Pharmacological activities of the constituents of atractylodes rhizomes

Sin, Kwan Seog; Kim, Hyun Pyo; Lee, Woo Cheol; Pachaly, P.

doi:10.1007/bf02911051

Cited by 24 publications

(15 citation statements)

References 6 publications

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“…Other studies reported that each medicinal herb has a different effect; Atractylon, a major component of Atractylodes japonica Koidzumi was reported to prevent hepatotoxicity in rats (Kiso et al, 1985) and has an anti-inflammatory activity (Sin et al, 1989) and anti-ulcer action (Matsuda et al, 1991). Phellodendron amurense Ruprecht has suppressive effect on the development of angiogenesis in a rat model of collageninduced arthritis, but the principal components have not yet been identified (Li et al, 2003).…”

Section: Discussionmentioning

confidence: 97%

Cheongyeolsaseuptang inhibits production of TNF-α, IL-6 and IL-8 as well as NF-κB activation in human mast cells

Kim

Lee

Song

et al. 2005

Journal of Ethnopharmacology

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Section: Discussionmentioning

confidence: 97%

Cheongyeolsaseuptang inhibits production of TNF-α, IL-6 and IL-8 as well as NF-κB activation in human mast cells

Kim

Lee

Song

et al. 2005

Journal of Ethnopharmacology

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“…ATR-I has been documented for a variety of pharmacological uses in eastern Asian countries regarding the treatment of edema, anorexia, splenic asthenia, excessive perspiration, and abnormal fetal movement [26,27]. Moreover, previous findings also advocate the in vivo and in vitro anti-inflammatory activities of ATR-I’s [12,28,29,30]. …”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Role of Atractylenolide-I in an In Vitro and In Vivo Model of Parkinson’s Disease

Choi

2017

Nutrients

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Parkinson’s disease (PD) is an age-related neurological disorder characterized by a loss of dopaminergic neurons within the midbrain. Neuroinflammation has been nominated as one of the key pathogenic features of PD. Recently, the inadequate pharmacotherapy and adverse effects of conventional drugs have spurred the development of unconventional medications in the treatment of PD. The purpose of this study is to investigate the anti-neuroinflammatory mechanisms of Atractylenolide-I (ATR-I) in in vivo and in vitro models of PD. Nitrite assay was measured via Griess reaction in lipopolysaccharide (LPS) stimulated BV-2 cells. mRNA and protein levels were determined by a reverse transcription-polymerase chain reaction (RT-PCR) and immunoblot analysis, respectively. Further, flow cytometry, immunocytochemistry, and immunohistochemistry were employed in BV-2 cells and MPTP-intoxicated C57BL6/J mice. Pre-treatment with ATR-I attenuated the inflammatory response in BV-2 cells by abating the nuclear translocation of nuclear factor-κB (NF-κB) and by inducing heme oxygenase-1 (HO-1). The intraperitoneal administration of ATR-I reversed MPTP-induced behavioral deficits, decreased microglial activation, and conferred protection to dopaminergic neurons in the mouse model of PD. Our experimental reports establish the involvement of multiple benevolent molecular events by ATR-I in MPTP-induced toxicity, which may aid in the development of ATR-I as a new therapeutic agent for the treatment of PD.

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“…These two compounds fractionated from A. japonica rhizomes were found to be active compounds in acetic acid-induced vascular permeability and chick embryo granuloma antiinflammatory assays (Endo et al, 1979). Atractylenolide I could inhibit cottonpellet granuloma formation (Sin et al, 1989). When atractylenolide I and atractylenolide III were tested for inhibitory activity against 5-lipoxygenase (5-LOX) and cyclooxygenase (COX), they showed no marked effects against either of those enzymes (Resch et al, 1998).…”

Section: Introductionmentioning

confidence: 98%

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

Jin

2007

Phytotherapy Research

124

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In order to clarify the mechanism involved in the antiinflammatory activity of atractylenolide I and atractylenolide III from the rhizomes of Atractylodes macrocephala Koidz, their effects on tumor necrosis factor-alpha (TNF-alpha) and nitric oxide (NO) production in peritoneal macrophages were examined. Atractylenolide I and atractylenolide III decreased the TNF-alpha level in LPS-stimulated peritoneal macrophages in a dose-dependent manner, their IC(50) values were 23.1 microm and 56.3 microm, respectively. RT-PCR analysis indicated that they inhibited TNF-alpha mRNA expression. Furthermore, they inhibited NO production in LPS-activated peritoneal macrophages, the IC(50) value of atractylenolide I was 41.0 microm, and the inhibition ratio of 100 microm of atractylenolide III was 45.1% +/- 6.2%. The activity analysis of inducible nitric oxide synthase (iNOS) indicated that they could inhibit the activity of iNOS, their IC(50) values were 67.3 microm and 76.1 microm, respectively. Western blot analysis showed that atractylenolide I and atractylenolide III attenuated LPS-induced synthesis of iNOS protein in the macrophages, in parallel. These results imply that the antiinflammatory mechanism of atractylenolide I and atractylenolide III may be explained at least in part, by the inhibition of TNF-alpha and NO production. Atractylenolide I showed more potent inhibition than atractylenolide III in the production of TNF-alpha and NO in LPS-activated peritoneal macrophages. So, atractylenolide I could be a candidate for the development of new drugs to treat inflammatory diseases accompanied by the overproduction of TNF-alpha and NO.

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Pharmacological activities of the constituents of atractylodes rhizomes

Cited by 24 publications

References 6 publications

Cheongyeolsaseuptang inhibits production of TNF-α, IL-6 and IL-8 as well as NF-κB activation in human mast cells

Cheongyeolsaseuptang inhibits production of TNF-α, IL-6 and IL-8 as well as NF-κB activation in human mast cells

Neuroprotective Role of Atractylenolide-I in an In Vitro and In Vivo Model of Parkinson’s Disease

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

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