Latest ArticlesInflammatory 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.
To investigate the molecular mechanism by which long-chain non-coding RNA (lncRNA) X-inactive specific transcript (XIST) regulates the biological activity of trophoblast cells. Methods Human HTR-8/Svneo trophoblast cells were cultured in vitro and separated into control, interference empty (transfected with small interfering RNA-normal control (si-NC)), si-XIST-1 (transfected with si-XIST-1), si-XIST-1+anti-NC (co-transfected with si-XIST-1 and anti-NC), and si-XIST-1+anti-182-5p (co-transfected with si-XIST-1 and anti-182-5p) groups. XIST, miR-182-5p, and hypoxia inducible factor-2α (HIF-2α) mRNA expression levels were measured by real-time fluorescence quantitative polymerase chain reaction (RT-qPCR). Cell proliferation was detected by Cell Counting Kit-8 (CCK-8) and 5-ethynyl-2′-deoxyuridine (EdU) assays. Apoptosis was detected by flow cytometry. Cell migration and invasion abilities were measured by scratch-healing and Transwell experiments. HIF-2α, cleaved-caspase-3, Bcl-2, Bax, matrix metalloproteinase (MMP)-2, and MMP-9 protein levels in cells were measured by Western blot. The targeting relationship of miR-182-5p with XIST and HIF-2α was verified by dualluciferase reporter assay.
XIST and HIF-2α mRNA levels, apoptosis rate, and HIF-2α, cleaved-caspase-3, and Bax protein levels in the si-XIST-1 group were lower than those in the control and interference empty groups, while miR-182-5p, cell viability, EdU-positive rate, scratch-healing rate, number of invaded cells, and Bcl-2, MMP-2, and MMP-9 protein levels were higher (P<0.05). HIF-2α mRNA level, apoptosis rate, and HIF-2α, cleaved-caspase-3, and Bax protein levels in the si-XIST-1+anti-182-5p group were higher than those in the si-XIST-1 and si-XIST-1+ anti-NC groups, while miR-182-5p, cell viability, EdU-positive rate, scratch-healing rate, number of invaded cells, and Bcl-2, MMP-2, and MMP-9 protein levels were lower (P<0.05). LncRNA XIST was able to target miR-182-5p in HTR-8/Svneo cells, and HIF-2α was the target of miR-182-5p.
Knocking-down lncRNA XIST may inhibit HIF-2α expression by competitively binding to miR-182-5p, thereby enhancing the proliferation, migration, and invasion abilities of HTR-8/Svneo cells and inhibiting cell apoptosis.
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