in macrophages, 14) the suppression of histamine release from mast cells via the regulation of interleukin (IL)-6 at the cellular level, 24) and the induction of lung carcinoma cell apoptosis via cell growth inhibition and increasing lactate dehydrogenase release. 15) Here, we describe for the first time the regulatory effects of AIII on glucose homeostasis and energy metabolism in skeletal muscle cells.…”

Section: Discussionmentioning

confidence: 99%

“…12) Atractylenolide III (AIII) is the primary bioactive compound of this extract. 13) AIII has been previously reported to have anti-inflammatory 14,15) and gastroprotective effects, 16) however its effects on skeletal muscle energy metabolism have not been investigated. Therefore, in the present study, we investigated the effects of AIII on energy metabolism via PGC1α/SIRT1/AMPK pathway activation in mouse skeletal muscle cells.…”

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confidence: 99%

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Atractylenolide III Enhances Energy Metabolism by Increasing the SIRT-1 and PGC1α Expression with AMPK Phosphorylation in C2C12 Mouse Skeletal Muscle Cells

Song

Jung

Kang

et al. 2017

Biological & Pharmaceutical Bulletin

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Targeting energy expenditure provides a potential alternative strategy for achieving energy balance to combat obesity and the development of type 2 diabetes mellitus (T2DM). In the present study, we investigated whether atractylenolide III (AIII) regulates energy metabolism in skeletal muscle cells. Differentiated C2C12 myotubes were treated with AIII (10, 20, or 50 µM) or metformin (2.5 mM) for indicated times. The levels of glucose uptake, the expressions of key mitochondrial biogenesis-related factors and their target genes were measured in C2C12 myotubes. AIII significantly increased the glucose uptake levels, and significantly increased the expressions of peroxisome proliferator-activated receptor coactivator-1α (PGC1α) and mitochondrial biogenesis-related markers, such as, nuclear respiratory factor-1 (NRF-1), and mitochondrial transcription factor A (TFAM) and mitochondrial mass and total ATP contents. In addition, AIII significantly increased the phosphorylation of AMP-activated protein kinase (AMPK) and the expression of sirtuin1 (SIRT1). These results suggest that AIII may have beneficial effects on obesity and T2DM by improving energy metabolism in skeletal muscle.Key words atractylenolide III; mitochondrial biogenesis; AMP-activated protein kinase; peroxisome proliferator-activated receptor coactivator-1α; sirtuin1; C2C12 cellThe prevalence of obesity, metabolic syndrome, and type 2 diabetes mellitus (T2DM) has increased over past decades, 1) and it is estimated over 1.9 billion adults worldwide are overweight, and that more than 600 million are clinically obese. 2)Obesity, T2DM, and metabolic syndrome are among the most frequent pathological consequences of chronic energy metabolism imbalance.3) The maintenance of energy balance depends on the regulations of energy intake and expenditure. However, the long-term efficacies of reduced energy intake, such as, by calorific restriction, are problematic, and thus, the targeting of energy expenditure could provide a more effective means of promoting energy balance and combating obesity and T2DM. 4)Skeletal muscle is regarded a target organ in the context of cellular bioenergetics, and is known to play an important role in the maintenance of glucose homeostasis and insulin sensitivity. Insulin resistance is associated with myocellular lipid accumulation, and it has been shown that insulin resistance is caused or accelerated by impaired oxidative capacity of skeletal muscle.5,6) One study conducted under euglycemic conditions showed that skeletal muscle is responsible for ca. 80% of total body glucose uptake. 7)Peroxisome proliferator-activated receptor coactivator 1α (PGC1α), AMP-activated protein kinase (AMPK) and sirtuin1 (SIRT1) compose an energy sensing network that controls energy expenditure in skeletal muscle.8) PGC1α plays a central role in the regulation of cellular energy metabolism, which results from the up-regulation of oxidative metabolism and the stimulation of mitochondrial biogenesis. 9) Furthermore, it is known metabolic sensors, such as A...

