Tanshinone I

CAS# 568-73-0

Tanshinone I

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Quality Control of Tanshinone I

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Chemical structure

Tanshinone I

3D structure

Chemical Properties of Tanshinone I

Cas No. 568-73-0 SDF Download SDF
PubChem ID 114917 Appearance Brown powder
Formula C18H12O3 M.Wt 276.3
Type of Compound Diterpenoids Storage Desiccate at -20°C
Synonyms Tanshinone A
Solubility DMSO : 2.5 mg/mL (9.05 mM; Need ultrasonic)
Chemical Name 1,6-dimethylnaphtho[1,2-g][1]benzofuran-10,11-dione
SMILES CC1=CC=CC2=C1C=CC3=C2C(=O)C(=O)C4=C3OC=C4C
Standard InChIKey AIGAZQPHXLWMOJ-UHFFFAOYSA-N
Standard InChI InChI=1S/C18H12O3/c1-9-4-3-5-12-11(9)6-7-13-15(12)17(20)16(19)14-10(2)8-21-18(13)14/h3-8H,1-2H3
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.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Source of Tanshinone I

The roots of Salvia miltiorrhiza

Biological Activity of Tanshinone I

DescriptionTanshinone I is an inhibitor of type IIA human recombinant sPLA2 (IC50=11 μM) and rabbit recombinant cPLA2 (IC50=82 μM). Tanshinone I possesses hepatocyte protective, anticancer, neuroprotection, and nephroprotective properties. Tanshinone I pretreatment causes significant suppression of skin cell death induces by solar simulated UV and riboflavin-sensitized UVA.
TargetsNO | IL Receptor | TNF-α | COX | NF-kB | P450 (e.g. CYP17) | ERK | Nrf2 | p53 | p21 | Bcl-2/Bax | Caspase | Wnt/β-catenin | GSK-3 | sPLA2
In vitro

Tanshinone I induces cyclin D1 proteasomal degradation in an ERK1/2 dependent way in human colorectal cancer cells.[Pubmed: 25615593]

Fitoterapia. 2015 Mar;101:162-8.

Tanshinone I (TAN I) as one of the naturally occurring diterpenes from Salvia miltiorrhizae Bunge (Danshen) has been reported to exhibit an anti-cancer activity. However, the underlying mechanisms are still poorly understood. Thus, we performed in vitro study to elucidate the biological mechanism by which TAN I may induce the inhibition of cell growth in human colorectal cancer cells.
METHODS AND RESULTS:
The treatment of TAN I suppressed the cell proliferation in HCT116 and SW480 cells and decreased the level of cyclin D1 protein. However, the mRNA level of cyclin D1 did not changed by TAN I treatment. Inhibition of proteasomal degradation by MG132 blocked TAN I-mediated cyclin D1 downregulation and the half-life of cyclin D1 was decreased in the cells treated with TAN I. In addition, phosphorylation of cyclin D1 at threonine-286 was increased by TAN I and a point mutation of threonine-286 to alanine attenuated TAN I-mediated cyclin D1 downregulation. Inhibition of ERK1/2 suppressed cyclin D1 phosphorylation and subsequent downregulation by TAN I. From these results, we suggest that TAN I-mediated cyclin D1 downregulation may result from proteasomal degradation through its ERK1/2-mediated phosphorylation of threonine-286.
CONCLUSIONS:
In conclusion, the current study provides new mechanistic link between TAN I, cyclin D1 downregulation and cell growth in human colorectal cancer cells.

In vivo

Tanshinone I selectively suppresses pro-inflammatory genes expression in activated microglia and prevents nigrostriatal dopaminergic neurodegeneration in a mouse model of Parkinson's disease.[Pubmed: 25666429]

J Ethnopharmacol. 2015 Apr 22;164:247-55.

