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tanshinone iia tsa  (Selleck Chemicals)
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Selleck Chemicals tanshinone iia tsa
Fig. 1. <t>TSA</t> inhibits Erastin/RSL3-induced cell death in HCAEC cells. A, Morphological observation of HCAECs. The HCAECs were treated with either TSA (50 nM), Era (10 mM), RSL3 (0.5 mM), or combination, as indicated, for 24 h. Cells were observed under light microscopy. B, HCAECs were treated as indicated, and cytotoxicity was determined by the LDH release assay. Treatments: TSA (50 nM), Era (10 mM), RSL3 (0.5 mM), Fer-1 (10 mM). C, HCAECs were treated with either TSA (50 nM), Era (10 mM), or both for 24 h; cell death rate was measured by PI staining. D, HCAECs were treated with either TSA (50 nM), RSL3 (0.5 mM), or both for 24 h; cell death rate was measured by PI staining. Data are shown as mean ± SD. ***p < 0.001, ANOVA with multiple comparisons. TSA, <t>Tanshinone</t> <t>IIA;</t> Era, Erastin.
Tanshinone Iia Tsa, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Fig. 1. TSA inhibits Erastin/RSL3-induced cell death in HCAEC cells. A, Morphological observation of HCAECs. The HCAECs were treated with either TSA (50 nM), Era (10 mM), RSL3 (0.5 mM), or combination, as indicated, for 24 h. Cells were observed under light microscopy. B, HCAECs were treated as indicated, and cytotoxicity was determined by the LDH release assay. Treatments: TSA (50 nM), Era (10 mM), RSL3 (0.5 mM), Fer-1 (10 mM). C, HCAECs were treated with either TSA (50 nM), Era (10 mM), or both for 24 h; cell death rate was measured by PI staining. D, HCAECs were treated with either TSA (50 nM), RSL3 (0.5 mM), or both for 24 h; cell death rate was measured by PI staining. Data are shown as mean ± SD. ***p < 0.001, ANOVA with multiple comparisons. TSA, Tanshinone IIA; Era, Erastin.

Journal: Biochemical and biophysical research communications

Article Title: Tanshinone IIA protects human coronary artery endothelial cells from ferroptosis by activating the NRF2 pathway.

doi: 10.1016/j.bbrc.2021.08.067

Figure Lengend Snippet: Fig. 1. TSA inhibits Erastin/RSL3-induced cell death in HCAEC cells. A, Morphological observation of HCAECs. The HCAECs were treated with either TSA (50 nM), Era (10 mM), RSL3 (0.5 mM), or combination, as indicated, for 24 h. Cells were observed under light microscopy. B, HCAECs were treated as indicated, and cytotoxicity was determined by the LDH release assay. Treatments: TSA (50 nM), Era (10 mM), RSL3 (0.5 mM), Fer-1 (10 mM). C, HCAECs were treated with either TSA (50 nM), Era (10 mM), or both for 24 h; cell death rate was measured by PI staining. D, HCAECs were treated with either TSA (50 nM), RSL3 (0.5 mM), or both for 24 h; cell death rate was measured by PI staining. Data are shown as mean ± SD. ***p < 0.001, ANOVA with multiple comparisons. TSA, Tanshinone IIA; Era, Erastin.

Article Snippet: Erastin (Era), Tanshinone IIA (TSA), Ferrostatin-1 (Fer-1), and ML385 were purchased from Selleckchem (Houston, USA).

Techniques: Light Microscopy, Lactate Dehydrogenase Assay, Staining

Fig. 2. TSA may attenuate ferroptosis by reducing ROS and iron accumulation in HCAEC cells. A, HCAECs were treated with either TSA (50 nM), Era (10 mM), or both for 24 h. Total cellular ROS was detected by DCFDA staining, and mean fluorescence intensity was measured by flow cytometry. B, HCAECs were treated with either TSA (50 nM), RSL3 (0.5 mM), or both for 24 h. Total cellular ROS was detected by DCFDA staining, and mean fluorescence intensity was measured by flow cytometry. C, HCAECs were treated as indicated for 24 h. Cellular lipid ROS was detected by C11-BODIPY staining, and mean fluorescence intensity was measured by flow cytometry. D, HCAECs were treated as indicated for 24 h. Cellular lipid ROS was detected by C11-BODIPY staining, and mean fluorescence intensity was measured by flow cytometry. E, HCAECs were treated with either TSA (50 nM), Era (10 mM), or both for 24 h. Cellular GSH level was measured. F&G, HCAECs were treated with either TSA (50 nM), Era (10 mM), or both for 24 h. FTH1 protein expression was detected by Western blot assay. H, HCAEC cells were treated as indicated. The FTH1 mRNA level was detected by qPCR. Data are shown as mean ± SD. ***p < 0.001, ANOVA with multiple comparisons. TSA, Tanshinone IIA; Era, Erastin.

