Tanshinone IIA (tanshinone + iia)

Distribution by Scientific Domains


Selected Abstracts


Neuroprotective effects of Tanshinone IIA on permanent focal cerebral ischemia in mice,

PHYTOTHERAPY RESEARCH, Issue 5 2009
Kenan Dong
Abstract The objective of this study was to evaluate whether Tanshinone IIA (TSA) was neuroprotective in permanent focal cerebral ischemia and to determine the possible mechanisms of its neuroprotection. Mice were subjected to permanent middle cerebral artery occlusion. The neuroprotection of TSA was investigated with respect to neurological deficit scores and infarct volume. Biochemical analyses for malondialdehyde (MDA) content and superoxide dismutase (SOD) activity in serum, and nitric oxide (NO) content and the inducible nitric oxide synthase (iNOS) activity in brain tissue were performed at 24 h after ischemia. Immunohistochemistry was used to measure the expression of iNOS. In vitro, the effects of TSA were tested in the cultured astrocytes exposed to hydrogen dioxide (H2O2). TSA (5, 10 and 20 mg/kg, i.p.) significantly reduced the infarct volume and improve neurological deficit. TSA also significantly increased the activity of SOD after 24 h of ischemia and decreased the MDA level, NO content, and iNOS expression. In vitro, the translocation of NF- ,B was inhibited by TSA and the survival rate of astrocytes was markedly increased and the NO production was decreased. In conclusion, these results illustrated that TSA protected the brain from ischemic injury by suppressing the oxidative stress and the radical-mediated inflammatory insult. Copyright 2008 John Wiley & Sons, Ltd. [source]


Characterization of metabolites of tanshinone IIA in rats by liquid chromatography/tandem mass spectrometry

JOURNAL OF MASS SPECTROMETRY (INCORP BIOLOGICAL MASS SPECTROMETRY), Issue 5 2006
Peng Li
Abstract The metabolism of tanshinone IIA was studied in rats after a single-dose intravenous administration. In the present study, 12 metabolites of tanshinone IIA were identified in rat bile, urine and feces with two LC gradients using LC-MS/MS. Seven phase I metabolites and five phase II metabolites of tanshinone IIA were characterized and their molecular structures proposed on the basis of the characteristics of their precursor ions, product ions and chromatographic retention time. The seven phase I metabolites were formed, through two main metabolic routes, which were hydroxylation and dehydrogenation metabolism. M1, M4, M5 and M6 were supposedly tanshinone IIB, hydroxytanshinone IIA, przewaquinone A and dehydrotanshinone IIA, respectively, by comparing their HPLC retention times and mass spectral patterns with those of the standard compounds. The five phase II metabolites identified in this research were all glucuronide conjugates, all of which showed a neutral loss of 176 Da. M9 and M12 were more abundant than other identified metabolites in the bile, which was the main excretion path of tanshinone IIA and the metabolites. M12 was the main metabolite of tanshinone IIA. M9 and M12 were proposed to be the glucuronide conjugates of two different semiquinones and these semiquinones were the hydrogenation products of dehydrotanshinone IIA and tanshinone IIA, respectively. This hydrogenized reaction may be catalyzed by the NAD(P)H: quinone acceptor oxidoreductase (NQO). The biotransformation pathways of tanshinone IIA were proposed on the basis of this research. Copyright 2006 John Wiley & Sons, Ltd. [source]


Separation and determination of active components in Radix Salviae miltiorrhizae and its medicinal preparations by nonaqueous capillary electrophoresis

JOURNAL OF SEPARATION SCIENCE, JSS, Issue 7-8 2004
An Jia Chen
Abstract A nonaqueous capillary electrophoresis (NACE) method was developed for simultaneous assay of three bioactive components (1: cryptotanshinone; 2: tanshinone IIA, and 3: tanshinone I) in Radix Salviae miltiorrhizae and in its herbal preparations for the first time. After optimization of separation conditions, a buffer of 250 mmol L,1 ammonium acetate containing 30% acetonitrile and 1.0% acetic acid (V : V) in methanol was selected for separating the three analytes, but baseline separation of tanshinon I and tanshinone IIA was not obtained. Therefore second-order derivative electropherograms were applied for resolving overlapping peaks. Regression equations revealed good linear relationships (correlation coefficients 0.9943,0.9991) between peak heights in second-order derivative electropherograms and concentrations of the three analytes. The relative standard deviations (RSD) of the migration times and the peak height of the three constituents were in the range of 0.81,0.88% and 0.34,1.13% (intra-day), 1.57,1.86% and 3.05,5.52% (inter-day), respectively. The recoveries of three constituents ranged from 90.2 to 108.5%. The results indicated that baseline separation of the analytes was sometimes hard to obtain and second-order derivative electropherograms were applicable for the resolving and analysis of overlapping peaks. [source]


Inhibition of microsomal triglyceride transfer protein expression and atherogenic risk factor apolipoprotein B100 secretion by tanshinone IIA in HepG2 cells

PHYTOTHERAPY RESEARCH, Issue 12 2008
Yun-Jeong Kang
Abstract Salvia miltiorrhiza Bunge is known to be effective for the treatment of cardiovascular diseases. Here, we have isolated tanshinone IIA (T-IIA) from S. miltiorrhiza Bunge. The aim of this study is to address the mechanisms where apolipoprotein B-100 (ApoB) regulation is associated with T-IIA, since T-IIA regulates the lipoprotein metabolism in liver cells. Human HepG2 cells treated with T-IIA for 24 h exerted a dose-dependent inhibitory effect on ApoB secretion together with triglyceride. However, another secretory protein, albumin, was unaffected by T-IIA treatment, indicating that the effect of T-IIA is specific for ApoB secretion. T-IIA decreased the transcription level of microsomal triglyceride transfer protein gene, suggesting that lipoprotein assembly is likely to be involved in the inhibited ApoB secretion. Interestingly, T-IIA inhibited ApoB secretion via a proteasome-dependent pathway. Our results suggest that T-IIA is an influential inhibitor of ApoB secretion and triglyceride secretion in liver cells. Copyright 2008 John Wiley & Sons, Ltd. [source]