triptolide treatment Search Results


94
Thermo Fisher triptolide treatment
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MedChemExpress triptolide
Pathological changes in the hippocampus of mTBI rat. A.HE staining showed that the swelling and rupture of rat cells were decreased after <t>triptolide</t> treatment. B. number of neuron cells. Swelling and ruptured nerve cells can be seen in the image, as shown by the black arrow. ## P < 0.01 mTBI compared with the sham group in both day 3 and day 7; *P < 0.05, mTBI+TP compared with the mTBI group day 3 and day 7. scale bar 100 µm, n=3. C. NeuN immunostaning (red). D. NeuN positive cells.comparison between groups on day 7, and day 3 each group. ## P < 0.01 mTBI compared with the sham group in both day 3 and day 7; *P < 0.05, mTBI+TP compared with the mTBI group day 3 and day 7. Data presented as mean + SD. n=5. The *,and # , indicate statistically significant differences.
Triptolide, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Millipore triptolide calbiochem triptolide
<t>Triptolide</t> treatment in neuroblastoma cells results in reduced cell viability with alternative mechanisms of cell death. Triptolide treatment in both neuroblastoma cell lines resulted in concentration- and time-dependent responses in vitro at minimal concentrations. (A) Cell death occurred in less than 72 hours at a 100 nmol/L concentration in both cell lines, with 45% cell death in IMR-32 cells and 50% cell death in SH-SY5Y cells. (B) A concentration- and time-dependent increase in caspase-3 activity was demonstrated with triptolide treatment in the IMR-32 cell line, which is consistent with cell death by apoptosis. However, this effect was not seen in the SH-SY5Y cell line, suggesting a method of cell death other than apoptosis. Data expressed as the mean ± SEM of 3 independent experiments. *P < .05 (t test) as compared with controls.
Triptolide Calbiochem Triptolide, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Selleck Chemicals inhibitor treatments
<t>Triptolide</t> treatment in neuroblastoma cells results in reduced cell viability with alternative mechanisms of cell death. Triptolide treatment in both neuroblastoma cell lines resulted in concentration- and time-dependent responses in vitro at minimal concentrations. (A) Cell death occurred in less than 72 hours at a 100 nmol/L concentration in both cell lines, with 45% cell death in IMR-32 cells and 50% cell death in SH-SY5Y cells. (B) A concentration- and time-dependent increase in caspase-3 activity was demonstrated with triptolide treatment in the IMR-32 cell line, which is consistent with cell death by apoptosis. However, this effect was not seen in the SH-SY5Y cell line, suggesting a method of cell death other than apoptosis. Data expressed as the mean ± SEM of 3 independent experiments. *P < .05 (t test) as compared with controls.
Inhibitor Treatments, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Dawley Inc triptolide
Summary of IL-10 traumatic brain injury preclinical studies.
Triptolide, supplied by Dawley Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Santa Cruz Biotechnology triptolide treatment
Figure 4. Paused Pol II Half-Life (t1/2) Decreases in FACT-Depleted S2 Cells (A–D) Chromatin from cells that had been treated with control dsRNA targeting EGFP or dsRNA targeting SSRP1 were incubated with 500-mM <t>triptolide</t> for 5, 10, 15, or 30 min or with 2% DMSO as control and subjected to ChIP-nexus using anti-Rpb3 antibodies. For each promoter where a typical Pol II ChIP-nexus footprint was observed (distance between positive and negative strand peak < 50 bp, position of Pol II footprint < 150 bp downstream of the TSS), spike-in normalized Pol II signal in a 51-bp window centered on the midpoint between paused Pol II positive and negative summits was determined, and the half-life of paused Pol II was calculated based on an exponential decay model. (A) Pol II in the pausing window at 18w as a function of time after addition of triptolide, in cells treated with EGFP (red) or SSRP1 (blue) dsRNAs. (B) Boxplot showing decreased paused Pol II half-life following SSRP1 depletion. p value was calculated with a two-sample Wilcoxon test, n = 998. (C) Heatmaps of Pol II ChIP-nexus data at various times after triptolide addition in EGFP and SSRP1 dsRNA-treated cells. (D) Boxplot showing fold change in pause half-life across highly paused (n = 411), moderately paused (n = 358), and lowly paused (n = 229) genes. p values were calculated using Wilcoxon rank sum test of pairwise comparisons. (E) A model for FACT function in promoter-proximal pausing and transcription-coupled histone modifications. In control cells (top panel), the +1 nucleosome is stabilized by FACT (Ramachandran et al., 2017). The +1 nucleosome in turn helps to maintain Pol II in the vicinity of the promoter-proximal pause, and tran- scription-coupled histone modifications H3K4me3 and H3K36me3 are normally deposited. Upon depletion of FACT, the +1 nucleosome is destabilized, and Pol II spends less time at the promoter-proximal pause. Hence, methyltransferases associated with elongating Pol II are allowed less time to place marks, leading to a broadening of H3K4me3 and relative depletion of H3K36me3 from more 50 portions of genes.
Triptolide Treatment, supplied by Santa Cruz Biotechnology, 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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BioMimetic Therapeutics prodrug triptolide palmitate ptp
