Inflammatory diseases are a type of disease caused by multiple factors, which are characterized by local or systemic tissue inflammatory reactions, commonly including atherosclerosis, osteoarthritis, non-alcoholic fatty liver, chronic kidney diseases, acute pancreatitis, and tumors. The prevalence of the above diseases is globally high and a growing threat to human health, as well as a huge healthcare burden. In recent years, Chinese herbal medicines have become an important reservoir for the discovery of new drugs and applications due to their unique molecular structures and potential biotherapeutic effects. Numerous studies have confirmed the beneficial effects of natural products in the prevention and treatment of different diseases. Scientific studies on the therapeutic potential of natural products have become a hot topic nowadays, especially regarding the active ingredients of herbs. Calycosin is a kind of isoflavonoid extracted from the root of Radix astragali, exhibiting anti-inflammatory, antioxidant, anti-cancer, cardioprotective, hepatoprotective, and neuroprotective activities. Therefore, this review aims to discuss the emerging roles, molecular mechanisms and therapeutic potential of calycosin in resolving inflammatory diseases.

The liver coordinately maintains cholesterol, triglyceride, and glucose homeostasis by integrating the synthesis, storage, utilization, and inter-conversion of these metabolic programs, and their dysregulation contributes to metabolic-associated steatotic liver disease (MASLD), hepatocellular carcinoma (HCC), type 2 diabetes mellitus (T2DM), and gestational diabetes mellitus (GDM). Long non-coding RNAs (lncRNAs), which are not translated into proteins, regulate gene expression through interactions with DNA, RNA, and proteins at transcriptional, post-transcriptional, and epigenetic levels, and have emerged as central determinants of hepatic metabolic balance. This review systematically summarizes how lncRNAs govern cholesterol biosynthesis and efflux, triglyceride synthesis and lipolysis, glycogen turnover, gluconeogenesis, and glycolysis in hepatocytes. Unlike pathway-by-pathway descriptions, we highlight that these programs are coupled through shared signaling networks, including PI3K/AKT/mechanistic target of rapamycin complex 1 (mTORC1), 5′-AMP-activated protein kinase (AMPK), SREBP, PPAR, and FoxO1, and that pleiotropic lncRNAs coordinate lipid and glucose outputs rather than controlling a single isolated process. We further examine how lncRNA dysregulation drives MASLD, HCC, T2DM, and GDM, and evaluate their potential as diagnostic biomarkers and therapeutic targets. Finally, we outline current limitations, including incomplete molecular characterization, low cross-species conservation, heterogeneous experimental validation, and unresolved delivery challenges, which must be addressed before lncRNA-based strategies reach clinical application.