It has been reported that oxidative stress plays a prominent role in diabetic macrovascular diseases. 3,4‑Dihydroxyacetophenone (3,4‑DHAP) has been found to have a variety of biological activities. However, few studies have assessed the antioxidant capacity of 3,4‑DHAP and the underlying mechanisms. Thus, the aim of the present study was to explore the effects of 3,4‑DHAP on oxidative stress in human umbilical vein endothelial cells (HUVECs). HUVECs were pre‑treated with 3,4‑DHAP and then exposed to high glucose conditions. Cell viability and cytotoxicity were measured using an MTT assay. Reactive oxygen species (ROS) levels were measured using an inverted fluorescence microscope and a fluorescent enzyme labeling instrument. Protein expression levels of nuclear factor E2‑related factor 2 (Nrf2), heme oxygenase‑1 (HO‑1), microtubule‑associated protein 1A/1B‑light chain 3 (LC3) and poly ADP‑ribose polymerase‑1 (PARP‑1) were measured using western blotting, and mRNA expression of Nrf2 and HO‑1 were measured through reverse transcription‑quantitative PCR (RT‑qPCR). Nrf2 nuclear translocation was evaluated using immunofluorescence analysis and autophagosomes were observed using transmission electron microscope (TEM). The results of the present study demonstrated that compared with the control group, cell viability of the high glucose group was reduced and cell cytotoxicity of the high glucose group was increased. ROS production in the high glucose group was clearly enhanced. In addition, high glucose upregulated Nrf2 and HO‑1 protein and mRNA expression levels. Nuclear translocation of Nrf2 in the high glucose group was also increased. The formation of autophagosomes in the high glucose group was also higher than that in the control group. Furthermore, LC3‑II/LC3‑I and PARP‑1 protein expression levels were increased after treatment with high glucose. However, compared to the high glucose group, 3,4‑DHAP (10 µmol/l) significantly enhanced cell viability. 3,4‑DHAP markedly decreased the production of ROS, increased Nrf2 and HO‑1 protein and mRNA expression levels, and promoted nuclear translocation of Nrf2 in HUVECs. In addition, 3,4‑DHAP promoted the formation of autophagosomes, and notably increased the protein expression levels of LC3‑II/LC3‑I and PARP‑1. Moreover, it was determined that compared to the 3,4‑DHAP group, treatment with 3,4‑DHAP and ML385 enhanced cell viability, and decreased ROS production, Nrf2 and HO‑1 protein and mRNA expression levels, nuclear translocation of Nrf2, and LC3‑II/LC3‑I and PARP‑1 protein expression levels. Collectively, the results of the present study showed that 3,4‑DHAP protected HUVECs against oxidative stress via regulation of the Nrf2/HO‑1 pathway, by increasing autophagy and promoting DNA damage repair.

Hepatocellular carcinoma has become one of the most shared cancers in the whole world because of its high morbidity, poor survival rate and low recovery rate. Especially in China, hepatocellular carcinoma has been regarded as one of the most malignant cancers. With the exploration of tumor diseases and the development of bioinformatics over the years, lncRNAs have been found to play a direct or indirect regulatory role in tumorigenesis and tumor development, which brings a new direction for the treatment of tumors. Previous studies had investigated that DIO3 opposite strand upstream RNA(DIO3OS) played a promoting role in the occurrence and development of thyroid carcinoma and uterine corpus endometrial carcinoma. However, research focusing on the role of DIO3OS in hepatocellular carcinoma is still uncleared. We found that low DIO3OS level often predicts poor prognosis in patients with hepatocellular carcinoma. In addition, there was significant correlation between different immune cells and their immune markers and DIO3OS. Our results suggest that DIO3OS can be used as an effective biomarker in the diagnosis and prognosis of hepatocellular carcinoma, affecting the development of hepatocellular carcinoma by influencing tumor immune cell infiltration.

Hepatocellular carcinoma(HCC) has become one of the most shared cancers in the whole world because of its high morbidity, poor survival rate and low recovery rate. Especially in China, HCC has been regarded as one of the most malignant cancers. With the development of tumor exploration and treatment over the years, it has been found that lncRNA plays a direct or indirect regulatory role in the process of tumorigenesis and cancer development, which brought a new direction for early diagnosis and therapy. Previous studies had investigated that DIO3OS played a promoting role in the occurrence and development of thyroid carcinoma and uterine corpus endometrial carcinoma. However, research focusing on the role of DIO3OS in HCC is still uncleared. Our work found that there was a significant negative correlation between low DIO3OS levels and HCC. In addition, there was also a correlation between immune cells and their surface markers and DIO3OS expression in HCC. Our findings demonstrated that DIO3OS may be a potential prognostic biomarker involved in the process of HCC by regulating immune cell infiltration.