Liver cancer is a malignant tumour with high morbidity and fatality rates that is common worldwide. At present, the clinical approaches to treating primary liver cancer include partial hepatectomy, systemic or local chemotherapy, radiotherapy, radiofrequency ablative surgery and liver transplantation. However, all of these approaches have shortcomings, including poor prognosis and numerous side-effects. A large number of studies have proven that many effective ingredients in traditional Chinese medicine, particularly the flavonoid compounds extracted from plants, have achieved breakthroughs in terms of enhancing the effects and reducing the toxicity of chemotherapy and radiotherapy, preventing tumour metastasis and relapse after surgery, alleviating the clinical symptoms of advanced tumours, improving the quality of life of the patient with tumours and extending patient long‑term survival. The purpose of the present study was to investigate the impact of isoquercitrin, the flavonoid from Bidens bipinnata L. extract, on the progression of liver cancer and to achieve a deeper understanding of the biological characteristics of isoquercitrin's involvement in the progression of liver cancer. In the in vitro experiments, isoquercitrin was found to strongly inhibit the proliferation of human liver cancer cells, promote the apoptosis of human liver cancer cells, and block the cell cycle in the G1 phase. Isoquercitrin activated caspase-3, -8 and -9, inhibited the expression level of ERK and p38MAPK protein phosphorylation, and promoted the phosphorylation of JNK. Additionally, isoquercitrin reduced the expression level of PKC in human liver cancer cells. In the in vivo experiments, isoquercitrin was also found to significantly inhibit the growth of transplanted tumours in nude mice. The present study confirmed that isoquercitrin could inhibit the progression of human liver cancer in vivo and in vitro, and the molecular mechanism of isoquercitrin may be closely associated with the MAPK and PKC signalling pathways.

Objectives: The metabolites of the ketogenic diet (KD), specifically ketone bodies (KB), are closely linked to brain health. The KD is widely used to treat epilepsy. It’s also getting more attention for treating neurodegenerative disorders like Alzheimer’s and Parkinson’s diseases, and its effectiveness in these areas is well - recognized. This study aims to explore the research hotspots in the field of KD and brain health from 2013 to 2024, providing references and directions for future research.Methods: This study utilized R software, VOSviewer, and CiteSpace to analyze 1,162 publications in this field from 2013 to 2024.Results: A total of 1,162 publications were included in this study. From 2013 to 2021, there was an upward trend in the number of publications in this field, followed by a slight decline from 2021 to 2023. The United States has the highest number of publications and exhibits the most extensive collaboration with other countries, positioning it as the leading nation in this field. The journal Nutrients has the highest number of publications, while Epilepsia is the most cited journal. Key subject terms include KD, Brain, Beta-Hydroxybutyrate, KB, Metabolism, and Oxidative Stress. The primary research focuses in this field are the application of the KD and its metabolites in treating brain disorders such as epilepsy, the role and mechanisms of the KD and its metabolites in brain metabolism, and the effects of the physiological properties of KD metabolites (e.g., KB) such as antioxidative stress and neuroprotection on brain health.Conclusion: The KD is beneficial for brain health, and its use in treating brain disorders has garnered widespread attention and recognition globally. This study provides a comprehensive and in-depth analysis of the literature in this field, offering valuable insights into the research hotspots and future directions for investigation.

Diabetes, as a prevalent chronic metabolic disease, imposes a heavy medical burden and economic pressure on society. The long-term dysregulation of glucose metabolism leads to multi-system (including cardiovascular, renal, neurological, etc.) damage, which constitutes the core pathological features of diabetic complications. In recent years, ferroptosis and epigenetic regulation have emerged as new research directions, gradually becoming a burgeoning field of study. Increasing evidence suggests that epigenetics may play a significant role in regulating the relationship between ferroptosis and diabetic complications. Notably, the epigenetics of certain key iron metabolism genes may influence the epigenetic “switch” of the ferroptosis pathway. This article systematically reviews the molecular mechanisms of ferroptosis and epigenetics in diabetic microvascular complications, neuropathy, and other related conditions, while exploring potential therapeutic targets based on epigenetic regulation to provide a theoretical basis for the treatment of diabetic complications.

Insulin resistance (IR) is a core mechanism leading to obesity and metabolic dysfunction of diabetes, and is the main cause of type 2 diabetes (T2DM). However, the etiology and mechanism of IR are very complex, which has not been clarified yet. Ferroptosis is a new type of iron dependent cell death, which is different from apoptosis, necrosis, autophagy and other typical cell death. It is not clear whether there is a direct relationship between Ferroptosis and IR. At present, only a few studies have explored the relationship between Ferroptosis and T2DM. The article starts from the mechanism of the two, reveals the possible relationship between them, so as to increase the understanding of IR and Ferroptosis, and hopes to lay a foundation for further clarifying the mechanism of insulin resistance.