Figure 4. Paused Pol II Half-Life (t1/2) Decreases in FACT-Depleted S2 Cells (A–D) Chromatin from cells that had been treated with control dsRNA targeting EGFP or dsRNA targeting SSRP1 were incubated with 500-mM <t>triptolide</t> for 5, 10, 15, or 30 min or with 2% DMSO as control and subjected to ChIP-nexus using anti-Rpb3 antibodies. For each promoter where a typical Pol II ChIP-nexus footprint was observed (distance between positive and negative strand peak < 50 bp, position of Pol II footprint < 150 bp downstream of the TSS), spike-in normalized Pol II signal in a 51-bp window centered on the midpoint between paused Pol II positive and negative summits was determined, and the half-life of paused Pol II was calculated based on an exponential decay model. (A) Pol II in the pausing window at 18w as a function of time after addition of triptolide, in cells treated with EGFP (red) or SSRP1 (blue) dsRNAs. (B) Boxplot showing decreased paused Pol II half-life following SSRP1 depletion. p value was calculated with a two-sample Wilcoxon test, n = 998. (C) Heatmaps of Pol II ChIP-nexus data at various times after triptolide addition in EGFP and SSRP1 dsRNA-treated cells. (D) Boxplot showing fold change in pause half-life across highly paused (n = 411), moderately paused (n = 358), and lowly paused (n = 229) genes. p values were calculated using Wilcoxon rank sum test of pairwise comparisons. (E) A model for FACT function in promoter-proximal pausing and transcription-coupled histone modifications. In control cells (top panel), the +1 nucleosome is stabilized by FACT (Ramachandran et al., 2017). The +1 nucleosome in turn helps to maintain Pol II in the vicinity of the promoter-proximal pause, and tran- scription-coupled histone modifications H3K4me3 and H3K36me3 are normally deposited. Upon depletion of FACT, the +1 nucleosome is destabilized, and Pol II spends less time at the promoter-proximal pause. Hence, methyltransferases associated with elongating Pol II are allowed less time to place marks, leading to a broadening of H3K4me3 and relative depletion of H3K36me3 from more 50 portions of genes.
Prodrug Triptolide Palmitate Ptp, supplied by BioMimetic Therapeutics, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Millipore triptolide treatment
Figure 4. Paused Pol II Half-Life (t1/2) Decreases in FACT-Depleted S2 Cells (A–D) Chromatin from cells that had been treated with control dsRNA targeting EGFP or dsRNA targeting SSRP1 were incubated with 500-mM <t>triptolide</t> for 5, 10, 15, or 30 min or with 2% DMSO as control and subjected to ChIP-nexus using anti-Rpb3 antibodies. For each promoter where a typical Pol II ChIP-nexus footprint was observed (distance between positive and negative strand peak < 50 bp, position of Pol II footprint < 150 bp downstream of the TSS), spike-in normalized Pol II signal in a 51-bp window centered on the midpoint between paused Pol II positive and negative summits was determined, and the half-life of paused Pol II was calculated based on an exponential decay model. (A) Pol II in the pausing window at 18w as a function of time after addition of triptolide, in cells treated with EGFP (red) or SSRP1 (blue) dsRNAs. (B) Boxplot showing decreased paused Pol II half-life following SSRP1 depletion. p value was calculated with a two-sample Wilcoxon test, n = 998. (C) Heatmaps of Pol II ChIP-nexus data at various times after triptolide addition in EGFP and SSRP1 dsRNA-treated cells. (D) Boxplot showing fold change in pause half-life across highly paused (n = 411), moderately paused (n = 358), and lowly paused (n = 229) genes. p values were calculated using Wilcoxon rank sum test of pairwise comparisons. (E) A model for FACT function in promoter-proximal pausing and transcription-coupled histone modifications. In control cells (top panel), the +1 nucleosome is stabilized by FACT (Ramachandran et al., 2017). The +1 nucleosome in turn helps to maintain Pol II in the vicinity of the promoter-proximal pause, and tran- scription-coupled histone modifications H3K4me3 and H3K36me3 are normally deposited. Upon depletion of FACT, the +1 nucleosome is destabilized, and Pol II spends less time at the promoter-proximal pause. Hence, methyltransferases associated with elongating Pol II are allowed less time to place marks, leading to a broadening of H3K4me3 and relative depletion of H3K36me3 from more 50 portions of genes.
Triptolide Treatment, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Cell Signaling Technology Inc triptolide treatments
The boxplots show the average ChIP-seq enrichment of Ser5P Pol II, Nipped-B, TBPH and Lark at active promoters, extragenic enhancers, and PREs in control cells, and cells treated with 10 μM <t>triptolide</t> for 1, 2, and 4 hours. The genome browser tracks at the right show the log2 ChIP-seq enrichment for the same proteins at the string gene and enhancers over the same time course of triptolide treatment.
Triptolide Treatments, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Millipore dmso-dissolved triptolide
The boxplots show the average ChIP-seq enrichment of Ser5P Pol II, Nipped-B, TBPH and Lark at active promoters, extragenic enhancers, and PREs in control cells, and cells treated with 10 μM <t>triptolide</t> for 1, 2, and 4 hours. The genome browser tracks at the right show the log2 ChIP-seq enrichment for the same proteins at the string gene and enhancers over the same time course of triptolide treatment.
Dmso Dissolved Triptolide, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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BioMimetic Therapeutics biomimetic nanoparticles triptolide
Promising areas for nanomedicine development in gastric cancer.
Biomimetic Nanoparticles Triptolide, supplied by BioMimetic Therapeutics, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Wolters Kluwer Health triptolide
Promising areas for nanomedicine development in gastric cancer.
Triptolide, supplied by Wolters Kluwer Health, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Pathological changes in the hippocampus of mTBI rat. A.HE staining showed that the swelling and rupture of rat cells were decreased after triptolide treatment. B. number of neuron cells. Swelling and ruptured nerve cells can be seen in the image, as shown by the black arrow. ## P < 0.01 mTBI compared with the sham group in both day 3 and day 7; *P < 0.05, mTBI+TP compared with the mTBI group day 3 and day 7. scale bar 100 µm, n=3. C. NeuN immunostaning (red). D. NeuN positive cells.comparison between groups on day 7, and day 3 each group. ## P < 0.01 mTBI compared with the sham group in both day 3 and day 7; *P < 0.05, mTBI+TP compared with the mTBI group day 3 and day 7. Data presented as mean + SD. n=5. The *,and # , indicate statistically significant differences.

