| 体外研究 |
Sodium sulfate (10-5-10-2 M; 24-72 h) can alter the morphology of human liver cell L02 in a time - and concentration dependent manner, and has significant toxic effects at concentrations of 10-3 M and 10-2 M [1].
Sodium sulfide (10-5-10-2 M; 72 h) can concentration dependently inhibit the viability of human liver cell L02, with an IC50 of 4.68 × 10-4 M after 72 h of incubation [1].
Sodium sulfide (10-5-10-2 M; 24-72 h) can inhibit the proliferation of human liver cell L02 in a time - and concentration dependent manner. When the concentration reaches 5 × 10-4 M or above, it can produce significant inhibitory effects [1].
Sodium sulfide (10-5-10-2 M; 72 h) induces apoptosis in human liver cell L02 in a concentration dependent manner, with significant apoptosis occurring at 10-4 M and severe cell death occurring within 24 h under 10-2 M conditions [1].
Sodium sulfate (4.68 × 10-4 M; 72 h) can alter the expression of 97 genes in human liver cell L02, with 13 genes significantly upregulated and 14 genes significantly downregulated; This substance can activate pathways that inhibit cell proliferation, induce cell apoptosis, and cause mitochondrial damage through the generation of reactive oxygen species.
Sodium sulfide (0.1-10 mM; 5-30 min) can induce the production of reactive oxygen species in freshly isolated human neutrophils in a concentration dependent manner within 5-30 min; After 30 minutes of pre incubation (0.1-10 mM; 30 min pre incubation followed by 5 min fMLP stimulation), these neutrophils were concentration dependent activated, enhancing fMLP induced reactive oxygen species production [2].
Sodium sulfide (0.1-10 mM; 4 h) can induce RNA synthesis in freshly isolated human neutrophils in a concentration dependent manner, but does not cause morphological changes in neutrophils [2].
Sodium sulfate (0.1-10 mM; 20 h) does not regulate the apoptosis rate of freshly isolated human neutrophils after 20 h incubation, nor can it reverse the delayed apoptosis effect of GM-CSF on these cells [2].
Sodium sulfate (0.001-10 mM; 5-24 h) can induce dose-dependent necrosis of RGM1 cells through oxidative stress, with an IC50 of 0.17 mM, and this cytotoxicity can be attenuated by the free radical scavenger Trolox [3].
Sodium sulfide (0-5 mM; 20 h) can induce necrotic cell death in RGM1 cells, and this process is independent of the apoptotic signaling pathway; This can be confirmed by unchanged caspase/PARP cleavage, caspase activity, DNA fragmentation, and dose-dependent LDH release [3].
Sodium sulfate (0-10 mM; 0-120 min, 24 h) can induce oxidative modification, aggregation, and inactivation of purified lysozyme through metal ion catalyzed free radical formation, without relying on the clearance of superoxide anions or hydrogen peroxide [3].
Cell Viability Assay
| Cell Line: |
human hepatocytes L02 |
| Concentration: |
10-5 M, 10-4 M, 2.5×10-4 M, 5×10-4 M, 5×10-3 M, 10-2 M |
| Incubation Time: |
72 hours |
| Result: |
Gradually decreased L02 cell viability with increasing sodium sulfite concentration.
Reached an IC50 of 4.68×10-4 M for L02 cells at 72 h. |
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Cell Proliferation Assay
| Cell Line: |
human hepatocytes L02 |
| Concentration: |
10-5 M, 10-4 M, 5×10-4 M, 5×10-3 M, 10-2 M |
| Incubation Time: |
24 h, 48 h, 72 h |
| Result: |
Significantly inhibited L02 cell proliferation at concentrations ≥5×10-4 M, with proliferation rate decreasing as incubation time increased.
Had no obvious effect on proliferation activity at low concentrations (10-5 M, 10-4 M). |
Apoptosis Analysis
| Cell Line: |
human hepatocytes L02 |
| Concentration: |
10-5 M, 10-4 M, 10-3 M, 10-2 M |
| Incubation Time: |
72 hours |
| Result: |
Caused cell color changes from green to orange/red (indicating apoptosis) at 10-4 M with increased incubation time.
Induced significant apoptosis as early as 24 h at 10-3 M, indicated by dominant orange and red staining.
Led to majority of cells being dead by 24 h at 10-2 M. |
Real Time qPCR
| Cell Line: |
human hepatocytes L02 |
| Concentration: |
4.68×10-4 M (IC50) |
| Incubation Time: |
72 hours |
| Result: |
Identified 97 significantly regulated differentially expressed genes between sodium sulfite-treated and control cells via transcriptomic analysis.
Confirmed the expression changes of 13 significantly upregulated genes (including SOCS3, FOSL1, PLK3, IL1B) and 14 significantly downregulated genes (including CPS1, FBN1, FKBP3) via qPCR.
Linked these genes to pathways including TNF signaling, IL-17 signaling, apoptosis, metabolism, and inflammatory responses. |
Apoptosis Analysis
| Cell Line: |
rat gastric mucosal epithelial cells (RGM1) |
| Concentration: |
0-5 mM (20 h incubation); 0-5 mM (1 h pre-incubation followed by 20 h in fresh medium) |
| Incubation Time: |
20 h; 1 h (pre-incubation) + 20 h (fresh medium) |
| Result: |
Did not alter levels of cleaved caspase-9, cleaved caspase-3, or cleaved PARP, nor change caspase-9 or caspase-3 activity.
Showed no apoptotic DNA fragmentation, but dose-dependently increased LDH release into the culture medium. |
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