Journal: Scientific Reports

Article Title: Hydroxytyrosol induced ferroptosis through Nrf2 signaling pathway in colorectal cancer cells

doi: 10.1038/s41598-025-04415-4

Figure Lengend Snippet: Network pharmacology and molecular docking predict HT-induced pathway in colorectal cancer cells. (A) Potential targets of HT; (B) Key targets of HT colorectal cancer; (C) Venn diagram plot screening on key targets of HT colorectal cancer ferroptosis; (D) PPI network topology analysis; (E) Degree value ranking of the 14 core targets; (F) HT with Nrf2 (NFE2L2), NQO1, TXNRD1, PTGS2, AKR1C3 molecular docking results; (G) molecular docking binding energy ranking.

Article Snippet: The culture conditions used in this study refer to ATCC standardised recommendations for colorectal cancer cells (HCT116: ATCC ® CCL-247TM; SW480 ATCC ® CCL-228TM), and the treatment time (48 h) was consistent with the literature to ensure comparable results .

Techniques: Binding Assay

Journal: Scientific Reports

Article Title: Hydroxytyrosol induced ferroptosis through Nrf2 signaling pathway in colorectal cancer cells

doi: 10.1038/s41598-025-04415-4

Figure Lengend Snippet: HT-induced ferroptosis in HCT116 and SW480 cells. (A , B) HT treatment caused morphological changes in cellular mitochondria, including smaller size, reduced cristae, and even membrane rupture (transmission electron microscopy). (C , D) HT promoted intracellular iron production in colorectal cancer cells. (E , F) HT inhibited intracellular GSH production in colorectal cancer cells. (G , H) HT promoted intracellular LPO production. (I , J) HT treatment promoted intracellular ROS production in colorectal cancer cells. (K , L) HT treatment caused a decrease in mitochondrial membrane potential in colorectal cancer cells. Statistical analyses of HT-treated and control groups: * p ≤ 0.05, ** p ≤ 0.01.

Article Snippet: The culture conditions used in this study refer to ATCC standardised recommendations for colorectal cancer cells (HCT116: ATCC ® CCL-247TM; SW480 ATCC ® CCL-228TM), and the treatment time (48 h) was consistent with the literature to ensure comparable results .

Techniques: Membrane, Transmission Assay, Electron Microscopy, Control

Journal: Scientific Reports

Article Title: Hydroxytyrosol induced ferroptosis through Nrf2 signaling pathway in colorectal cancer cells

doi: 10.1038/s41598-025-04415-4

Figure Lengend Snippet: HT inhibited Nrf2 signalling pathway-induced ferroptosis in colorectal cancer cells. (A) After 48 h of HT treatment, the expression level of Tfr1 protein was elevated while the expression level of SLC7A11 and GPX4 protein were reduced; at the same time, the expression levels of the key proteins of the Nrf2 signalling pathway, Nrf2 and NQO1, were reduced; (B) HT treatment notably increased Tfr1 protein levels while reducing SLC7A11 and GPX4 protein expression in SW480 cells. Similarly, Nrf2 and NQO1 protein expression were suppressed in these cells. Statistical analyses were performed for the HT-treated and control groups: * p ≤ 0.05, ** p ≤ 0.01.

Article Snippet: The culture conditions used in this study refer to ATCC standardised recommendations for colorectal cancer cells (HCT116: ATCC ® CCL-247TM; SW480 ATCC ® CCL-228TM), and the treatment time (48 h) was consistent with the literature to ensure comparable results .

Techniques: Expressing, Control

Journal: Scientific Reports

Article Title: Hydroxytyrosol induced ferroptosis through Nrf2 signaling pathway in colorectal cancer cells

doi: 10.1038/s41598-025-04415-4

Figure Lengend Snippet: Fer-1, a ferroptosis inhibitor, inhibits HT-induced ferroptosis in colorectal cancer cells. (A) Fer-1 effectively attenuated HT cytotoxicity in HCT116 cells (HCT116 cells were exposed to 1µM Fer-1 for 2 h before treatment with specified concentrations of HT, followed by cell viability assessment using the CCK8 method). (B) Fer-1 reduced the toxic effects of HT in SW480 cells. Cells were also pretreated with (1µM) Fer-1 and then treated with HT (45, 90,and 180 µM) and cell viability was determined using the CCK8 assay. (C) In HCT116 cells, HT treatment raised Trf1 protein levels while reducing SLC7A11 and GPX4 protein levels; the addition of 1 µM Fer-1 with HT reversed these protein expression levels. (D) The expression levels of Trf1, SLC7A11, and GPX4 proteins were similarly reversed by 1µM Fer-1 in SW480 cells. Statistical analyses were performed for the HT-treated and control groups: ns p > 0.05.

Article Snippet: The culture conditions used in this study refer to ATCC standardised recommendations for colorectal cancer cells (HCT116: ATCC ® CCL-247TM; SW480 ATCC ® CCL-228TM), and the treatment time (48 h) was consistent with the literature to ensure comparable results .

Techniques: CCK-8 Assay, Expressing, Control

Journal: BioMed Research International

Article Title: Gene Expression Profiling of Clostridium botulinum under Heat Shock Stress

doi: 10.1155/2013/760904

Figure Lengend Snippet: The COG functional categorization of differentially expressed genes in response to heat shock stress in Clostridium botulinum ATCC 3502. The number in parentheses showed the total number of genes classified in each COG functional category in Clostridium botulinum ATCC 3502. The bar diagram represented the percentage of differentially expressed genes (including upregulated and down-regulated genes) relative to the total number of genes in each COG functional category. The number beside the bar diagram indicated the percentage of differentially expressed genes in each COG functional category relative to the total number of differentially expressed genes under heat shock stress.

Article Snippet: In addition, previous studies showed that C. botulinum ATCC 3502 alters the protein expression of botulinum toxin cluster genes ha-33 under temperature shift from 37°C to 45°C, indicating that ha-33 is a heat shock protein [ , ].

Techniques: Functional Assay

Journal: BioMed Research International

Article Title: Gene Expression Profiling of Clostridium botulinum under Heat Shock Stress

doi: 10.1155/2013/760904

Figure Lengend Snippet: The top 40 differentially expressed genes in response to heat shock stress in Clostridium botulinum ATCC 3502.

Article Snippet: In addition, previous studies showed that C. botulinum ATCC 3502 alters the protein expression of botulinum toxin cluster genes ha-33 under temperature shift from 37°C to 45°C, indicating that ha-33 is a heat shock protein [ , ].

Techniques: Modification, Membrane, Chemotaxis Assay, Transduction, Control