Journal: IBRO Neuroscience Reports

Article Title: Neuroprotective effect of triptolide on neuronal inflammation in rats with mild brain injury

doi: 10.1016/j.ibneur.2024.05.007

Figure Lengend Snippet: Pathological changes in the hippocampus of mTBI rat. A.HE staining showed that the swelling and rupture of rat cells were decreased after triptolide treatment. B. number of neuron cells. Swelling and ruptured nerve cells can be seen in the image, as shown by the black arrow. ## P < 0.01 mTBI compared with the sham group in both day 3 and day 7; *P < 0.05, mTBI+TP compared with the mTBI group day 3 and day 7. scale bar 100 µm, n=3. C. NeuN immunostaning (red). D. NeuN positive cells.comparison between groups on day 7, and day 3 each group. ## P < 0.01 mTBI compared with the sham group in both day 3 and day 7; *P < 0.05, mTBI+TP compared with the mTBI group day 3 and day 7. Data presented as mean + SD. n=5. The *,and # , indicate statistically significant differences.

Article Snippet: The rats in the triptolide treatment group were intraperitoneally injected with 0.2 mg/kg triptolide ( ) for a week.TP (Med Chem Express, USA#39,836) was dissolved in DMSO at a concentration of 2 mg/mL and diluted with normal saline to a final concentration of 0.2 mg/ mL.

Techniques: Staining, Comparison

Inflammatory-related factors A. IL-1β, B. TNF-α and C. IL-10; changes after triptolide treatment. D&E individual raw data of each factors after 3 days and 7 days. Comparison between groups on day 3, comparison between groups on day 7, and day 3 and day 7 for each group. Data presented as mean + SD. The *, # , indicate statistically significant differences. IL-1β; mTBI Vs. Sham day3 ** P < 0.01, day 7 ** P < 0.01 , mTBI+TP Vs. mTBI; day3 ## P < 0.01, day 7 # P < 0.05, TNF-ɑ; mTBI Vs. Sham day3 ** P < 0.01, day 7 ** P < 0.01, mTBI+TP Vs. mTBI; day3 ## P < 0.01, day 7 ## P < 0.01, IL-10; mTBI Vs. Sham day3 * P < 0.05 , day 7 * P < 0.05, mTBI+TP Vs . mTBI; day3 ** P < 0.01, day 7 ** P < 0.01, n=10.

Journal: IBRO Neuroscience Reports

Article Title: Neuroprotective effect of triptolide on neuronal inflammation in rats with mild brain injury

doi: 10.1016/j.ibneur.2024.05.007

Figure Lengend Snippet: Inflammatory-related factors A. IL-1β, B. TNF-α and C. IL-10; changes after triptolide treatment. D&E individual raw data of each factors after 3 days and 7 days. Comparison between groups on day 3, comparison between groups on day 7, and day 3 and day 7 for each group. Data presented as mean + SD. The *, # , indicate statistically significant differences. IL-1β; mTBI Vs. Sham day3 ** P < 0.01, day 7 ** P < 0.01 , mTBI+TP Vs. mTBI; day3 ## P < 0.01, day 7 # P < 0.05, TNF-ɑ; mTBI Vs. Sham day3 ** P < 0.01, day 7 ** P < 0.01, mTBI+TP Vs. mTBI; day3 ## P < 0.01, day 7 ## P < 0.01, IL-10; mTBI Vs. Sham day3 * P < 0.05 , day 7 * P < 0.05, mTBI+TP Vs . mTBI; day3 ** P < 0.01, day 7 ** P < 0.01, n=10.