Radix Salviae Miltiorrhizae, known as Danshen, is a well-known traditional Chinese herb which has been used extensively for the treatment of various diseases, including cardiovascular and cerebrovascular disease and neurodegenerative diseases for thousands of years. Tanshinone I is one of major bioactive flavonoids of Radix Salviae Miltiorrhizae. Modulation of microglial over-reaction may represent a therapeutic target to alleviate the progression of neurodegenerative diseases. Here, we tested the effect of Tanshinone I on neuro-inflammation and whether it can provide neuroprotection through inhibition of neuro-inflammation.
METHODS AND RESULTS:
The effects of Tanshinone I on the production and/or mRNA expression of pro-inflammatory and anti-inflammatory factors in lipopolysaccharide(LPS)-induced BV-2 microglia cells were tested by Griess reaction, enzyme-linked immunosorbent assay (Elisa) or real time polymerase chain reaction. Activation of nuclear factor κ B (NF-κB) was measured by the nuclear translocation p65 and DNA binding activity. A model of Parkinson׳s disease was established by treatment of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in C57BL/6 mice. The effect of Tanshinone I on the behavioral changes, dopamine and its metabolites levels, expression of tyrosine hydroxylase (TH) and IBA-1, production of cytokines in the midbrain were investigated by the rotarod test, high-performance liquid chromatography (HPLC)-ECD, immunohistochemistry and Elisa. 1-methyl-4-phenylpyridinium (MPP+) concentration was tested by HPLC. Liver toxicity was determined by biochemical assay and histochemistry. We found that the productions and/or expressions of several pro-inflammatory M1 factors such as nitric oxide (NO), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-6 were highly suppressed by Tanshinone I in LPS-induced microglia. Interestingly, it did not affect the enhancement of expression of some anti-inflammatory M2 microglia markers, including IL-10, IL-1 receptor antagonist (IL-1Ra) and Cox-2. But it could significantly inhibit LPS-induced granulocyte colony-stimulating factor (G-CSF) expression. Tanshinone I could also inhibit LPS-induced NF-κB activation in microglia. Furthermore, it improved motor functions, normalized striatal neurotransmitters, and provided dopaminergic neuronal protection in MPTP-intoxicated mice. In vivo results also indicated that Tanshinone I could modulate MPTP-induced microglial activation, attenuated the increase of TNF-α, reserved the increase of IL-10 concentrain of MPTP-intoxicated mice. Tanshinone I does not alter MPTP toxic metabolite (MPP+) concentration. Oral administration of Tanshinone I at 10mg/kg daily for 2 weeks did not show liver toxicity.
CONCLUSIONS:
Tanshinone I selectively suppressed pro-inflammatory M1 genes expression in activated microglia, interestingly, partially reserved anti-inflammatory M2 genes expression. It also could provide neuroprotection in a mouse model of Parkinson׳s disease. These data indicated that Tanshinone I could make the most of the beneficial side and minimize the detrimental side of activated microglia simultaneously, and provide neuroprotection by modulating the immune response of microglia.

Tanshinone I protects mice from aristolochic acid I-induced kidney injury by induction of CYP1A.[Pubmed: 23981375]

Environ Toxicol Pharmacol. 2013 Nov;36(3):850-7.

Hepatic CYP1A especially CYP1A2 plays an important role in the reduction of aristolochic acid I (AAI) nephrotoxicity.
METHODS AND RESULTS:
In this study, we investigated the effects of Tanshinone I, a strong inducer of Cyp1a, on the nephrotoxicity induced by AAI. Histopathology and blood biochemistry assays showed that Tanshinone I could reduce AAI-induced acute kidney injury. Pharmacokinetics analysis revealed that Tanshinone I markedly decreased AUC of AAI in plasma and the content of AAI in both liver and kidney, indicating the enhancement of AAI metabolism. Real-time PCR and Western blot analysis confirmed that Tanshinone I effectively increased the mRNA and protein levels of hepatic CYP1A1 and CYP1A2 in vivo. Luciferase assay showed that Tanshinone I strongly increased the transcriptional activity of CYP1A1 and CYP1A2 in the similar extent.
CONCLUSIONS:
In summary, our data suggested that Tanshinone I facilitated the metabolism of AAI and prevented AAI-induced kidney injury by induction of hepatic CYP1A 1/2 in vivo.

Protocol of Tanshinone I

Cell Research

Growth inhibition and apoptosis induction by tanshinone I in human colon cancer Colo 205 cells.[Pubmed: 18949381]

The Nrf2-inducers tanshinone I and dihydrotanshinone protect human skin cells and reconstructed human skin against solar simulated UV.[Pubmed: 24273736]

Protective properties of tanshinone I against oxidative DNA damage and cytotoxicity.[Pubmed: 24021569]

Food Chem Toxicol. 2013 Dec;62:407-12.

