Inflammatory pain and depression are clinically common disorders with a high comorbidity rate. They mutually exacerbate their pathological processes and severely reduce the quality of life of patients. The pathogenesis of the comorbidity of inflammatory pain and depression is highly complex, posing significant challenges for clinical diagnosis and treatment. Recent studies have revealed that sustained activation of neuroinflammation is a central pathological link in the comorbidity of inflammatory pain and depression. As a non-pharmacological intervention, exercise can effectively improve both pain and depressive symptoms in patients with comorbidity. However, its specific mechanisms of action remain incompletely elucidated. This article summarizes recent research advances on the effects of exercise in inhibiting central inflammation, modulating the balance of microglial M1/M2 polarization, regulating neuronal excitatory-inhibitory homeostasis, and promoting hippocampal neurogenesis. It systematically reviews the molecular and neural mechanisms by which exercise modulates neuroinflammation to treat the comorbidity of inflammatory pain and depression, with the aim of providing a theoretical basis and practical guidance for clinical exercise therapy.

The blood-brain barrier (BBB) plays a critical role in maintaining brain homeostasis. BBB dysfunction is closely associated with various neurodegenerative diseases and acute brain injuries, which impair brain defense mechanisms and can exacerbate the progression of pathological conditions. Nitric oxide (NO), an important biological signaling molecule, exerts a wide range of effects on the central nervous system, influencing both physiological and pathological states. This review summarizes the production and metabolism of NO and their effects on BBB permeability, followed by an introduction to the role of NO in pathological conditions such as cerebral ischemia-reperfusion injury, neurodegenerative diseases, and brain tumors. NO regulates BBB integrity through the regulation of tight junction proteins and vascular endothelial growth factor receptor 2 (VEGFR2). The review also delves into the potential of NO as a therapeutic target in drug delivery and gene therapy, and explores its potential to enhance drug penetration across the BBB. These explorations provide novel perspectives for future therapeutic strategies.

We conducted a systematic review of the construction method and pathological mechanisms of animal and cellular models for diminished ovarian reserve (DOR), to provide a theoretical basis for understanding its pathophysiological mechanisms and references for future drug development and therapeutic strategies. We carried out extensive retrieval and analysis of the recent literature to identify the detailed diverse modeling approaches (including pharmaceutical induction, environmental factors, natural factors, and composite factors) and explored the roles of their mechanisms in DOR pathogenesis. The pathogenesis of DOR involves multiple factors, including oxidative stress, apoptosis and autophagy dysregulation, impaired angiogenesis, and imbalances in follicular development and the immune microenvironment. Studies also revealed intrinsic correlations among key signaling pathways in DOR models. Although existing DOR modeling method can effectively replicate Western medicine pathological features, models incorporating traditional Chinese medicine (TCM) syndrome characteristics remain scarce. Given the unique advantages of TCM in regulating the complex pathological network of DOR, future research is needed to prioritize the construction of TCM syndrome-oriented DOR models. This will support investigations into the scientific basis of TCM's multi-target regulatory mechanisms and provide a robust theoretical foundation for clinical applications.