Article Snippet: The rats in the triptolide treatment group were intraperitoneally injected with 0.2 mg/kg triptolide ( ) for a week.TP (Med Chem Express, USA#39,836) was dissolved in DMSO at a concentration of 2 mg/mL and diluted with normal saline to a final concentration of 0.2 mg/ mL.

Techniques: Comparison

Triptolide downregulated IL-1β and NF-κB expressions. The relative mRNA expression was calculated using the formula 2– ΔΔ Ct. Comparison between groups on day 3, comparison between groups on day 7, and day 3 and day 7 for each group. Data presented as mean + SD. The indicate statistically significant differences. IL-1β; mTBI Vs. Sham day3 ** P < 0.01, day 7 ** P < 0.01 , mTBI+TP Vs. mTBI; day3 ## P < 0.01, day 7 # P < 0.05, NF-kB; mTBI Vs. Sham day3 ** P < 0.01, day 7 ** P < 0.01, mTBI+TP Vs. mTBI; day3 ## P < 0.01, day 7 ## P < 0.01, n=8.

Journal: IBRO Neuroscience Reports

Article Title: Neuroprotective effect of triptolide on neuronal inflammation in rats with mild brain injury

doi: 10.1016/j.ibneur.2024.05.007

Figure Lengend Snippet: Triptolide downregulated IL-1β and NF-κB expressions. The relative mRNA expression was calculated using the formula 2– ΔΔ Ct. Comparison between groups on day 3, comparison between groups on day 7, and day 3 and day 7 for each group. Data presented as mean + SD. The indicate statistically significant differences. IL-1β; mTBI Vs. Sham day3 ** P < 0.01, day 7 ** P < 0.01 , mTBI+TP Vs. mTBI; day3 ## P < 0.01, day 7 # P < 0.05, NF-kB; mTBI Vs. Sham day3 ** P < 0.01, day 7 ** P < 0.01, mTBI+TP Vs. mTBI; day3 ## P < 0.01, day 7 ## P < 0.01, n=8.

Article Snippet: The rats in the triptolide treatment group were intraperitoneally injected with 0.2 mg/kg triptolide ( ) for a week.TP (Med Chem Express, USA#39,836) was dissolved in DMSO at a concentration of 2 mg/mL and diluted with normal saline to a final concentration of 0.2 mg/ mL.

Techniques: Expressing, Comparison

LC3B expression changes after triptolide treatment at different time points. (A): Representative LC3B positive (green) and DAPI (blue) merged image is shown. In the mTBI group, the positive expression index of autophagy protein LC3B was higher than both sham and mTBI + TP groups. The autophagy protein experimental group can be seen in the image. Scale bar = 50 μm. Immunofluorescence showed decreased expression of autophagy and aquaporin in rats treated with triptolide. (B): Comparison between groups on day 3, comparison between groups on day 7, and day 3 and day 7 for each group. Data presented as mean + SD. The *, #, indicate statistically significant differences. mTBI Vs. Sham day3 ** P < 0.01, day 7 ** P < 0.01 , mTBI+TP Vs. mTBI; day3 ## P < 0.01, day 7 ## P < 0.01 day 7, n=8. C. LC3B Western blot, D. Quantitative analysis of LC3B; mTBI Vs. Sham day3 ** P < 0.01, day 7 ** P < 0.01, mTBI+TP Vs. mTBI; day3 ## P < 0.01, day 7 ## P < 0.01 day 7, n=3.

Journal: IBRO Neuroscience Reports

Article Title: Neuroprotective effect of triptolide on neuronal inflammation in rats with mild brain injury

doi: 10.1016/j.ibneur.2024.05.007

Figure Lengend Snippet: LC3B expression changes after triptolide treatment at different time points. (A): Representative LC3B positive (green) and DAPI (blue) merged image is shown. In the mTBI group, the positive expression index of autophagy protein LC3B was higher than both sham and mTBI + TP groups. The autophagy protein experimental group can be seen in the image. Scale bar = 50 μm. Immunofluorescence showed decreased expression of autophagy and aquaporin in rats treated with triptolide. (B): Comparison between groups on day 3, comparison between groups on day 7, and day 3 and day 7 for each group. Data presented as mean + SD. The *, #, indicate statistically significant differences. mTBI Vs. Sham day3 ** P < 0.01, day 7 ** P < 0.01 , mTBI+TP Vs. mTBI; day3 ## P < 0.01, day 7 ## P < 0.01 day 7, n=8. C. LC3B Western blot, D. Quantitative analysis of LC3B; mTBI Vs. Sham day3 ** P < 0.01, day 7 ** P < 0.01, mTBI+TP Vs. mTBI; day3 ## P < 0.01, day 7 ## P < 0.01 day 7, n=3.

