Heart failure （HF） is the end-stage of various cardiovascular diseases， with high morbidity and mortality. The existing “new quadruple” standard treatment can hardly reverse the core pathological process of myocardial remodeling， and long-term medication may pose risks of drug resistance and adverse reactions. Therefore， new therapeutic targets and strategies are urgently needed. Metabolic reprogramming is the upstream core mechanism regulating phenotypic polarization and functional activation of macrophages， which drives the occurrence and development of HF through the core axis of metabolic reprogramming-immune imbalance-ventricular remodeling and has become a cutting-edge potential target for the prevention and treatment of HF. Traditional Chinese medicine （TCM） has a long history in the prevention and treatment of HF. A large number of studies in recent years have confirmed that different therapeutic methods of TCM can correct the polarization imbalance， restore the homeostasis of myocardial immune microenvironment， inhibit myocardial injury， and delay the pathological process of HF by targeting and regulating the metabolic reprogramming of glucose， lipids， mitochondria， and amino acids in macrophages. This paper systematically expounds the core pathological mechanism of metabolic reprogramming of macrophages in HF， sorts out the research progress of TCM in preventing and treating HF by intervening this target， analyzes the regulatory rules， summarizes the limitations of existing research， and puts forward future directions. This review aims to provide a systematic theoretical reference and new research ideas for TCM clinical diagnosis and treatment and new drug development of HF.

BACKGROUND:In osteoarthritis cartilage degeneration, connective tissue growth factors as the important effector molecules play an important role in chondrocyte proliferation and differentiation. Clinical application of diacerein for the treatment of osteoarthritis has achieved good effect, but the exact mechanism of the treatment is unclear. OBJECTIVE:To observe the effect of different concentrations of diacerein on the expression of connective tissue growth factor in the articular cartilage induced with interleukin-1βin vitro. METHODS: Chondrocytes of Sprague Dawley rats were culturedin vitro, and then the chondrocytes were induced with recombinant human interleukin-1β to prepare the osteoarthritis model. Rats in the normal control group received no treatment; rats in the model group were treated with recombinant human interleukin-1β; rats in the experimental group were treated with different concentrations of diacerein+10 μg/L recombinant human interleukin-1β. The proliferation of chondrocytes was observed withMTT assay, and Western blot was used to detect the expression of connective tissue growth factor. The experiments above were repeated for three times. RESULTS AND CONCLUSION:The MTT assay results showed that compared with the normal control group, the diacerein could promote the proliferation activity of chondrocytes, and more significant in the concentration of 10-5 mol/L (P < 0.01); the proliferation capacity of chondrocytes in the experimental group was decreased after induced with interleukin-1β (P < 0.05), but when compared with the normal control group, the diacerein with the concentrations of 10-4 mol/L and 10-5 mol/L could promote the MTT proliferation capacity of chondrocytes with or without interleukin-1β (P < 0.05). Western blot results showed that interleukin-1β could reduce the expression of connective tissue growth factor (P< 0.01), and 10-5 mol/L diacerein could significantly promote the expression of connective tissue growth factor induced with interleukin-1β, and the effect was significantly higher than that in the model group (P < 0.01). Diacerein can promote expression of connective tissue growth factor induced with interleukin-1β, it may be one the mechanism of diacerein for promoting chondrocytes differentiation and proliferation and the treatment of osteoarthritis.