Tanshinone IIA-sulfonic sodium

The roots of Salvia miltiorrhiza

Tanshinone IIA sulfonate (sodium) is a water-soluble derivative of tanshinone IIA, which acts as an inhibitor of store-operated Ca2+ entry (SOCE), and is used to treat cardiovascular disorders.

In Vitro:Sodium Tanshinone IIA sulfonate (12.5 μM) inhibits hypoxia-induced PKG and PPAR-γ downregulation in PASMCs and distal pulmonary arteries of rats. The suppressive effects of Sodium Tanshinone IIA sulfonate on TRPC1 and TRPC6 expression in hypoxic PASMCs can be prevented by specific knockdown PKG or PPAR-γ. The suppressive effects of Sodium Tanshinone IIA sulfonate on basal calcium concentration and SOCE in hypoxic PASMCs can be reversed by specific knockdown of PKG or PPAR-γ. PKG-PPAR-γ signaling axis participates in the suppressive effects of Sodium Tanshinone IIA sulfonate on proliferation in hypoxic PASMCs. PPAR-γ agonist promotes the protective role of Sodium Tanshinone IIA sulfonate on basal [Ca2+]i and SOCE in hypoxic PASMCs[2]. Sodium tanshinone IIA sulfonate inhibits the activity of CYP3A4 in a dose-dependent manner by the HLMs and CYP3A4 isoform. The KM and Vmax values of STS are 54.8±14.6 µM and 0.9±0.1 nmol/mg protein/min, respectively, for the HLMs and 7.5±1.4 µM and 6.8±0.3 nmol/nmol P450/min, respectively, for CYP3A4. CYP1A2, CYP2A6, CYP2C9, CYP2D6, CYP2E1, and CYP2C19 show minimal or no effects on the metabolism of STS[3]. Sodium Tanshinone IIA sulfonate inhibits the activity of CYP3A4 in a dose-dependent manner in the HLMs and CYP3A4 isoform. Sodium Tanshinone IIA sulfonate primarily inhibits the activities of CYP3A4 in vitro, and Sodium Tanshinone IIA sulfonate has the potential to perpetrate drug-drug interactions with other CYP3A4 substrates[4].

In Vivo:Sodium Tanshinone IIA sulfonate (10 mg/kg, 20 mg/kg) and Donepezil shorten escape latency, increase crossing times of the original position of the platform, and increase the time spent in the target quadrant. Sodium Tanshinone IIA sulfonate decreases the activity of acetylcholinesterase (AChE) and increases the activity of choline acetyltransferase (ChAT) in the hippocampus and cortex of SCOP-treated mice. Sodium Tanshinone IIA sulfonate increases the activity of superoxide dismutase (SOD) and decreases the levels of malondialdehyde (MDA) and reactive oxygen species (ROS) in hippocampus and cortex[1]. Sodium Tanshinone IIA sulfonate prevention (30 mg/kg/day) alleviates hypoxia-induced characteristic changes in chronic hypoxia PH rat model[2]. Sodium Tanshinone IIA sulfonate (20, 10, and 5 mg/kg, i.p.) effectively prevents peritoneal adhesion without affecting anastomotic healing in the rats. Compared with the adhesion model group, the Sodium Tanshinone IIA sulfonate-treated groups show increased peritoneal lavage fluid tPA activity and tPA/PAI-1 ratio in the ischemic tissues with loared TGF-β1 and collagen I expressions in the ischemic tissues[5].

References:
[1]. Xu QQ, et al. Sodium Tanshinone IIA Sulfonate Attenuates Scopolamine-Induced Cognitive Dysfunctions via Improving Cholinergic System. Biomed Res Int. 2016;2016:9852536. [2]. Jiang Q, et al. Sodium tanshinone IIA sulfonate inhibits hypoxia-induced enhancement of SOCE in pulmonary arterial smooth muscle cells via the PKG-PPAR-γ signaling axis. Am J Physiol Cell Physiol. 2016 Jul 1;311(1):C136-49. [3]. Ouyang DS, et al. Kinetics of cytochrome P450 enzymes for metabolism of sodium tanshinone IIA sulfonate in vitro. Chin Med. 2016 Mar 22;11:11. [4]. Chen D, et al. Sodium tanshinone IIA sulfonate and its interactions with human CYP450s. Xenobiotica. 2016 Dec;46(12):1085-1092. Epub 2016 Mar 2. [5]. Lin S, et al. [Sodium tanshinone IIA sulfonate prevents postoperative peritoneal adhesions in rats by enhancing the activity of the peritoneal fibrinolytic system]. Nan Fang Yi Ke Da Xue Xue Bao. 2016 Feb;36(2):260-4.

[The inhibitive effect of sodium tanshinone II A sulfonic acid on intimal hyperplasia in rabbit iliac artery ballon injury model].[Pubmed:17944192]

Zhong Yao Cai. 2007 Jul;30(7):811-5.