Article Snippet: The rats in the triptolide treatment group were intraperitoneally injected with 0.2 mg/kg triptolide ( ) for a week.TP (Med Chem Express, USA#39,836) was dissolved in DMSO at a concentration of 2 mg/mL and diluted with normal saline to a final concentration of 0.2 mg/ mL.

Techniques: Expressing, Immunofluorescence, Comparison, Western Blot

AQP4 expression changes after triptolide treatment at different time points. (A): Representative AQP4 positive (green) and DAPI (blue) merged image is shown. In the mTBI group, the positive expression index of AQP4 was higher than the sham and mTBI + TP groups. The Aquaporin of an experimental group can be seen in the image. Scale bar = 50 μm. Immunofluorescence showed decreased expression of autophagy and aquaporin in rats treated with triptolide. (B): Comparison between groups on day 3, comparison between groups on day 7, and day 3 and day 7 for each group. Data presented as mean + SD, n=8. The *, #, indicate statistically significant differences. mTBI Vs. Sham day3 ** P < 0.01, day 7 ** P < 0.01 , mTBI+TP Vs. mTBI; day3 # P < 0.05, day 7 # P < 0.05 day 7, n=8. C. LC3B Western blot, D. Quantitative analysis of LC3B; mTBI Vs. Sham day3 ** P < 0.01, day 7 ** P < 0.01, mTBI+TP Vs. mTBI; day3 ## P < 0.01, day 7 ## P < 0.01 day 7, n=3.

Journal: IBRO Neuroscience Reports

Article Title: Neuroprotective effect of triptolide on neuronal inflammation in rats with mild brain injury

doi: 10.1016/j.ibneur.2024.05.007

Figure Lengend Snippet: AQP4 expression changes after triptolide treatment at different time points. (A): Representative AQP4 positive (green) and DAPI (blue) merged image is shown. In the mTBI group, the positive expression index of AQP4 was higher than the sham and mTBI + TP groups. The Aquaporin of an experimental group can be seen in the image. Scale bar = 50 μm. Immunofluorescence showed decreased expression of autophagy and aquaporin in rats treated with triptolide. (B): Comparison between groups on day 3, comparison between groups on day 7, and day 3 and day 7 for each group. Data presented as mean + SD, n=8. The *, #, indicate statistically significant differences. mTBI Vs. Sham day3 ** P < 0.01, day 7 ** P < 0.01 , mTBI+TP Vs. mTBI; day3 # P < 0.05, day 7 # P < 0.05 day 7, n=8. C. LC3B Western blot, D. Quantitative analysis of LC3B; mTBI Vs. Sham day3 ** P < 0.01, day 7 ** P < 0.01, mTBI+TP Vs. mTBI; day3 ## P < 0.01, day 7 ## P < 0.01 day 7, n=3.

Article Snippet: The rats in the triptolide treatment group were intraperitoneally injected with 0.2 mg/kg triptolide ( ) for a week.TP (Med Chem Express, USA#39,836) was dissolved in DMSO at a concentration of 2 mg/mL and diluted with normal saline to a final concentration of 0.2 mg/ mL.

Techniques: Expressing, Immunofluorescence, Comparison, Western Blot

Triptolide treatment in neuroblastoma cells results in reduced cell viability with alternative mechanisms of cell death. Triptolide treatment in both neuroblastoma cell lines resulted in concentration- and time-dependent responses in vitro at minimal concentrations. (A) Cell death occurred in less than 72 hours at a 100 nmol/L concentration in both cell lines, with 45% cell death in IMR-32 cells and 50% cell death in SH-SY5Y cells. (B) A concentration- and time-dependent increase in caspase-3 activity was demonstrated with triptolide treatment in the IMR-32 cell line, which is consistent with cell death by apoptosis. However, this effect was not seen in the SH-SY5Y cell line, suggesting a method of cell death other than apoptosis. Data expressed as the mean ± SEM of 3 independent experiments. *P < .05 (t test) as compared with controls.

Journal: American journal of surgery

Article Title: Triptolide-mediated cell death in neuroblastoma occurs by both apoptosis and autophagy pathways and results in inhibition of nuclear factor–kappa B activity

doi: 10.1016/j.amjsurg.2013.01.008

Figure Lengend Snippet: Triptolide treatment in neuroblastoma cells results in reduced cell viability with alternative mechanisms of cell death. Triptolide treatment in both neuroblastoma cell lines resulted in concentration- and time-dependent responses in vitro at minimal concentrations. (A) Cell death occurred in less than 72 hours at a 100 nmol/L concentration in both cell lines, with 45% cell death in IMR-32 cells and 50% cell death in SH-SY5Y cells. (B) A concentration- and time-dependent increase in caspase-3 activity was demonstrated with triptolide treatment in the IMR-32 cell line, which is consistent with cell death by apoptosis. However, this effect was not seen in the SH-SY5Y cell line, suggesting a method of cell death other than apoptosis. Data expressed as the mean ± SEM of 3 independent experiments. *P < .05 (t test) as compared with controls.

