Effect of pinolenic acid on oxidative stress injury in HepG2 cells induced by H2O2. Issue 10 (25th August 2021)

• Record Type: Journal Article
• Authors: Zhao, Yang; Liu, Sainan; Sheng, Zhili; Li, Xue; Chang, Yanan; Dai, Weichang; Chang, Sui Kiat; Liu, Junmei; Yang, Yuchun
• Is Part Of: Food science & nutrition. Volume 9:Issue 10(2021)
• Page Start: 5689
• Page End: 5697
• Publication Date: 2021-08-25
• Subjects: antioxidant defense responses -- antioxidant enzymes system -- HepG2 cells -- oxidative stress -- Pinolenic acid; Food industry and trade -- Periodicals; Food -- Periodicals; Nutrition -- Periodicals; 664
• DOI: 10.1002/fsn3.2534
• Languages: English
• ISSNs: 2048-7177

Abstract

Abstract: To investigate the effect and mechanism of pinolenic acid (PNA) on H2 O2 ‐induced oxidative stress injury in HepG2 cells. Methods: PNA was used to regulate oxidative stress injury of HepG2 cells induced by H2 O2 . 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 H2 O2 (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 H2 O2 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. Abstract : Oxidative stress injury of HepG2 cells induced by H2 O2 was regulated by Pinolenic acid. The antioxidant ability of the body was strengthened by Pinolenic acid; thus, the ability to regulate oxidative stress from outside was enhanced. The cellular oxidative stress was regulated by Pinolenic acid, which was dose‐dependent, and the higher the concentration, and the better the regulation ability.