Journal: Biochemical and biophysical research communications

Article Title: Tanshinone IIA protects human coronary artery endothelial cells from ferroptosis by activating the NRF2 pathway.

doi: 10.1016/j.bbrc.2021.08.067

Figure Lengend Snippet: Fig. 2. TSA may attenuate ferroptosis by reducing ROS and iron accumulation in HCAEC cells. A, HCAECs were treated with either TSA (50 nM), Era (10 mM), or both for 24 h. Total cellular ROS was detected by DCFDA staining, and mean fluorescence intensity was measured by flow cytometry. B, HCAECs were treated with either TSA (50 nM), RSL3 (0.5 mM), or both for 24 h. Total cellular ROS was detected by DCFDA staining, and mean fluorescence intensity was measured by flow cytometry. C, HCAECs were treated as indicated for 24 h. Cellular lipid ROS was detected by C11-BODIPY staining, and mean fluorescence intensity was measured by flow cytometry. D, HCAECs were treated as indicated for 24 h. Cellular lipid ROS was detected by C11-BODIPY staining, and mean fluorescence intensity was measured by flow cytometry. E, HCAECs were treated with either TSA (50 nM), Era (10 mM), or both for 24 h. Cellular GSH level was measured. F&G, HCAECs were treated with either TSA (50 nM), Era (10 mM), or both for 24 h. FTH1 protein expression was detected by Western blot assay. H, HCAEC cells were treated as indicated. The FTH1 mRNA level was detected by qPCR. Data are shown as mean ± SD. ***p < 0.001, ANOVA with multiple comparisons. TSA, Tanshinone IIA; Era, Erastin.

Article Snippet: Erastin (Era), Tanshinone IIA (TSA), Ferrostatin-1 (Fer-1), and ML385 were purchased from Selleckchem (Houston, USA).

Techniques: Staining, Cytometry, Expressing, Western Blot

Fig. 3. TSA combined with Erastin activates the NRF2 pathway in HCAEC cells. A-E, HCAECs were treated with either TSA (50 nM), Era (10 mM), or both for 24 h. The indicated proteins were detected by Western blot assay. The intensity of protein bands was quantified using ImageJ software. FeI, HCAECs were treated with either TSA (50 nM), Era (10 mM), or both for 24 h. The mRNA levels of the indicated genes were detected by qPCR. Data are shown as mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001, ANOVA with multiple comparisons. TSA, Tanshinone IIA; Era, Erastin.

Journal: Biochemical and biophysical research communications

Article Title: Tanshinone IIA protects human coronary artery endothelial cells from ferroptosis by activating the NRF2 pathway.

doi: 10.1016/j.bbrc.2021.08.067

Figure Lengend Snippet: Fig. 3. TSA combined with Erastin activates the NRF2 pathway in HCAEC cells. A-E, HCAECs were treated with either TSA (50 nM), Era (10 mM), or both for 24 h. The indicated proteins were detected by Western blot assay. The intensity of protein bands was quantified using ImageJ software. FeI, HCAECs were treated with either TSA (50 nM), Era (10 mM), or both for 24 h. The mRNA levels of the indicated genes were detected by qPCR. Data are shown as mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001, ANOVA with multiple comparisons. TSA, Tanshinone IIA; Era, Erastin.

Article Snippet: Erastin (Era), Tanshinone IIA (TSA), Ferrostatin-1 (Fer-1), and ML385 were purchased from Selleckchem (Houston, USA).

Techniques: Western Blot, Software

Fig. 4. NRF2 inhibition abolishes the protective effect of TSA on HCAEC cells. A, TSA promotes the nuclear translocation of NRF2. HCAECs were treated with either TSA, Era, or both for 24 h. NRF2 staining is indicated as green, and the cell nucleus was stained with DAPI (blue). B, HCAECs were treated as indicated for 24 h. The cytoplasmic and nuclear proteins were extracted, and NRF2 protein levels were detected by Western blot assay. The intensity of the protein bands was quantified. C, NRF2 inhibition by ML385 abolished the protective effect of TSA on HCAECs. HCAECs were treated as indicated, and cell death rate was determined by PI staining. Treatments: TSA (50 nM), Era (10 mM), ML385 (a NRF2 inhibitor, 10 mM). D, HCAECs were treated as indicated, and cellular lipid ROS was detected by C11-BODIPY staining. Mean fluorescence intensity was measured by flow cytometry. Data are shown as mean ± SD. **p < 0.01, ***p < 0.001, ANOVA with multiple comparisons. TSA (50 nM), Era (10 mM), ML385 (a NRF2 inhibitor, 10 mM). TSA, Tanshinone IIA; Era, Erastin; H3, histone H3. . (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)

Journal: Biochemical and biophysical research communications

Article Title: Tanshinone IIA protects human coronary artery endothelial cells from ferroptosis by activating the NRF2 pathway.

doi: 10.1016/j.bbrc.2021.08.067

Figure Lengend Snippet: Fig. 4. NRF2 inhibition abolishes the protective effect of TSA on HCAEC cells. A, TSA promotes the nuclear translocation of NRF2. HCAECs were treated with either TSA, Era, or both for 24 h. NRF2 staining is indicated as green, and the cell nucleus was stained with DAPI (blue). B, HCAECs were treated as indicated for 24 h. The cytoplasmic and nuclear proteins were extracted, and NRF2 protein levels were detected by Western blot assay. The intensity of the protein bands was quantified. C, NRF2 inhibition by ML385 abolished the protective effect of TSA on HCAECs. HCAECs were treated as indicated, and cell death rate was determined by PI staining. Treatments: TSA (50 nM), Era (10 mM), ML385 (a NRF2 inhibitor, 10 mM). D, HCAECs were treated as indicated, and cellular lipid ROS was detected by C11-BODIPY staining. Mean fluorescence intensity was measured by flow cytometry. Data are shown as mean ± SD. **p < 0.01, ***p < 0.001, ANOVA with multiple comparisons. TSA (50 nM), Era (10 mM), ML385 (a NRF2 inhibitor, 10 mM). TSA, Tanshinone IIA; Era, Erastin; H3, histone H3. . (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)

Article Snippet: Erastin (Era), Tanshinone IIA (TSA), Ferrostatin-1 (Fer-1), and ML385 were purchased from Selleckchem (Houston, USA).

Techniques: Inhibition, Translocation Assay, Staining, Western Blot, Cytometry