Food Science and Human Wellness
·
2019
·
IF 0
Shaokang Wang,Lingmeng Fu,Yi Wu,Hongmei Xiao,Jing Wang,Guiju Sun
The present study was conducted to verify the influence of luteolin on apoptosis of Eca109 cells and to further investigate the possible mechanisms underlying its effect on apoptosis. The cells were exposed to different concentrations of luteolin (0, 40, 80, 120, 160, 200, 240 μM) for 24, 48, and 72 h respectively. The influence of luteolin on proliferation of Eca109 cells was detected using MTT assay. Eca109 cells were then treated with luteolin (0, 40, 160, 240 μM) for 24 h. The effect of luteolin on cell cycle progression and apoptosis was assayed by using flow cytometry (FCM). Expression of caspase9 and caspase3 mRNA and protein was analyzed by real-time PCR and Western blot respectively. The results showed that luteolin could inhibit the proliferation of Eca109 cells at all concentrations in a time-dependent manner and the relative inhibition rate showed an inverted U-shaped association with the concentration of luteolin. Further, the cell cycle was arrested in the S phase following treatment with luteolin. Apoptosis analysis indicated that luteolin could induce the apoptosis of Eca109 cells across the three concentration groups, which exhibited a trend of first promotional and then inhibitory with the increases in luteolin concentration. The effect of luteolin on the mRNA and protein expression of caspase 9 and caspase3 first manifested as promotion, then inhibition. Therefore, luteolin may serve a role in promoting cell apoptosis by inducing Eca109 cell apoptosis that involves the expression of caspase3, caspase9 mRNA and protein. This study provides theoretical basis for further study and clinical application of luteolin. The specific mechanism has not yet been clarified and the other activation pathways inducing apoptosis need to be further studied.
研究领域:
肿瘤学
·
细胞生物学
·
药理学
✓ 已验证
产品关联
DOI
COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY C-TOXICOLOGY & PHARMACOLOGY
·
2024
·
IF 3.9
Ying Sun,Xiaohui Jin,Zuwang Yang,Zunhan Hu,Qiulu Li,Jingquan Dong,Mian Fu
Difenoconazole (DFZ) is a widely used triazole fungicide in agricultural production. However, the presence of DFZ residue in the environment poses a significant risk to non-target organisms. Ferulic acid (FA) is a phenolic compound known for its antioxidant and anti-inflammatory properties. This study aims to investigate the hepatic damage caused by DFZ in carp and explore the mechanism through which FA alleviates this damage. The findings revealed that FA enhanced the antioxidant capability of the carp's liver and reduced the accumulation of reactive oxygen species (ROS) in the liver tissue. Moreover, FA regulated the transcriptional levels of inflammation-related factors, effectively preventing the inflammatory response triggered by the NF-κB signaling pathway. Additionally, TUNEL results demonstrated that DFZ initiated apoptosis, while dietary supplementation with FA decreased the protein expression levels of Bax and Cytochrome C (Cyt c) and the transcriptional levels of bax , caspase3 , caspase9 , p53 genes. Furthermore, FA increased the protein expression and transcriptional levels of Bcl-2. In conclusion, FA protects against liver injury induced by DFZ exposure in carp by modulating oxidative damage, inflammation, and apoptosis.
研究领域:
环境毒理学
·
水生生物学
·
药理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH
·
2022
·Vol. 30
·期 1
·1060-1071
·
IF 5.19
Zhang Xinyu,Sun Kexin,Wang Xu,Shi Xu,Gong Duqiang
Chlorpyrifos (CPF), an organophosphorus pesticide, is detected commonly in environments, where it is thought to be highly toxic to non-target organisms. However, the mechanism of CYP450s pathway mediated by nuclear receptors on CPF-induced apoptosis and necroptosis at the cellular level and the effect of CPF on the cytotoxicity of the chicken hepatocarcinoma cell line (LMH) has also not been reported in detail. Therefore, this experiment aims to explore whether CPF can improve apoptosis and necroptosis in LMH cells by activating the nuclear receptors/CYP450s axis. LMH cells, the subject of this study, were exposed to 5 μg/mL, 10 μg/mL, and 15 μg/mL doses of CPF. With the increase of CPF concentration, the increase of nuclear receptor level led to the up-regulation of CYP450s activity. With the massive production of ROS, the expression of apoptotic pathway genes (Bax, Caspase9, and Caspase3) enhanced, while Bcl-2 expression dropped sharply. The expression of programmed necroptosis genes (RIPK1, RIPK3, and MLKL) heightened, and Caspase8 reduced considerably. In short, our data suggests that excessive activation of nuclear receptors and CYP450s induced by CPF promotes ROS production, which directs apoptosis and programmed necroptosis in LMH cells. Graphical abstract
研究领域:
毒理学
·
细胞生物学
·
分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）