Tanshinone I, a naturally occurring diterpene from Danshen, has been shown to possess hepatocyte protective, anticancer, and memory enhancing properties. However, there are few stringent pharmacological tests for neuroprotection of Tanshinone I thus far. Since peroxynitrite is involved in the pathogenesis of neurodegenerative disorders, this study was undertaken to investigate whether the neuroprotective effect of Tanshinone I is associated with inhibition of peroxynitrite-caused DNA damage, a critical event leading to peroxynitrite-induced cytotoxicity.
METHODS AND RESULTS:
Our results show that Tanshinone I can significantly inhibit peroxynitrite-induced DNA damage both in φX-174 plasmid DNA and rat primary astrocytes. EPR spectroscopy indicates that Tanshinone I potently diminished the DMPO-hydroxyl radical adduct signal from peroxynitrite.
CONCLUSIONS:
Taken together, these results demonstrate for the first time that Tanshinone I can protect against peroxynitrite-induced DNA damage, hydroxyl radical formation and cytotoxicity, which might have implications for Tanshinone I-mediated neuroprotection.

Redox Biol. 2013 Oct 29;1:532-41.

Exposure to solar ultraviolet (UV) radiation is a causative factor in skin photocarcinogenesis and photoaging, and an urgent need exists for improved strategies for skin photoprotection. The redox-sensitive transcription factor Nrf2 (nuclear factor-E2-related factor 2), a master regulator of the cellular antioxidant defense against environmental electrophilic insult, has recently emerged as an important determinant of cutaneous damage from solar UV, and the concept of pharmacological activation of Nrf2 has attracted considerable attention as a novel approach to skin photoprotection. In this study, we examined feasibility of using tanshinones, a novel class of phenanthrenequinone-based cytoprotective Nrf2 inducers derived from the medicinal plant Salvia miltiorrhiza, for protection of cultured human skin cells and reconstructed human skin against solar simulated UV.
METHODS AND RESULTS:
Using a dual luciferase reporter assay in human Hs27 dermal fibroblasts pronounced transcriptional activation of Nrf2 by four major tanshinones [Tanshinone I (T-I), dihydrotanshinone (DHT), Tanshinone IIA (T-II-A) and cryptotanshinone (CT)] was detected. In fibroblasts, the more potent tanshinones T-I and DHT caused a significant increase in Nrf2 protein half-life via blockage of ubiquitination, ultimately resulting in upregulated expression of cytoprotective Nrf2 target genes (GCLC, NQO1) with the elevation of cellular glutathione levels. Similar tanshinone-induced changes were also observed in HaCaT keratinocytes. T-I and DHT pretreatment caused significant suppression of skin cell death induced by solar simulated UV and riboflavin-sensitized UVA. Moreover, feasibility of tanshinone-based cutaneous photoprotection was tested employing a human skin reconstruct exposed to solar simulated UV (80 mJ/cm(2) UVB; 1.53 J/cm(2) UVA). The occurrence of markers of epidermal solar insult (cleaved procaspase 3, pycnotic nuclei, eosinophilic cytoplasm, acellular cavities) was significantly attenuated in DHT-treated reconstructs that displayed increased immunohistochemical staining for Nrf2 and γ-GCS together with the elevation of total glutathione levels.
CONCLUSIONS:
Taken together, our data suggest the feasibility of achieving tanshinone-based cutaneous Nrf2-activation and photoprotection.

Int J Mol Med. 2008 Nov;22(5):613-8.

Tanshinone I (Tan-I) and Tanshinone IIA (Tan-IIA) were isolated from Danshen (Salviae Miltiorrhizae Radix), a widely prescribed traditional herbal medicine that is used to treat cardiovascular and dysmenorrhea diseases. In our previous study, Tan-IIA was demonstrated to induce apoptosis in human colon cancer Colo 205 cells. However, the effect of Tan-I on human colon cancer cells is not clearly understood yet.
METHODS AND RESULTS:
In this study, the anti-growth and apoptosis-eliciting effects of Tan-I, as well as its cellular mechanisms of actions, were investigated in Colo 205 human colon cancer cells. Tan-I reduced cell growth in a concentration-dependent manner, inducing apoptosis accompanied by an increase in TUNEL staining and in cells in the sub-G1 fraction. The expression of p53, p21, bax and caspase-3 increased in Tan-I-treated cells. In addition, the cell cycle analysis showed G0/G1 arrest.
CONCLUSIONS:
These findings suggest that Tan-I induces apoptosis in Colo 205 cells through both mitochondrial-mediated intrinsic cell-death pathways and p21-mediated G0/G1cell cycle arrest. Accordingly, the therapeutic potential of Tan-I for colon cancer deserves further study.

