Rheumatoid arthritis (RA) is a chronic autoimmunity illness, mainly featured with synovitis of the joint. The specificity of ferroptosis is disparate in different diseases, and the mechanism of ferroptosis in RA has some uncertainty yet. Therefore, the mechanism of ferroptosis was deeply observed in RA patients and animal models. In this paper, plasma of RA patients, the tumor necrosis factor‐alpha‐induced human synovial fibroblasts, and an animal model of arthritis induced by collagen were applied to initially inquire about the therapeutic effect of ferroptosis. For the RA patients, ELISA detected protein expression of glutathione (GSH), GPX4, Nrf2, Keap‐1, and ferritin. In cell experiments, erastin or fer‐1 regulated the invasion of human synovial fibroblast cells, mitochondrial membrane potential, reactive oxygen species (ROS) expression, marker protein, and so on. For the animal experiments, 32 Sprague–Dawley male rats were randomly separated into four groups with a collagen‐induced RA model for 14 days and administered with erastin or fer‐1 for 35 days. The expressions of GSH, GPX4, Nrf2, and Keap‐1 were lower, and the ferritin was higher in RA patients, and the expressions of these proteins varied significantly after disease remission. In addition, ferroptosis inactivation also reduced the proliferation and migration ability, mitochondrial membrane potential, and ROS in cells. We discovered unexpectedly that activation of ferroptosis meaningfully forbore the foot swelling in animals with CIA, reduced arthritis scores, destruction of bone, and articular synovitis, and also decreased the high expression of inflammatory factors in plasma. There is a nonlinear relationship between human disease manifestations and animal model pathology. Ferroptosis regulating in RA for humans or animals may produce different effects.

Isochlorogenic acid C (ICAC) is found in a variety of natural foods and medicinal plant materials. This study aims to validate the biological activity of isochlorogenic acid C in limiting inflammation by the Erk/JNK/NF-κB pathway. In this study, TNF-α-induced human fibroblast-like synoviocytes and collagen-induced arthritis animal models were used to perceive the potential anti-inflammation mechanism of ICAC. The role of isochlorogenic acid C was evaluated by observing the migration, invasion ability, and apoptotic activity of TNF-α-induced fibroblast-like synoviocytes cells in humans and analysing foot swelling, joint index, and histopathological changes in a collagen-induced RA animal model. The results reveal that ICAC inhibited the proliferation of human fibroblast-like synoviocytes and promoted their apoptosis. ICAC also blocked the nuclear transfer of NF-κB, Erk, and JNK. It was observed that ICAC significantly inhibited the degree of posterior foot swelling in CIA, reducing arthritis scores, bone tissue injury, and articular synovitis. ICAC may promote cell apoptosis and inhibit the hyperactivation of inflammatory cells to alleviate inflammation-induced synovial proliferation through the Erk/JNK/NF-κB pathway.

Mulberroside A, naturally existent from the mulberry plant, is known for its diverse biological activities. Our research indicates that mulberroside A may possess significant anti-aging effects. We assessed its anti-aging properties using naturally aging animal models and by inducing senescence in human-derived endothelial cells and mouse-derived endothelial cells through treatment with angiotensin II. We found that mulberroside A promotes the proliferation of HMEC-1 and bEnd.3 endothelial cells, while significantly reducing the levels of senescence biomarkers p16, p21, and Rb in both these endothelial cell types and in the hippocampus, kidney, spleen and liver of naturally aging animals. Additionally, mulberroside A was found to mitigate telomerase depletion in the blood of naturally aging animals, enhance the body’s resistance ability to oxidative stress, and inhibit the overexpression of inflammatory factors in vivo.

A simple and efficient hydroxide-mediated S_NAr rearrangement was reported to synthesize new depside derivatives containing the diaryl ether skeleton from the natural product barbatic acid. The prepared compounds were determined using ¹H NMR, ¹³C NMR, HRMS, and X-ray crystallographic analysis and were also screened in vitro for cytotoxicity against three cancer cell lines and one normal cell line. The evaluation results showed that compound 3b possessed the best antiproliferative activity against liver cancer HepG2 cell line and low toxicity, which made it worth further study.

The current therapeutic interventions of chronic obstructive pulmonary disease offer only partial alleviation of symptoms, leaving the majority of patients with persistent and significant clinical manifestations. This investigation seeks to elucidate the underlying pharmacological mechanisms of Qing Fei Bao Yuan Decoction (QFBYD) employing a multidisciplinary approach that includes network pharmacology and molecular docking techniques. The QFBYD formulation were subjected to mass spectrometry analysis, while critical compounds and biological targets were subsequently identified through the TCMSP database. Disease- and drug-specific targets were collated from a plethora of databases, including Batman-TCM, Stitch, Swiss Target Prediction and GeneCards. GO and KEGG pathways were analyzed for the collected targets. A PPI network was constructed using STRING database to isolate core targets. Molecular docking was executed using Auto Dock Tools and PyMOL software, and an animal model of COPD was developed for experimental validation. Seven salient compounds and five core biological targets were ascertained through our analysis. Additionally, four compounds demonstrated high-affinity binding to the identified targets. Pathways involving bacterial endotoxin response, oxidative stress regulation, and endothelial cell migration were significantly enriched according to the KEGG database. Animal models substantiated that QFBYD ameliorated pathological hallmarks, enhanced respiratory functionality, mitigated overexpression of pro-inflammatory cytokines, augmented the antioxidant defense mechanism, and suppressed the hyperactivity of the five core targets. The efficacy of QFBYD in COPD treatment may be primarily attributed to its role in moderating inflammatory responses and rectifying oxidative imbalances.

Depression is often associated with gastrointestinal issues, forming a self-sustaining cycle known as the emotion-gastrointestinal axis. Traditional Chinese Medicine (TCM) provides multi-component and multi-target therapies, though its mechanisms are not fully understood. This article reviews key studies on how TCM, including herbal formulas, single herbs, active ingredients, and acupuncture, influences the brain-gut axis in treating depression and gastrointestinal problems. This article reviews recent research on the pharmacological mechanisms of Chinese medicine, providing a basis for its targeted molecular therapy and future development. Additionally, it provides insights into enhanced treatment strategies for clinical patients and investigates the potential role of TCM in addressing depression and gastrointestinal-related health disorders.