Article Snippet: Treatment of cells with triptolide Calbiochem triptolide (EMD Millipore Chemicals, Billerica, MA) was dissolved in dimethyl sulfoxide (DMSO) (Sigma-Aldrich, St. Louis, MO) and added to the cells at the indicated concentrations in serum-free medium (SFM).

Techniques: Concentration Assay, In Vitro, Activity Assay

Triptolide treatment induces autophagy in SH-SY5Y neuroblastoma cells. (A) Investigation of SH-SY5Y LC3 protein levels by Western blotting showed increased expression of LC3II in triptolide-treated cells at 6 and 24 hours, which is consistent with autophagy. Actin served as a loading control; results representative of n =3. (B and C) Treatment of SH-SY5Y cells with triptolide at 100 nmol/L for 20 hours shows a significant increase in the LC3 punctate staining pattern when compared with untreated controls. This finding was not observed in the apoptotic IMR-32 neuroblastoma cell line. Data are expressed as the mean ± SEM of 3 independent experiments.

Journal: American journal of surgery

Article Title: Triptolide-mediated cell death in neuroblastoma occurs by both apoptosis and autophagy pathways and results in inhibition of nuclear factor–kappa B activity

doi: 10.1016/j.amjsurg.2013.01.008

Figure Lengend Snippet: Triptolide treatment induces autophagy in SH-SY5Y neuroblastoma cells. (A) Investigation of SH-SY5Y LC3 protein levels by Western blotting showed increased expression of LC3II in triptolide-treated cells at 6 and 24 hours, which is consistent with autophagy. Actin served as a loading control; results representative of n =3. (B and C) Treatment of SH-SY5Y cells with triptolide at 100 nmol/L for 20 hours shows a significant increase in the LC3 punctate staining pattern when compared with untreated controls. This finding was not observed in the apoptotic IMR-32 neuroblastoma cell line. Data are expressed as the mean ± SEM of 3 independent experiments.

Article Snippet: Treatment of cells with triptolide Calbiochem triptolide (EMD Millipore Chemicals, Billerica, MA) was dissolved in dimethyl sulfoxide (DMSO) (Sigma-Aldrich, St. Louis, MO) and added to the cells at the indicated concentrations in serum-free medium (SFM).

Techniques: Western Blot, Expressing, Control, Staining

mRNA and protein levels in the heat shock protein pathway are decreased after triptolide treatment, with a sustained increase in intracellular calcium levels. (A) Triptolide treatment (100 nmol/L) of SH-SY5Y and IMR-32 neuroblastoma cell lines for 24 hours resulted in a significant decrease in expression of HSF1, HSP70, and HSP27 mRNA levels compared with untreated controls. Data is representative of results obtained from 3 separate quantitative PCR analyses. (B) Representative Western blots show triptolide treatment (50 and 100 nmol/L) results in a depletion of the heat shock protein transcription factor, HSF1, as well as downstream proteins HSP70 and HSP27. Actin served as a loading control. (C) Both cell lines demonstrated a time- and dose-dependent increase in intracellular calcium levels with triptolide treatment to levels greater than 200% of control at 72 hours (with 100 nmol/L triptolide). Data are expressed as the mean ± SEM of 3 independent experiments. *P < .05 (t test) as compared with controls.

Journal: American journal of surgery

Article Title: Triptolide-mediated cell death in neuroblastoma occurs by both apoptosis and autophagy pathways and results in inhibition of nuclear factor–kappa B activity

doi: 10.1016/j.amjsurg.2013.01.008

Figure Lengend Snippet: mRNA and protein levels in the heat shock protein pathway are decreased after triptolide treatment, with a sustained increase in intracellular calcium levels. (A) Triptolide treatment (100 nmol/L) of SH-SY5Y and IMR-32 neuroblastoma cell lines for 24 hours resulted in a significant decrease in expression of HSF1, HSP70, and HSP27 mRNA levels compared with untreated controls. Data is representative of results obtained from 3 separate quantitative PCR analyses. (B) Representative Western blots show triptolide treatment (50 and 100 nmol/L) results in a depletion of the heat shock protein transcription factor, HSF1, as well as downstream proteins HSP70 and HSP27. Actin served as a loading control. (C) Both cell lines demonstrated a time- and dose-dependent increase in intracellular calcium levels with triptolide treatment to levels greater than 200% of control at 72 hours (with 100 nmol/L triptolide). Data are expressed as the mean ± SEM of 3 independent experiments. *P < .05 (t test) as compared with controls.

Article Snippet: Treatment of cells with triptolide Calbiochem triptolide (EMD Millipore Chemicals, Billerica, MA) was dissolved in dimethyl sulfoxide (DMSO) (Sigma-Aldrich, St. Louis, MO) and added to the cells at the indicated concentrations in serum-free medium (SFM).