Animal Research

Tanshinone I Enhances Neurogenesis in the Mouse Hippocampal Dentate Gyrus via Increasing Wnt-3, Phosphorylated Glycogen Synthase Kinase-3β and β-Catenin Immunoreactivities.[Pubmed: 27053301 ]

Neurochem. Res., 2016,41(8):1958-68.

Tanshinone I (TsI), a lipophilic diterpene extracted from Danshan (Radix Salvia miltiorrhizae), exerts neuroprotection in cerebrovascular diseases including transient ischemic attack. In this study, we examined effects of TsI on cell proliferation and neuronal differentiation in the subgranular zone (SGZ) of the mouse dentate gyrus (DG) using Ki-67, BrdU and doublecortin (DCX) immunohistochemistry.
METHODS AND RESULTS:
Mice were treated with 1 and 2 mg/kg TsI for 28 days. In the 1 mg/kg TsI-treated-group, distribution patterns of BrdU, Ki-67 and DCX positive ((+)) cells in the SGZ were similar to those in the vehicle-treated-group. However, in the 2 mg/kg TsI-treated-group, double labeled BrdU(+)/NeuN(+) cells, which are mature neurons, as well as Ki-67(+), DCX(+) and BrdU(+) cells were significantly increased compared with those in the vehicle-treated-group. On the other hand, immunoreactivities and protein levels of Wnt-3, β-catenin and serine-9-glycogen synthase kinase-3β (p-GSK-3β), which are related with morphogenesis, were significantly increased in the granule cell layer of the DG only in the 2 mg/kg TsI-treated-group.
CONCLUSIONS:
Therefore, these findings indicate that TsI can promote neurogenesis in the mouse DG and that the neurogenesis is related with increases of Wnt-3, p-GSK-3β and β-catenin immunoreactivities.

Tanshinone I Dilution Calculator

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Preparing Stock Solutions of Tanshinone I

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.6193 mL 18.0963 mL 36.1925 mL 72.3851 mL 90.4814 mL
5 mM 0.7239 mL 3.6193 mL 7.2385 mL 14.477 mL 18.0963 mL
10 mM 0.3619 mL 1.8096 mL 3.6193 mL 7.2385 mL 9.0481 mL
50 mM 0.0724 mL 0.3619 mL 0.7239 mL 1.4477 mL 1.8096 mL
100 mM 0.0362 mL 0.181 mL 0.3619 mL 0.7239 mL 0.9048 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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Background on Tanshinone I

Tanshinone I is an inhibitor of type IIA human recombinant sPLA2 (IC50=11 μM) and rabbit recombinant cPLA2 (IC50=82 μM).

In Vitro:Tanshinone I inhibits PGE2 formation from LPS-induced RAW macrophages (IC50=38 μM). When Tanshinone I is added simultaneously with LPS, this compound clearly inhibits PGE2 production (IC50=38 μM) at 10-100 μM. Tanshinone I also reduces PGE2 production (IC50=46 μM) when added after COX-2 is fully induced. The fact that Tanshinone I inhibits PGE2 production by pre-induced COX-2 strongly suggests that this compound may directly inhibit COX-2 activity and/or affect PLA2 activity. When Tanshinone I is incubated with two different forms of phospholipase A2 (PLA2), it clearly inhibits sPLA2 (IC50=11 μM) in a concentration-dependent manner. Although being less potent, Tanshinone I also inhibits cPLA2 (IC50=82 μM)[1].

In Vivo:Tanshinone I shows antiinflammatory activity in rat carrageenan-induced paw oedema and adjuvant-induced arthritis. In order to establish the anti-inflammatory activity of Tanshinone I, the classical animal models of acute and chronic inflammation [rat carrageenan (CGN)-induced paw oedema and rat adjuvant-induced arthritis (AIA)] are employed. When Tanshinone I is orally administered, it shows significant anti-inflammatory activity against CGN-induced paw oedema (47% inhibition at 160 mg/kg), while the IC50 of indomethacin is 7.1 mg/kg. In AIA, Tanshinone I gives 27% inhibition of secondary inflammation at 18 day with an oral dose of 50 mg/kg/day, whereas prednisolone (5 mg/kg/day) shows potent inhibition (65%)[1].

