A Newly Isolated Antispasmodic—butylidenephthalide—

Ko, Wun-Chang

doi:10.1254/jjp.30.85

Cited by 47 publications

(27 citation statements)

References 16 publications

(9 reference statements)

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“…Chao et al (2010) reported that the components of AS ethyl acetate extract, including ferulic acid and Z-ligustilide, have anti-inflammatory activity through inhibition of the NF-jB pathway of macrophage on murine model. n-Butylidenephthalide (BP), derived from a chloroform extract of AS, has been examined for its antispasmodic action (Ko 1980), anti-platelet effect (Teng et al 1987), anti-anginal effect (Ko et al 1998), anti-atherosclerotic treatment (Mimura et al 1995), and tumor suppression effects (Lin et al 2008;Tsai et al 2005;Wei et al 2009). However, no study has described immunomodulatory effects of BP.…”

Section: Introductionmentioning

confidence: 99%

Lipopolysaccharide-stimulated activation of murine DC2.4 cells is attenuated by n-butylidenephthalide through suppression of the NF-κB pathway

Hran

Chu

et al. 2011

Biotechnol Lett

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Modulation of dendritic cell (DC) fate and function may be one approach for the treatment of inflammatory and autoimmune diseases. n-Butylidenephthalide (BP), derived from Angelica sinensis, at 40 μg/ml significantly decreased the secretion of interleukin-6 and tumor necrosis factor-α by lipopolysaccharide (LPS)-stimulated activation of cultured murine DC2.4 cells (P<0.01). LPS-induced major histocompatibility complex class II (P<0.05), CD86 (P<0.01) and CD40 (P<0.01) expression on DC2.4 cells was also inhibited by BP. The endocytic capacity of LPS-stimulated DC2.4 cells was increased by BP (P<0.01). The antigen-presenting capacity of LPS-stimulated DC2.4 cells was decreased by BP (P<0.05). Moreover, we confirmed BP attenuates the responses of LPS-stimulated activation of DCs via suppression of NF-κB-dependent pathways.

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Section: Introductionmentioning

confidence: 99%

Lipopolysaccharide-stimulated activation of murine DC2.4 cells is attenuated by n-butylidenephthalide through suppression of the NF-κB pathway

Hran

Chu

et al. 2011

Biotechnol Lett

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“…In this situation, if Z-Bdph binds to the L-type ROCCs, it still does not relax the TC further, as TC was completely inhibited and remained no detectable tension. In fact, we have reported that Bdph alone inhibited ACh-induced PC and TC of GPI in a similar extent (Ko 1980). Thus, Bdph may block L-type ROCCs in the GPI.…”

Section: Discussionmentioning

confidence: 70%

“…It was suggested that Bdph had a non-specific antispasmodic action to inhibit Ca 2+ influx from extracellular fluid like papaverine, a phosphodiesterase inhibitor (Ko 1980). However, Bdph was reported to inhibit ACh-induced phasic (PC) and tonic contraction (TC) in a similar extent, but papaverine more potently inhibited TC than PC in the GPI (Ko 1980). Bdph (mol.…”

Section: Introductionmentioning

confidence: 99%

Lack of effect of Z-butylidenephthalide on presynaptic N-type Ca2+ channels in isolated guinea-pig ileum