OBJECTIVE: To study the preventive effect of Sodium Tanshinone II A sulfonic acid on intimal hyperplasia in rabbit iliac artery balloon injury model and explore the possible mechanism. METHODS: Thirty male pure hreed New Zealand white rabbits were undertaken experimental balloon injury in left iliac artery. Then the rabbits were assigned into treatment group (n=15) and control group (n=15), paired with weights. Sodium Tanshinone II A sulfonic acid had been injected intravenously with 7.5 - 9 mg/day for 6 days in treatment group. Saline of equivalence was given in contol group. The balloon injured arteries were harvested in the 7th, 14th, and 28th days after balloon injuy, and Paraffin sections were made. At last, HE staining, apoptosis TUNEL assay were undertaken. RESULTS: (1) HE staining analysis: Media and intimal areas in treatment group at 14th day post-operation were larger than that in the 7th day (P = 0.003 and < 0.001, respectively). Media and intimal areas in treatment group decreased at the 28th day post-operation, while increased in control. Both media and intimal areas were significantly different (P < 0.001 respectively. (2) Tunel analysis discovered that, apoptosis reached peak in both treatment and control groups at the 28th post-operation. Differences of apoptosis cells counts in media and intimal between treatment and control groups were non-significant at the 7th, and 28th days, while differences at the 14th day were significant(p = 0.031 and 0.029 respectively). Apoptosis cells counting in treatment group at the 14th day increased more dramatically than that in the control. CONCLUSION: Intravenous Sodium Tanshinone II A sulfonic acid inhibites intimal proliferation after arterial balloon injury in rabits. The effect can e partially explaineArte by the induction of apoptosis in injured artery. Clinical effect of tanshinone II A still needs further evaluation. Sodium TA-II A sulfonic acid may be of potential therapeutic value in the prevention of OBJECTIVE: To study the preventive effect of Sodium Tanshinone II A sulfonic acid on intimal by perplasia in rabbit iliac artery balloon injury model and explore the possible mechanism. METHODS: Thirty male pure breed Nexw Zealand white rabbits were un-dertaken experimental balloon injury in left iliac artery. Then the rabbits were assigned into treatment group (n=15) and control group (n=15), paired with weights. Sodium Tanshinone II A sulfonie acid had been injected intraxenously with 7.5 - 9 mg/day for 6 days in treatment group. Saline of equivalence was given in contol group. The balloon injured arteries were harvested in the 7th, 14th, and 28th days after balloon injury, and Paraffin sections were made. At last, HE staining, apoptosis TUNEL assay were undertaken. RESULTS: (1) HE staining analysis: Media and intimal areas in treatment group at 14th day post-operation were larger than that in the 7th day (P = 0.003 and < 0.001, respectively). Media and intimal areas in treatment group decreased at the 28th day post-operation, while increased in control. Both media and intimal areas were significantly different (P < 0.001 respectively. (2) Tunel analysis discovered that, apoptosis reached peak in both treatment and control groups at the 28th post-operation. Differences of apoptosis cells counts in media and intimal between treatment and control groups were non-significant at the 7th, and 28th days, while differences at the 14th day were significant (p = 0.031 and 0.029 respectively). Apoptosis cells counting in treatment group at the 14th day increased more dramatically than that in the control. CONCLUSION: Intravenous Sodium Tanshinone II A sulfonic acid inhibites intimal proliferation after arterial balloon injury in rabbits. The effect can he partially explained by the induction of apoptosis in injured artery. Clinical effect of tanshinone II A still needs further evaluation. Sodium TA-II A sulfonic acid may be of potential therapeutic value in the prevention of restenosis after angioplasty.

Tanshinone IIA sodium sulfonate protects against cardiotoxicity induced by doxorubicin in vitro and in vivo.[Pubmed:19358873]

Food Chem Toxicol. 2009 Jul;47(7):1538-44.

Although doxorubicin (DXR) is an effective antineoplastic agent; the serious cardiotoxicity mediated by the production of reactive oxygen species has remained a considerable clinical problem. Our hypothesis is that tanshinone IIA sodium sulfonate (TSNIIA-SS), which holds significant affects on cardioprotection in clinic, protects against DXR-induced cardiotoxicity. In vitro investigation on H9c2 cell line, as well as in vivo study in animal model of DXR-induced chronic cardiomyopathy were performed. TSNIIA-SS significantly increased cell viability and ameliorated apoptosis of DXR-injured H9c2 cells using CCK-8 assay and Hoechst 33342 stain respectively. Furthermore, the cardio-protective effects of TSNIIA-SS were confirmed with decreasing ST-interval and QRS interval by electrocardiography (ECG); improving appearance of myocardium with haematoxylin and eosin (H&E) stain; increasing myocardial tensile strength using tension to rupture (TTR) assay and decreasing fibrosis through picric-sirius red staining comparing with those receiving DXR alone. These data have provided the considerable evidences that TSNIIA-SS is a protective agent against DXR-induced cardiac injury.

Tanshinone IIA sulfonate (sodium) is a derivative of tanshinone IIA, which acts as an inhibitor of store-operated Ca2+ entry (SOCE), and is used to treat cardiovascular disorders.

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