References:
[1]. Kim SY, et al. Effects of Tanshinone I isolated from Salvia miltiorrhiza bunge on arachidonic acid metabolism and in vivo inflammatory responses. Phytother Res. 2002 Nov;16(7):616-20.

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References on Tanshinone I

Tanshinone I induces cyclin D1 proteasomal degradation in an ERK1/2 dependent way in human colorectal cancer cells.[Pubmed:25615593]

Fitoterapia. 2015 Mar;101:162-8.

Tanshinone I (TAN I) as one of the naturally occurring diterpenes from Salvia miltiorrhizae Bunge (Danshen) has been reported to exhibit an anti-cancer activity. However, the underlying mechanisms are still poorly understood. Thus, we performed in vitro study to elucidate the biological mechanism by which TAN I may induce the inhibition of cell growth in human colorectal cancer cells. The treatment of TAN I suppressed the cell proliferation in HCT116 and SW480 cells and decreased the level of cyclin D1 protein. However, the mRNA level of cyclin D1 did not changed by TAN I treatment. Inhibition of proteasomal degradation by MG132 blocked TAN I-mediated cyclin D1 downregulation and the half-life of cyclin D1 was decreased in the cells treated with TAN I. In addition, phosphorylation of cyclin D1 at threonine-286 was increased by TAN I and a point mutation of threonine-286 to alanine attenuated TAN I-mediated cyclin D1 downregulation. Inhibition of ERK1/2 suppressed cyclin D1 phosphorylation and subsequent downregulation by TAN I. From these results, we suggest that TAN I-mediated cyclin D1 downregulation may result from proteasomal degradation through its ERK1/2-mediated phosphorylation of threonine-286. In conclusion, the current study provides new mechanistic link between TAN I, cyclin D1 downregulation and cell growth in human colorectal cancer cells.

Tanshinone I Enhances Neurogenesis in the Mouse Hippocampal Dentate Gyrus via Increasing Wnt-3, Phosphorylated Glycogen Synthase Kinase-3beta and beta-Catenin Immunoreactivities.[Pubmed:27053301]

Neurochem Res. 2016 Aug;41(8):1958-68.

Tanshinone I (TsI), a lipophilic diterpene extracted from Danshan (Radix Salvia miltiorrhizae), exerts neuroprotection in cerebrovascular diseases including transient ischemic attack. In this study, we examined effects of TsI on cell proliferation and neuronal differentiation in the subgranular zone (SGZ) of the mouse dentate gyrus (DG) using Ki-67, BrdU and doublecortin (DCX) immunohistochemistry. Mice were treated with 1 and 2 mg/kg TsI for 28 days. In the 1 mg/kg TsI-treated-group, distribution patterns of BrdU, Ki-67 and DCX positive ((+)) cells in the SGZ were similar to those in the vehicle-treated-group. However, in the 2 mg/kg TsI-treated-group, double labeled BrdU(+)/NeuN(+) cells, which are mature neurons, as well as Ki-67(+), DCX(+) and BrdU(+) cells were significantly increased compared with those in the vehicle-treated-group. On the other hand, immunoreactivities and protein levels of Wnt-3, beta-catenin and serine-9-glycogen synthase kinase-3beta (p-GSK-3beta), which are related with morphogenesis, were significantly increased in the granule cell layer of the DG only in the 2 mg/kg TsI-treated-group. Therefore, these findings indicate that TsI can promote neurogenesis in the mouse DG and that the neurogenesis is related with increases of Wnt-3, p-GSK-3beta and beta-catenin immunoreactivities.

The Nrf2-inducers tanshinone I and dihydrotanshinone protect human skin cells and reconstructed human skin against solar simulated UV.[Pubmed:24273736]

Redox Biol. 2013 Oct 29;1:532-41.

