Asarinin, a mammalian lignan precursor, has immunosuppression activity and can inhibit acute rejection in vitro. Asarinin may have a role on TLR4 pathway and produce prolongation of allograft heart survival. Asarinin induces dopamine biosynthesis via activation of the PKA-CREB-TH system and protects against 6-OHDA-induced cytotoxicity by inhibiting the sustained activation of the ERK-p38MAPK-JNK1/2-caspase-3 system in PC12 cells.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C)
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
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The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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Experimental study of the effects of Asarinin on immunosuppression activity in vitro.[Reference: WebLink
To test the extract of Asarum heterotropides called Asarinin in the immunosuppression activity in vitro and compared with cyclosporine A(CsA).
METHODS AND RESULTS:
Cardiomyocytes of adult wistar rats and spleen cells of adult SD rats were separated. 0.1 ml of the cardiomyocytes(2×10~(6)/ml) as stimulate cells and 0.1 ml of spleen cells(1×10~(7)/ml) as response cells were cultured in 96 culture plates. The model of rejection reaction in vitro was set up. Then the 0.1 ml serum including Asarinin was given to culture plates, the inhibition rate of lymphocyte transformation was investigated with MTT after 108 hours and IL-2、INF-#gamma#、IL-4 were detected with ELISA. Asarinin inhibited the lymphocyte transformation (inhibition rate 60.37%) in vitro. Compared with positive control group, it significantly decreased IL-2(69.11±17.47 pg/ml vs 160.44±19.79 pg/ ml, P<0.01)、INF-#gamma#(183.11± 95.24 pg/ml vs 521.89± 133.18 pg/ml, P<0.01) and increased IL-4(53.14±11.80 pg/ml vs 14.44± 4.21 pg/ml, P<0.01)in culture plates.
Transplant Proc. 2015 Mar;47(2):545-8.
The effect of Asarinin on Toll-like pathway in rats after cardiac allograft implantation.[Pubmed: 25769604
The objective of this study was to study the mechanism of the anti-rejection effect of Asarinin in rats that underwent cardiac allograft implantation.
METHODS AND RESULTS:
Hearts from Wistar rats were transplanted into the abdominal cavity of Sprague Dawley rats (SD rats) 64 SD rats received either cyclosporin A (CsA), Asarinin, or demi-dose of cyclosporine A and Asarinin through oral administration. On the seventh day post-transplantation, the expression of Toll-like receptor 4 (TLR4), chemokine (C-X-C motif) receptor 3 (CXCR3) in myocardium, and the level of interleukin (IL)-12 in the peripheral blood were analyzed 7 days after transplantation.
The survival time in 3 groups (CsA group, Asarinin group, and semi-dose CsA group) prolonged (P < .01), the microscope myocardial histopathology in 3 groups (CsA group, Asarinin group and semi-dose CsA group) relieved, the expression of TLR4 and CXCR3 in 3 groups was significantly decreased (P < .01) when compared with the control group. The level of IL-12 decreased remarkably (P < .05) in the 3 groups when compared with the control group.
The combined data suggested that Asarinin decreased peripheral blood concentration of IL-12 and inhibited the expression of TLR4 and CXCR3, which means Asarinin may have a role on TLR4 pathway and produced prolongation of allograft heart survival.
Arch Pharm Res. 2017 May;40(5):631-639.
Effects of asarinin on dopamine biosynthesis and 6-hydroxydopamine-induced cytotoxicity in PC12 cells.[Pubmed: 28397192
This study investigated the effects of Asarinin on dopamine biosynthesis and 6-hydroxydopamine (6-OHDA)-induced cytotoxicity in rat adrenal pheochromocytoma (PC12) cells.
METHODS AND RESULTS:
Treatment with Asarinin (25-50 μM) increased intracellular dopamine levels and enhanced L-DOPA-induced increases in dopamine levels. Asarinin (25 μM) induced cyclic AMP-dependent protein kinase A (PKA) signaling, leading to increased cyclic AMP-response element binding protein (CREB) and tyrosine hydroxylase (TH) phosphorylation, which in turn stimulated dopamine production. Asarinin (25 μM) also activated transient phosphorylation of extracellular signal-regulated kinase (ERK1/2) and Bad phosphorylation at Ser 112, both of which have been shown to promote cell survival. In contrast, Asarinin (25 μM) inhibited sustained ERK1/2, Bax, c-Jun N-terminal kinase (JNK1/2) and p38 mitogen-activated protein kinase (p38MAPK) phosphorylation and caspase-3 activity, which were induced by 6-OHDA (100 μM).
These results suggest that Asarinin induces dopamine biosynthesis via activation of the PKA-CREB-TH system and protects against 6-OHDA-induced cytotoxicity by inhibiting the sustained activation of the ERK-p38MAPK-JNK1/2-caspase-3 system in PC12 cells.
Food Chemistry, 2011, 124(3):895-899.
A new mammalian lignan precursor, asarinin.[Reference: WebLink
Enterolactone (ENL) and enterodiol are mammalian lignans. Several plant lignans have been reported as precursors of mammalian lignans. However, Asarinin (AS), a furofuran type lignan which occurs in medicinal plants and foods, has not been reported as mammalian lignan precursor to date.
METHODS AND RESULTS:
After the incubation of AS with human intestinal microflora, AS was converted to not only ENL, but also two more metabolites (mono-demethylenated and ring-cleaved compounds). Under the same conditions, sesamin (SM) was converted to ENL. Furthermore, chiral HPLC analysis showed that ENL produced from AS and SM was (−)-ENL.
This is the first report which shows that AS is a mammalian lignan precursor.