Chen

2015

Naunyn-Schmiedeberg's Arch Pharmacol

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Z-Butylidenephthalide (Bdph) was reported to more potently inhibit electrically induced twitch responses than acetylcholine-induced tonic contraction in isolated guinea-pig ileum (GPI). The aim of the present study was to investigate the inhibitory effects of Z-Bdph on Ca2+ and K+ channels on GPI. In Locke-Ringer’s solution, both responses were isometrically recorded on a polygraph. Incubation of ω-conotoxin MVIIC, but not Z-Bdph, in the electrically stimulated GPI prior to adding ω-conotoxin GVIA, an irreversible blocker of N-type voltage-dependent Ca2+ channels (VDCCs), protected the binding sites and resulted in the twitch responses reversible by washing, suggesting that Z-Bdph did not bind to the N-type VDCCs. Interestingly, we found Z-Bdph concentration dependently delayed the onsets of K+-induced twitch responses, suggesting that Z-Bdph may be a blocker of K+ channels to interfere extracellular K+ across through the pre-junctional membrane of nerve ending in K+-free medium. Z-Bdph similar to nifedipine non-competitively inhibited cumulative ACh-induced phasic contractions, suggesting that Z-Bdph may bind to L-type of inositol-1,4,5-trisphosphate (IP3)-sensitive Ca2+ channels on the endoplasmic reticulum (ER) membrane. In the presence of verapamil, a L-type Ca2+ channel blocker or Z-Bdph, the twitch inhibitions by either were effectively reversed by exogenous Ca2+, suggesting that they may freely pass through pre-junctional N-type, but not L-type which was blocked at least a part by either, of VDDCs open when each electrical coaxial stimulation (ECS) into intracellular space of cholinergic nerve terminal and trigger release of transmitters. In conclusion, results confirm that Z-Bdph more potently inhibits ECS-induced twitch responses than ACh-induced PCs in GPI and suggest that this effect is not mediated by interaction with presynaptic N-type VDCCs.

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“…The earliest literature reported that butylidenephthalide (Bdph), 3-Butylidene-4, 4a, 7, 7a-tetrahydrophthalide ( Fig. 1a), was one of the major active constituents in the essential oil from Rhizoma Chuanxiong (Ko 1980). It inhibits platelet aggregation in rabbit (Teng et al 1987) and strongly increases peripheral blood flow in rats (Yorozu, Sato, and Komoto 1994).…”

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confidence: 99%

A GC-SIM-MS Method for the Determination of Butylidenephthalide in Rat Plasma and Tissue: Application to the Pharmacokinetic and Tissue Distribution Study

Wang¹,

Shi²,

Chen³

et al. 2008

Analytical Letters

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Butylidenephthalide is one of the major active components isolated from Rhizoma Chuanxiong. This paper describes a simple, rapid, specific and sensitive method for the quantification of butylidenephthalide in rat plasma and tissue distribution using a liquid-liquid extraction procedure followed by capillary gas chromatography-selected ion monitoring mode-mass spectrometry (GC-SIM-MS) analysis. The calibration curves were linear over the concentration ranging from 0.02-10.0 mg=mL (r > 0.99) for plasma samples and 0.18-7.25 mg=g (r > 0.99) for the tissue samples. The limit of quantification (LOQ) was 1.0 ng=mL or 1.0 ng=g (ten times signal=noise ratio). Within-and between-day precisions expressed as the relative standard deviation (RSD) for the method were 2.39-2.98% and 2.97-4.26%, respectively. The methods of recovery for all samples were greater than 80% at the low, medium, and high concentrations. The method has been successfully applied to a pharmacokinetics study in rats after an oral administration of Butylidenephthalide with a dose of 20.0 mg=kg. The main pharmacokinetic parameters obtained were T max ¼ (0.22 AE 0.06) h, C max ¼ (3 AE 1) mg=mL, AUC ¼ (32 AE 6) h . mg=mL, and K a ¼ (8.5 AE 0.8)=h. The results showed that the butylidenephthalide was easily absorbed. The concentrations of butylidenephthalide in rat kidney, lung, heart, and cerebellum were higher than those in other organs. To determine free fraction in serum, samples were filtered using ultrafiltration membranes with a molecular weight cut-off of 10,000 Da and extracted using liquid-liquid extraction. The extracts were evaporated and analyzed by GC-MS. The protein binding in rat plasma, human plasma, and human serum albumin were 83 AE 4%, 94 AE 3%, and 89 AE 3%, respectively.

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A Newly Isolated Antispasmodic—butylidenephthalide—

Abstract: Abstract-Butylidenephthalide(BdPh

Cited by 47 publications

References 16 publications

Lipopolysaccharide-stimulated activation of murine DC2.4 cells is attenuated by n-butylidenephthalide through suppression of the NF-κB pathway

Lipopolysaccharide-stimulated activation of murine DC2.4 cells is attenuated by n-butylidenephthalide through suppression of the NF-κB pathway

Lack of effect of Z-butylidenephthalide on presynaptic N-type Ca2+ channels in isolated guinea-pig ileum

A GC-SIM-MS Method for the Determination of Butylidenephthalide in Rat Plasma and Tissue: Application to the Pharmacokinetic and Tissue Distribution Study

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