Exposure to solar ultraviolet (UV) radiation is a causative factor in skin photocarcinogenesis and photoaging, and an urgent need exists for improved strategies for skin photoprotection. The redox-sensitive transcription factor Nrf2 (nuclear factor-E2-related factor 2), a master regulator of the cellular antioxidant defense against environmental electrophilic insult, has recently emerged as an important determinant of cutaneous damage from solar UV, and the concept of pharmacological activation of Nrf2 has attracted considerable attention as a novel approach to skin photoprotection. In this study, we examined feasibility of using tanshinones, a novel class of phenanthrenequinone-based cytoprotective Nrf2 inducers derived from the medicinal plant Salvia miltiorrhiza, for protection of cultured human skin cells and reconstructed human skin against solar simulated UV. Using a dual luciferase reporter assay in human Hs27 dermal fibroblasts pronounced transcriptional activation of Nrf2 by four major tanshinones [Tanshinone I (T-I), dihydrotanshinone (DHT), Tanshinone IIA (T-II-A) and cryptotanshinone (CT)] was detected. In fibroblasts, the more potent tanshinones T-I and DHT caused a significant increase in Nrf2 protein half-life via blockage of ubiquitination, ultimately resulting in upregulated expression of cytoprotective Nrf2 target genes (GCLC, NQO1) with the elevation of cellular glutathione levels. Similar tanshinone-induced changes were also observed in HaCaT keratinocytes. T-I and DHT pretreatment caused significant suppression of skin cell death induced by solar simulated UV and riboflavin-sensitized UVA. Moreover, feasibility of tanshinone-based cutaneous photoprotection was tested employing a human skin reconstruct exposed to solar simulated UV (80 mJ/cm(2) UVB; 1.53 J/cm(2) UVA). The occurrence of markers of epidermal solar insult (cleaved procaspase 3, pycnotic nuclei, eosinophilic cytoplasm, acellular cavities) was significantly attenuated in DHT-treated reconstructs that displayed increased immunohistochemical staining for Nrf2 and gamma-GCS together with the elevation of total glutathione levels. Taken together, our data suggest the feasibility of achieving tanshinone-based cutaneous Nrf2-activation and photoprotection.

Protective properties of tanshinone I against oxidative DNA damage and cytotoxicity.[Pubmed:24021569]

Food Chem Toxicol. 2013 Dec;62:407-12.

Tanshinone I, a naturally occurring diterpene from Danshen, has been shown to possess hepatocyte protective, anticancer, and memory enhancing properties. However, there are few stringent pharmacological tests for neuroprotection of Tanshinone I thus far. Since peroxynitrite is involved in the pathogenesis of neurodegenerative disorders, this study was undertaken to investigate whether the neuroprotective effect of Tanshinone I is associated with inhibition of peroxynitrite-caused DNA damage, a critical event leading to peroxynitrite-induced cytotoxicity. Our results show that Tanshinone I can significantly inhibit peroxynitrite-induced DNA damage both in phiX-174 plasmid DNA and rat primary astrocytes. EPR spectroscopy indicates that Tanshinone I potently diminished the DMPO-hydroxyl radical adduct signal from peroxynitrite. Taken together, these results demonstrate for the first time that Tanshinone I can protect against peroxynitrite-induced DNA damage, hydroxyl radical formation and cytotoxicity, which might have implications for Tanshinone I-mediated neuroprotection.

Tanshinone I protects mice from aristolochic acid I-induced kidney injury by induction of CYP1A.[Pubmed:23981375]

Environ Toxicol Pharmacol. 2013 Nov;36(3):850-7.

Hepatic CYP1A especially CYP1A2 plays an important role in the reduction of aristolochic acid I (AAI) nephrotoxicity. In this study, we investigated the effects of Tanshinone I, a strong inducer of Cyp1a, on the nephrotoxicity induced by AAI. Histopathology and blood biochemistry assays showed that Tanshinone I could reduce AAI-induced acute kidney injury. Pharmacokinetics analysis revealed that Tanshinone I markedly decreased AUC of AAI in plasma and the content of AAI in both liver and kidney, indicating the enhancement of AAI metabolism. Real-time PCR and Western blot analysis confirmed that Tanshinone I effectively increased the mRNA and protein levels of hepatic CYP1A1 and CYP1A2 in vivo. Luciferase assay showed that Tanshinone I strongly increased the transcriptional activity of CYP1A1 and CYP1A2 in the similar extent. In summary, our data suggested that Tanshinone I facilitated the metabolism of AAI and prevented AAI-induced kidney injury by induction of hepatic CYP1A 1/2 in vivo.

Growth inhibition and apoptosis induction by tanshinone I in human colon cancer Colo 205 cells.[Pubmed:18949381]

Int J Mol Med. 2008 Nov;22(5):613-8.