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Atractylenolide III Enhances Energy Metabolism by Increasing the SIRT-1 and PGC1α Expression with AMPK Phosphorylation in C2C12 Mouse Skeletal Muscle Cells

Song

Jung

Kang

et al. 2017

Biological & Pharmaceutical Bulletin

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“…It was reported that atractylenolide III possesses various pharmacological activities, such as antiinflammatory activity, [11][12][13] anti-cancer activity, 14,15) protective effects, 16) and inhibition of the movement of uterus smooth muscle. 17) In this study, an in vitro Gli reporter gene assay in MSCs was used to isolate Shh signaling activators, in order to identify molecules that enhance chondrogenic differentiation in MSCs.…”

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confidence: 99%

Targeting of the Sonic Hedgehog Pathway by Atractylenolides Promotes Chondrogenic Differentiation of Mesenchymal Stem Cells

Wei

Wang

et al. 2012

Biological & Pharmaceutical Bulletin

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Molecules that enhance chondrogenic differentiation in mesenchymal stem cells (MSCs) were identified and isolated using an in vitro Gli reporter gene assay in MSCs incorporating a Sonic Hedgehog (Shh) target. Atractylenolide III, which promoted Gli1-mediated transcriptional activity, was isolated from an ethyl acetate extract of the Rhizoma, Atractylodis macrocephalae. After dehydration, atractylenolide III was transformed to atractylenolide I. Both atractylenolides were confirmed by MS, UV, IR, 1 H-and 13 C-NMR spectra. Atractylenolide III (which contains -OH at the 8-position) and atractylenolide I (which lacks -OH at the 8-position) were found to effectively promote the activity of the Gli promoter. While the hydroxyl group of atractylenolide III was not essential for the effect of atractylenolide, its effect was dependent on Shh signaling. Phenotypic cellular analysis indicated that atractylenolides induced MSCs to differentiate into chondrocytes, as shown by increased expression of specific chondrogenic markers including collagen II, aggrecan and the cartilage related transcription factor, Sox9. Atractylenolides significantly increased the expression of Shh and its target gene Gli-1, indicating that Shh signaling was activated by atractylenolides. Moreover, inhibition of Shh signaling reduced the effect of atractylenolides on the chondrogenic phenotype. The discovery that atractylenolides induce chondrocytes from MSCs is promising for bony disease therapy.

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“…(Li et al, 2007). NO•can react with O 2 to form nitrogen dioxide (NO 2 -), with O 2 -to form peroxynitrite (ONOO-), or with transition metal ions to form metalnitrosyl (M-NO) complexes.…”

Section: Resultsmentioning

confidence: 99%

Antitumor and immunomodulatory effects of the naphthoquinone 5-methoxy-3,4-dehydroxanthomegnin

Kitagawa¹,

Vilegas²,

Carlos³

et al. 2011

Rev. bras. farmacogn.

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Large number of quinones has been associated with antitumor, antibacterial, antimalarial and antifungal activities. In this work we describe the effect of the naphthoquinone, 5-methoxy-3,4-dehydroxanthomegnin, on murine tumor cells (LP07 and LM2) and its immunomodulatory effect on nitric oxide (NO) production on LPS-stimulated macrophages. The results have shown that 5-methoxy-3,4-dehydroxanthomegnin was a significant inhibitor of LPS-stimulated NO generation from macrophage (inhibition percentage ranged from 97.4 to 98.9%) and a strong cytotoxic agent against both tumor cells LP07 and LM2 (CI50 6.2±0.36 µM and 74.6±1.9 µM, respectively). These results indicate that the 5-methoxy-3,4-dehydroxanthomegnin may show promising activity in the treatment of murine breast and lung cancer by immunomodulatory and antiproliferative activities.

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Atractylenolide I and atractylenolide III inhibit Lipopolysaccharide‐induced TNF‐α and NO production in macrophages

Cited by 123 publications

References 23 publications

Atractylenolide III Enhances Energy Metabolism by Increasing the SIRT-1 and PGC1α Expression with AMPK Phosphorylation in C2C12 Mouse Skeletal Muscle Cells

Atractylenolide III Enhances Energy Metabolism by Increasing the SIRT-1 and PGC1α Expression with AMPK Phosphorylation in C2C12 Mouse Skeletal Muscle Cells

Targeting of the Sonic Hedgehog Pathway by Atractylenolides Promotes Chondrogenic Differentiation of Mesenchymal Stem Cells

Antitumor and immunomodulatory effects of the naphthoquinone 5-methoxy-3,4-dehydroxanthomegnin

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