Effect of pinolenic acid on oxidative stress injury in HepG2 cells induced by H<sub>2</sub>O<sub>2</sub>
Why this work is in the frame
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Bibliographic record
Abstract
Abstract To investigate the effect and mechanism of pinolenic acid (PNA) on H 2 O 2 ‐induced oxidative stress injury in HepG2 cells. Methods: PNA was used to regulate oxidative stress injury of HepG2 cells induced by H 2 O 2 . Quantification of cell survival rate, accumulation of intracellular reactive oxygen species (ROS), and expression levels of anti‐oxidation‐related genes were determined using MTT, fluorescent probe technology (DCFH‐DA), and real‐time quantitative reverse transcription polymerase chain technology (qRT‐PCR) method, respectively. Meanwhile, the activity of intracellular antioxidant enzymes was determined by biochemical methods. The results showed that PNA improved the survival rate of HepG2 cells induced by H 2 O 2 (29.59%, high‐dose group), reduced the accumulation of intracellular ROS (65.52%, high‐dose group), and reduced the level of intracellular malondialdehyde (MDA; 65.52%, high‐dose group). All these results were dose‐dependent, which indicated that PNA can improve oxidative stress damage of cells. Furthermore, the mechanism of PNA regulating oxidative stress was investigated from the gene level. Results showed that under supplementation of PNA, the activity of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH‐Px) had been improved (39.74%, 17.58%, and 23.83%, high‐dose group). Further studies on gene expression which controls the activity of antioxidant enzymes showed that under the regulation of PNA, the expression level of Keap1 gene was decreased, while Nrf2 gene was increased. The expression levels of HO‐1 and NQO1 in the downstream of Nrf2 were increased. Results indicated that under the regulation of PNA, Nrf2 was separated from Keap1, entered the nucleus, bound to ARE, and up‐regulated the expression levels of HO‐1 and NQO1 genes. Conclusion: PNA has a conspicuous improvement effect on oxidative stress damage induced by H 2 O 2 in HepG2 cells. We also found the antioxidant mechanisms of PNA where it protected cells from oxidative stress damage by causing nuclear translocation of Nrf2 gene and up‐regulated the expression levels of antioxidant enzymes in the downstream. This shows that PNA prevented oxidative stress by mediating the Keap1/Nrf2 transcriptional pathway and down‐regulating enzyme activities.
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Full frame distilled prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.
Codex and Gemma teacher scores by category
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.000 | 0.000 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.000 | 0.000 |
| Bibliometrics | 0.000 | 0.001 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.000 | 0.000 |
| Insufficient payload (model declined to judge) | 0.000 | 0.000 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it