Tanshinone I (Tan-I) and Tanshinone IIA (Tan-IIA) were isolated from Danshen (Salviae Miltiorrhizae Radix), a widely prescribed traditional herbal medicine that is used to treat cardiovascular and dysmenorrhea diseases. In our previous study, Tan-IIA was demonstrated to induce apoptosis in human colon cancer Colo 205 cells. However, the effect of Tan-I on human colon cancer cells is not clearly understood yet. In this study, the anti-growth and apoptosis-eliciting effects of Tan-I, as well as its cellular mechanisms of actions, were investigated in Colo 205 human colon cancer cells. Tan-I reduced cell growth in a concentration-dependent manner, inducing apoptosis accompanied by an increase in TUNEL staining and in cells in the sub-G1 fraction. The expression of p53, p21, bax and caspase-3 increased in Tan-I-treated cells. In addition, the cell cycle analysis showed G0/G1 arrest. These findings suggest that Tan-I induces apoptosis in Colo 205 cells through both mitochondrial-mediated intrinsic cell-death pathways and p21-mediated G0/G1cell cycle arrest. Accordingly, the therapeutic potential of Tan-I for colon cancer deserves further study.

Tanshinone I selectively suppresses pro-inflammatory genes expression in activated microglia and prevents nigrostriatal dopaminergic neurodegeneration in a mouse model of Parkinson's disease.[Pubmed:25666429]

J Ethnopharmacol. 2015 Apr 22;164:247-55.

ETHNOPHARMACOLOGICAL RELEVANCE: Radix Salviae Miltiorrhizae, known as Danshen, is a well-known traditional Chinese herb which has been used extensively for the treatment of various diseases, including cardiovascular and cerebrovascular disease and neurodegenerative diseases for thousands of years. Tanshinone I is one of major bioactive flavonoids of Radix Salviae Miltiorrhizae. Modulation of microglial over-reaction may represent a therapeutic target to alleviate the progression of neurodegenerative diseases. Here, we tested the effect of Tanshinone I on neuro-inflammation and whether it can provide neuroprotection through inhibition of neuro-inflammation. MATERIALS AND METHODS: The effects of Tanshinone I on the production and/or mRNA expression of pro-inflammatory and anti-inflammatory factors in lipopolysaccharide(LPS)-induced BV-2 microglia cells were tested by Griess reaction, enzyme-linked immunosorbent assay (Elisa) or real time polymerase chain reaction. Activation of nuclear factor kappa B (NF-kappaB) was measured by the nuclear translocation p65 and DNA binding activity. A model of Parkinsons disease was established by treatment of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in C57BL/6 mice. The effect of Tanshinone I on the behavioral changes, dopamine and its metabolites levels, expression of tyrosine hydroxylase (TH) and IBA-1, production of cytokines in the midbrain were investigated by the rotarod test, high-performance liquid chromatography (HPLC)-ECD, immunohistochemistry and Elisa. 1-methyl-4-phenylpyridinium (MPP+) concentration was tested by HPLC. Liver toxicity was determined by biochemical assay and histochemistry. RESULTS: We found that the productions and/or expressions of several pro-inflammatory M1 factors such as nitric oxide (NO), tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and IL-6 were highly suppressed by Tanshinone I in LPS-induced microglia. Interestingly, it did not affect the enhancement of expression of some anti-inflammatory M2 microglia markers, including IL-10, IL-1 receptor antagonist (IL-1Ra) and Cox-2. But it could significantly inhibit LPS-induced granulocyte colony-stimulating factor (G-CSF) expression. Tanshinone I could also inhibit LPS-induced NF-kappaB activation in microglia. Furthermore, it improved motor functions, normalized striatal neurotransmitters, and provided dopaminergic neuronal protection in MPTP-intoxicated mice. In vivo results also indicated that Tanshinone I could modulate MPTP-induced microglial activation, attenuated the increase of TNF-alpha, reserved the increase of IL-10 concentrain of MPTP-intoxicated mice. Tanshinone I does not alter MPTP toxic metabolite (MPP+) concentration. Oral administration of Tanshinone I at 10mg/kg daily for 2 weeks did not show liver toxicity. CONCLUSIONS: Tanshinone I selectively suppressed pro-inflammatory M1 genes expression in activated microglia, interestingly, partially reserved anti-inflammatory M2 genes expression. It also could provide neuroprotection in a mouse model of Parkinsons disease. These data indicated that Tanshinone I could make the most of the beneficial side and minimize the detrimental side of activated microglia simultaneously, and provide neuroprotection by modulating the immune response of microglia.

Description

Tanshinone I is an inhibitor of type IIA human recombinant sPLA2 (IC50=11 μM) and rabbit recombinant cPLA2 (IC50=82 μM).

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