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Objective(s): Hyperglycemia, a prevalent metabolic condition observed in diabetes, leads to oxidative damage, inflammatory responses, and other consequences. Natural compounds alleviate the adverse impacts of diabetes. We aimed to explore the effects of alpha-pinene (AP) as a monoterpene on oxidative damage and inflammation caused by high glucose (HG) in the human hepatocellular liver carcinoma (HepG2) cell line. Materials and Methods: The HepG2 cells were subjected to non or HG concentration (50 mM) and treated with or without AP (8, 16, and 32 µg/ml) for 48 hr. The effect of treatments on cellular viability, malondialdehyde (MDA), glutathione (GSH), and activity of anti-oxidant enzymes, including glutathione peroxidase (GPx), catalase (CAT), superoxide dismutase (SOD), was determined. The gene expression levels of nuclear factor-κβ (NF-κB), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and dipeptidyl peptidase-4 (DPP-4) were estimated using quantitative real-time polymerase chain reaction (qRT-PCR). Results: HG exposure significantly increased cell death, MDA formation, and depletion of GSH content and GPx, CAT, and SOD activity (P<0.05). We have also seen a significant induction in NF-κB, TNF-α, IL-6, and DPP-4 gene expression in hepatocytes under HG conditions (P<0.05). Interestingly, co-treatment with AP in a dose-dependent manner improved cell death and altered levels of MDA and GSH, and activity of GPx and CAT (P<0.05). AP could also modulate the gene expression of NF-κB and inflammatory biomarkers dose-dependently (P<0.05). Conclusion: Our findings suggested the protective effect of AP on hepatocytes under HG conditions through attenuating oxidative stress markers and suppression of inflammatory pathways. [ABSTRACT FROM AUTHOR]

Background: Cinnamic acid, a phenylpropanoid acid, has been investigated as a potential alternative therapy for diabetes and its complications in some studies. Methods: In the first stage, the viability of HepG2 cells at different concentrations of glucose and CA was assessed by MTT assay. Oxidative stress markers) CAT, GPx, GSH, and MDA) were measured spectrophotometrically. After RNA extraction, the effect of different concentrations of CA on the expression of DPP4 and inflammatory factors (IL-6, NF- κB) in HepG2 cells was assessed using realtime PCR. Results: In HepG2 cells, CA increased catalase and glutathione peroxidase activity and GSH production in a dose-dependent manner in the presence of high glucose concentrations, with the greatest effect seen at a concentration of 75 mg/ml. Also, it reduced the amount of MDA in highglucose HepG2 cells. Furthermore, CA decreased the expression of DPP4, NF- κB, and IL-6 genes in HepG2 cells in the presence of high glucose levels. Conclusions: The results of our study indicated that CA reduced hyperglycemia-induced complications in HepG2 cells by decreasing inflammatory gene expression, including IL-6 and NF- κB and inhibiting the expression of DPP4, and limiting oxidative stress. [ABSTRACT FROM AUTHOR]