Dexin Li’s research while affiliated with Peking University and other places

Background The standardized extract of milk thistle seeds, known as silibinin, has been utilized in herbal medicine for over two centuries, with the aim of safeguarding the liver against the deleterious effects of various toxic substances. However, the role of silibinin in Particulate Matter (PM2.5)-induced intrahepatic triglyceride accumulation remains unclear. This study seeks to investigate the impact of silibinin on PM2.5-induced intrahepatic triglyceride accumulation and elucidate potential underlying mechanisms. Methods A model of intrahepatic triglyceride accumulation was established in male C57BL/6J mice through intratracheal instillation of PM2.5, followed by assessment of liver weight, body weight, liver index, and measurements of intrahepatic triglycerides and cholesterol after treatment with silibinin capsules. Hep G2 cells were exposed to PM2.5 suspension to create an intracellular triglyceride accumulation model, and after treatment with silibinin, cell viability, intracellular triglycerides and cholesterol, fluorescence staining for Nile Red (lipid droplets), and DCFH-DA (Reactive Oxygen Species, ROS), as well as proteomics, real-time PCR, and mitochondrial function assays, were performed to investigate the mechanisms involved in reducing triglycerides. Results PM2.5 exposure leads to triglyceride accumulation, increased ROS production, elevated expression of inflammatory factors, decreased expression of antioxidant factors, and increased expression of downstream genes of aryl hydrocarbon receptor. Silibinin can partially or fully reverse these factors, thereby protecting cells and animal livers from PM2.5-induced damage. In vitro studies show that silibinin exerts its protective effects by preserving oxidative phosphorylation of mitochondrial complexes I and II, particularly significantly enhancing the function of mitochondrial complex II. Succinate dehydrogenase (mitochondrial complex II) is a direct target of silibinin, but silibinin A and B exhibit different affinities for different subunits of complex II. Conclusion Silibinin improved the accumulation of intrahepatic triglycerides induced by PM2.5, and this was, at least in part, explained by an enhancement of oxidative phosphorylation in mitochondrial Complexes I and II.

Obesity is a chronic disease that endangers human health. In recent years, the phenomenon of obesity has become more and more common, and it has become a global epidemic. Obesity is closely associated with many adverse metabolic changes and diseases, such as insulin resistance, type 2 diabetes mellitus, coronary heart disease, nervous system diseases and some malignant tumors, which have caused a huge burden on the country’s medical finance. In most countries of the world, the incidence of cancer caused by obesity is increasing year on year. Diabetes associated with obesity can lead to secondary neuropathy. How to treat obesity and its secondary diseases has become an urgent problem for patients, doctors and society. This article will summarize the multidisciplinary research on obesity and its complications.

Background TCDD-inducible poly (ADP-ribose) polymerase (TiPARP) is a DNA repair enzyme with functions in energy metabolism, signal transduction, cell differentiation, and other biological processes, which may closely related to lipid metabolism and is highly expressed in adipose tissue. Adipose tissue can be divided into white adipose tissue (WAT) that stores energy and brown adipose tissue (BAT) that releases energy and generates heat. In the present study, we investigated whether TiPARP can affect adipogenesis in adipose tissue and thus participate in the development of obesity. Methods BAT primary cells or 3T3-L1 cells infected with adenovirus expressing TiPARP or TiPARP-targeted short hairpin RNA (shTiPARP) were cultured to induce adipogenic differentiation. The expression of TiPARP was detected by real-time PCR and Western blotting. The expression of specific BAT- and WAT-related markers was detected by real-time PCR. The accumulation of lipid droplets in differentiated cells was detected by Oil Red O staining. Results TiPARP was highly expressed in both subcutaneous WAT and BAT, and TiPARP mRNA level increased significantly along with adipogenic differentiation. Activation of TiPARP or overexpression of TiPARP upregulated BAT-related markers in primary BAT cells and WAT-related markers in 3T3-L1 cells, together with increased lipid accumulation. On the contrary, knockdown of TiPARP downregulated expression of specific markers in both BAT primary cells and 3T3-L1 cells, together with decreased lipid accumulation. Conclusion TiPARP regulates adipogenesis in both BAT primary cells and 3T3-L1 cells and therefore plays an important role in modulating maturity and lipid accumulation in brown and white adipocytes. These findings provide us with a new strategy for combating obesity.