Techniques: Expressing, Real-time Polymerase Chain Reaction, Western Blot, Control

Effects of triptolide therapy in neuroblastoma. Our study shows that triptolide treatment in neuroblastoma cells leads to inhibition of NF-κB activity while also inhibiting mRNA and protein expression in the heat shock pathway, specifically by reducing HSF1, and thereby reducing HSP70 and HSP27. NF-κB is known to serve as a transcription initiator for HSP70 (UCSC Genome Bioinformatics Site), providing a possible common link among the pathways (dotted line). Ultimately, the inhibition of these pathways has been previously demonstrated to result in increased intracellular calcium levels, leading to cell death. In our study, we demonstrate triptolide’s induction of different cell death mechanisms, based on the cell type, ultimately leading to reduced cell viability or death.

Journal: American journal of surgery

Article Title: Triptolide-mediated cell death in neuroblastoma occurs by both apoptosis and autophagy pathways and results in inhibition of nuclear factor–kappa B activity

doi: 10.1016/j.amjsurg.2013.01.008

Figure Lengend Snippet: Effects of triptolide therapy in neuroblastoma. Our study shows that triptolide treatment in neuroblastoma cells leads to inhibition of NF-κB activity while also inhibiting mRNA and protein expression in the heat shock pathway, specifically by reducing HSF1, and thereby reducing HSP70 and HSP27. NF-κB is known to serve as a transcription initiator for HSP70 (UCSC Genome Bioinformatics Site), providing a possible common link among the pathways (dotted line). Ultimately, the inhibition of these pathways has been previously demonstrated to result in increased intracellular calcium levels, leading to cell death. In our study, we demonstrate triptolide’s induction of different cell death mechanisms, based on the cell type, ultimately leading to reduced cell viability or death.

Article Snippet: Treatment of cells with triptolide Calbiochem triptolide (EMD Millipore Chemicals, Billerica, MA) was dissolved in dimethyl sulfoxide (DMSO) (Sigma-Aldrich, St. Louis, MO) and added to the cells at the indicated concentrations in serum-free medium (SFM).

Techniques: Inhibition, Activity Assay, Expressing

Summary of IL-10 traumatic brain injury preclinical studies.

Journal: Frontiers in Neurology

Article Title: Role of Interleukin-10 in Acute Brain Injuries

doi: 10.3389/fneur.2017.00244

Figure Lengend Snippet: Summary of IL-10 traumatic brain injury preclinical studies.

Article Snippet: IP Triptolide , CCI , Triptolide treatment increases brain IL-10 levels at 1d and improves anatomical and neurobehavioral outcomes , Sprague-Dawley , ( ) .

Techniques:

Figure 4. Paused Pol II Half-Life (t1/2) Decreases in FACT-Depleted S2 Cells (A–D) Chromatin from cells that had been treated with control dsRNA targeting EGFP or dsRNA targeting SSRP1 were incubated with 500-mM triptolide for 5, 10, 15, or 30 min or with 2% DMSO as control and subjected to ChIP-nexus using anti-Rpb3 antibodies. For each promoter where a typical Pol II ChIP-nexus footprint was observed (distance between positive and negative strand peak < 50 bp, position of Pol II footprint < 150 bp downstream of the TSS), spike-in normalized Pol II signal in a 51-bp window centered on the midpoint between paused Pol II positive and negative summits was determined, and the half-life of paused Pol II was calculated based on an exponential decay model. (A) Pol II in the pausing window at 18w as a function of time after addition of triptolide, in cells treated with EGFP (red) or SSRP1 (blue) dsRNAs. (B) Boxplot showing decreased paused Pol II half-life following SSRP1 depletion. p value was calculated with a two-sample Wilcoxon test, n = 998. (C) Heatmaps of Pol II ChIP-nexus data at various times after triptolide addition in EGFP and SSRP1 dsRNA-treated cells. (D) Boxplot showing fold change in pause half-life across highly paused (n = 411), moderately paused (n = 358), and lowly paused (n = 229) genes. p values were calculated using Wilcoxon rank sum test of pairwise comparisons. (E) A model for FACT function in promoter-proximal pausing and transcription-coupled histone modifications. In control cells (top panel), the +1 nucleosome is stabilized by FACT (Ramachandran et al., 2017). The +1 nucleosome in turn helps to maintain Pol II in the vicinity of the promoter-proximal pause, and tran- scription-coupled histone modifications H3K4me3 and H3K36me3 are normally deposited. Upon depletion of FACT, the +1 nucleosome is destabilized, and Pol II spends less time at the promoter-proximal pause. Hence, methyltransferases associated with elongating Pol II are allowed less time to place marks, leading to a broadening of H3K4me3 and relative depletion of H3K36me3 from more 50 portions of genes.

