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In RKO cells treated with Hyrtios sp. extract, cell death occurred by induction of p53 and p21 proteins.
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Since, PE extract induced cell death was highest among the CGN extracts, with maximum cancer cell death occurred in ZR751 cells; we carried out mechanism study of PE extract induced ZR751 cell death.
Flow cytometric analysis of apoptosis showed that the methanol extract induced apoptosis in HepG2 cells similarly to sorafenib suggesting that the methanol extract induced cell death was though early apoptosis.
The protective effect of WBM leaf extract against cell death induced by menadione (2-methyl-1, 4-naphthoquinone) was measured by the method of Klausc et al. ([2010]).
The protective effect of WBM leaf extract against cell death induced by sodium nitroprusside (SNP) was determined by the method of Bastianetto et al. ([2010]).
As shown in Figure 2, the extract induced cell death in a dose- and time-dependent manner as compared with vehicle controls.
The treatment of cells with various concentrations of extract prevented cell death and generation of reactive oxygen species following hypoxia exposure and the protective effects were dose dependent– 3 d) and 4(a)– 4(d), light gray bars).
Morphological changes in LNCaP cells were clearly observed 24 hours after treatment with both sprout extracts, and it was obvious that treatment with SeSp extracts induced cell death more effectively than CSp in LNCaP cells.
PE extract induced maximum cell death in ZR751 cells (P < 0.001) indicating the selective cytotoxicity of PE extract towards breast cancer cells.
The caspase 3/7 was activated in the cancer cells treated with BTB extract leading to cell death by apoptosis.
Overall, these results indicate that PE extract induced ZR751 cell death may be due to the induction of G2 cell cycle arrest and subsequent apoptotic process.
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