Kaerophyllin CAS NO.75590-33-9

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General tips：For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
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Chemical Properties of Kaerophyllin

Source of Kaerophyllin

The roots of Bupleurum chinense DC.

Biological Activity of Kaerophyllin

Preparing Stock Solutions of Kaerophyllin

References on Kaerophyllin

Kaerophyllin, a new lignan from Chaerophyllum maculatum.[Pubmed:17402063]

Planta Med. 1981 Dec;43(4):378-80.

From the methanolic extract of roots of spotted cow parsley (Chaerophyllum maculatum Willd.) a new lignan, named Kaerophyllin, has been isolated and identified as A-(trans-3,4-dimethoxybenzylidene)- beta-(3,4-methylenedioxylbenzyl)-gamma-butyrolactone. Its structure has been established on the basis of the analysis of UV, IR-, (1)H-NMR, (13)C-NMR and mass spectra.

Protective effects of kaerophyllin against liver fibrogenesis in rats.[Pubmed:22103576]

Eur J Clin Invest. 2012 Jun;42(6):607-16.

BACKGROUND: We previously demonstrated that Kaerophyllin, a lignan, isolated from a widely used traditional Chinese herb, Bupleurum scorzonerifolium, leading to the inhibition of hepatic stellate cells (HSCs) activation in vitro. This current study evaluated the in vivo role of Kaerophyllin in protecting the liver against injury and fibrogenesis caused by thioacetamide (TAA) in rats and further explored the underlying mechanisms. MATERIALS AND METHODS: Liver fibrosis in Sprague-Dawley rats was induced by intraperitoneal injection of TAA (200 mg/kg) twice per week for 6 weeks. Animals were divided into five groups: vehicle control, TAA control, TAA + low dose Kaerophyllin, TAA + high dose Kaerophyllin and TAA + curcumin groups. Kaerophyllin (10 or 30 mg/kg) or curcumin (150 mg/mL) was given by gavage twice per day consecutively for 4 weeks starting 2 weeks after TAA injection. Rat HSCs were used to investigate the anti-inflammatory role of Kaerophyllin against tumour necrosis factor alpha (TNF-alpha) in vitro. Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) expression was knocked down in rat HSCs using PPAR-gamma small interfering RNAs. RESULTS: Kaerophyllin significantly protected liver from injury by reducing serum aspartate transaminase and alanine transaminase levels and by improving the histological architecture and fibrosis score. In addition, Kaerophyllin suppressed inflammation by reducing the mRNA of TNF-alpha, interleukin-1beta (IL-1beta) and monocyte chemoattractant protein-1 (MCP-1) genes. In HSCs, Kaerophyllin elevated PPAR-gamma activity and reduced TNF-alpha-stimulated mRNA levels of intracellular adhesion molecule-1 (ICAM-1), MCP-1 and IL-1beta genes, which were reversed by small interfering RNA knockdown of PPAR-gamma gene. CONCLUSIONS: Our results demonstrated that Kaerophyllin protected the rat liver from TAA-caused injury and fibrogenesis by suppressing hepatic inflammation and inhibiting HSC activation, possibly through upregulation of PPAR-gamma expression.

Kaerophyllin inhibits hepatic stellate cell activation by apoptotic bodies from hepatocytes.[Pubmed:21457435]

Liver Int. 2011 May;31(5):618-29.

BACKGROUND: Hepatic stellate cells (HSCs), the key cell type for hepatic fibrosis, become activated and profibrogenic in the presence of hepatocyte apoptotic bodies (ABs). Bupleurum scorzonerifolium (BS), a widely used traditional Chinese herb for liver diseases, was fractionated, and the inhibitory effects of BS extracts on AB-induced HSC migration were screened. The activity-guided fractionation led to a lignan, Kaerophyllin. In this study, the anti-fibrotic effects of Kaerophyllin were studied in the presence of ABs. METHODS: LX-2 cells phagocytosing ultraviolet (UV)-induced HepG2 ABs were investigated by confocal microscopy and flow cytometry. AB-induced HSC activation was evaluated by immunoblotting and real-time PCR analyses. HSC migration was measured by wound-healing assays. RESULTS: HepG2 ABs induced LX-2 activation, with the production of collagen I and alpha-smooth muscle actin, upregulated profibrogenic gene transcriptions and increased NF-kappaB activity, cell migration and phagocytosis. Kaerophyllin from BS antagonized AB-induced HSC migration and activation. CONCLUSIONS: Kaerophyllin inhibited AB-induced LX-2 activation and migration with downregulation of Akt/ERK phosphorylations and NF-kappaB activity. Our study suggests a novel platform for screening anti-fibrotic compounds with ABs.

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