Journal: Cell reports

Article Title: A Role for FACT in RNA Polymerase II Promoter-Proximal Pausing.

doi: 10.1016/j.celrep.2019.05.099

Figure Lengend Snippet: Figure 4. Paused Pol II Half-Life (t1/2) Decreases in FACT-Depleted S2 Cells (A–D) Chromatin from cells that had been treated with control dsRNA targeting EGFP or dsRNA targeting SSRP1 were incubated with 500-mM triptolide for 5, 10, 15, or 30 min or with 2% DMSO as control and subjected to ChIP-nexus using anti-Rpb3 antibodies. For each promoter where a typical Pol II ChIP-nexus footprint was observed (distance between positive and negative strand peak < 50 bp, position of Pol II footprint < 150 bp downstream of the TSS), spike-in normalized Pol II signal in a 51-bp window centered on the midpoint between paused Pol II positive and negative summits was determined, and the half-life of paused Pol II was calculated based on an exponential decay model. (A) Pol II in the pausing window at 18w as a function of time after addition of triptolide, in cells treated with EGFP (red) or SSRP1 (blue) dsRNAs. (B) Boxplot showing decreased paused Pol II half-life following SSRP1 depletion. p value was calculated with a two-sample Wilcoxon test, n = 998. (C) Heatmaps of Pol II ChIP-nexus data at various times after triptolide addition in EGFP and SSRP1 dsRNA-treated cells. (D) Boxplot showing fold change in pause half-life across highly paused (n = 411), moderately paused (n = 358), and lowly paused (n = 229) genes. p values were calculated using Wilcoxon rank sum test of pairwise comparisons. (E) A model for FACT function in promoter-proximal pausing and transcription-coupled histone modifications. In control cells (top panel), the +1 nucleosome is stabilized by FACT (Ramachandran et al., 2017). The +1 nucleosome in turn helps to maintain Pol II in the vicinity of the promoter-proximal pause, and tran- scription-coupled histone modifications H3K4me3 and H3K36me3 are normally deposited. Upon depletion of FACT, the +1 nucleosome is destabilized, and Pol II spends less time at the promoter-proximal pause. Hence, methyltransferases associated with elongating Pol II are allowed less time to place marks, leading to a broadening of H3K4me3 and relative depletion of H3K36me3 from more 50 portions of genes.

Article Snippet: To control for the loss of Pol II ChIP signal after triptolide treatment, a spike-in control was prepared by incubating human chromatin extracts from GM12878 cells with a 1:1 mixture of Dynabeads Protein A and Dynabeads Protein G coupled to antibodies against human Pol II (N20, Santa Cruz) followed by washing with nexus washing buffers A to D. A fixed amount of Dynabeads and human Pol II ChIP mixture was then spiked into each S2 ChIP-nexus experiment.

Techniques: Control, Incubation

The boxplots show the average ChIP-seq enrichment of Ser5P Pol II, Nipped-B, TBPH and Lark at active promoters, extragenic enhancers, and PREs in control cells, and cells treated with 10 μM triptolide for 1, 2, and 4 hours. The genome browser tracks at the right show the log2 ChIP-seq enrichment for the same proteins at the string gene and enhancers over the same time course of triptolide treatment.

Journal: PLoS Genetics

Article Title: Drosophila TDP-43 RNA-Binding Protein Facilitates Association of Sister Chromatid Cohesion Proteins with Genes, Enhancers and Polycomb Response Elements

doi: 10.1371/journal.pgen.1006331

Figure Lengend Snippet: The boxplots show the average ChIP-seq enrichment of Ser5P Pol II, Nipped-B, TBPH and Lark at active promoters, extragenic enhancers, and PREs in control cells, and cells treated with 10 μM triptolide for 1, 2, and 4 hours. The genome browser tracks at the right show the log2 ChIP-seq enrichment for the same proteins at the string gene and enhancers over the same time course of triptolide treatment.

Article Snippet: The Ser5P Pol II rabbit monoclonal antibody was purchased from Cell Signaling Technology (#13523) and validated by western blots of cell extracts with and without triptolide treatments.

Techniques: ChIP-sequencing, Control

The log2 ChIP-seq enrichment for Ser5P Pol II, Nipped-B, TBPH and Lark at all individual active promoters, enhancers and PREs in control untreated (Mock) cells is plotted against the enrichment after treatment of cells with 10 μM triptolide for 1, 2 and 4 hours.

Journal: PLoS Genetics

Article Title: Drosophila TDP-43 RNA-Binding Protein Facilitates Association of Sister Chromatid Cohesion Proteins with Genes, Enhancers and Polycomb Response Elements

doi: 10.1371/journal.pgen.1006331

Figure Lengend Snippet: The log2 ChIP-seq enrichment for Ser5P Pol II, Nipped-B, TBPH and Lark at all individual active promoters, enhancers and PREs in control untreated (Mock) cells is plotted against the enrichment after treatment of cells with 10 μM triptolide for 1, 2 and 4 hours.

Article Snippet: The Ser5P Pol II rabbit monoclonal antibody was purchased from Cell Signaling Technology (#13523) and validated by western blots of cell extracts with and without triptolide treatments.

Techniques: ChIP-sequencing, Control

Promising areas for nanomedicine development in gastric cancer.

Journal: Frontiers in Bioengineering and Biotechnology

Article Title: Advances in nanomedicine and delivery systems for gastric cancer research

doi: 10.3389/fbioe.2025.1565999

Figure Lengend Snippet: Promising areas for nanomedicine development in gastric cancer.

Article Snippet: Biomimetic Nanoparticles , , PTX, Triptolide , NPs , RP (P/T).

Techniques: