Potential mechanism of tea for treating osteoporosis, osteoarthritis, and rheumatoid arthritis.

Osteoporosis (OP), osteoarthritis (OA), and rheumatoid arthritis (RA) are common bone and joint diseases with a high incidence and long duration. Thus, these conditions can affect the lives of middle-aged and elderly people. Tea drinking is a traditional lifestyle in China, and the long-term intake of tea and its active ingredients is beneficial to human health. However, the mechanisms of action of tea and its active ingredients against OP, OA, and RA are not completely elucidated. This study aimed to assess the therapeutic role and related mechanisms of tea and its active ingredients in OP, OA, and RA. Moreover, it expanded the potential mechanisms of tea efficacy based on network pharmacology and molecular docking. Results showed that tea has potential anti-COX properties and hormone-like effects. Compared with a single component, different tea components synergize or antagonize each other, thereby resulting in a more evident dual effect. In conclusion, tea has great potential in the medical and healthcare fields. Nevertheless, further research on the composition, proportion, and synergistic mechanism of several tea components should be performed.

Role of the major histocompatibility complex class II protein presentation pathway in bone immunity imbalance in postmenopausal osteoporosis.

Bone immunity regulates osteoclast differentiation and bone resorption and is a potential target for the treatment of postmenopausal osteoporosis (PMOP). The molecular network between bone metabolism and the immune system is complex. However, the molecular mechanism underlying the involvement of the major histocompatibility complex class II (MHC-II) molecule protein presentation pathway in PMOP remains to be elucidated. The MHC-II molecule is a core molecule of the protein presentation pathway. It is combined with the processed short peptide and presented to T lymphocytes, thereby activating them to become effector T cells. T-cell-derived inflammatory factors promote bone remodeling in PMOP. Moreover, the MHC-II molecule is highly expressed in osteoclast precursors. MHC-II transactivator (CIITA) is the main regulator of MHC-II gene expression and the switch for protein presentation. CIITA is also a major regulator of osteoclast differentiation and bone homeostasis. Therefore, we hypothesized that the MHC-II promotes osteoclast differentiation, providing a novel pathogenic mechanism and a potential target for the treatment of PMOP.