Mood disorders mainly affect the patient’s daily life, lead to suffering and disability, increase the incidence rate of many medical illnesses, and even cause a trend of suicide. The glucocorticoid (GC)-mediated hypothalamus–pituitary–adrenal (HPA) negative feedback regulation plays a key role in neuropsychiatric disorders. The balance of the mineralocorticoid receptor (MR)/glucocorticoid receptor (GR) level contributes to maintaining the homeostasis of the neuroendocrine system. Consistently, a chronic excess of GC can also lead to HPA axis dysfunction, triggering anxiety, depression, memory loss, and cognitive impairment. The animal model induced by chronic corticosterone (CORT) administration has been widely adopted because of its simple replication and strong stability. This review summarizes the behavioral changes and underlying mechanisms of chronic CORT administration-induced animal models, including neuroinflammatory response, pyroptosis, oxidative stress, neuroplasticity, and apoptosis. Notably, CORT administration at different doses and cycles can destroy the balance of the MR/GR ratio to make dose-dependent effects of CORT on the central nervous system (CNS). This work aims to offer an overview of the topic and recommendations for future cognitive function research.

Traumatic heterotopic ossification (HO) is the abnormal formation of bone in soft tissues as a consequence of injury. However, the pathological mechanisms leading to traumatic HO remain unknown. Here, we report that aberrant expression of IL‐17 promotes traumatic HO formation by activating β‐catenin signalling in mouse model. We found that elevated IL‐17 and β‐catenin levels are correlated with a high degree of HO formation in specimens from patients and HO animals. We also show that IL‐17 initiates and promotes HO progression in mice. Local injection of an IL‐17 neutralizing antibody attenuates ectopic bone formation in a traumatic mouse model. IL‐17 enhances the osteoblastic differentiation of mesenchymal stem cells (MSCs) by activating β‐catenin signalling. Moreover, inhibition of IL‐17R or β‐catenin signalling by neutralizing antibodies or drugs prevents the osteogenic differentiation of isolated MSCs and decreases HO formation in mouse models. Together, our study identifies a novel role for active IL‐17 as the inducer and promoter of ectopic bone formation and suggests that IL‐17 inhibition might be a potential therapeutic target in traumatic HO.

Aims: Electroacupuncture (EA) promotes the regeneration and repair of peripheral nerve injury (PNI) in clinical, and its underlying neuroimmune mechanisms have still not been fully clarified. Our study investigates the role of exosomal lncRNA MIAT in EA-mediated repair of PNI. Methods: The study observed EA’s effect on PNI in a rat model established by sciatic nerve injuries. The sciatic nerve function was observed via sciatic nerve function index. Serum exosomal and sciatic nerve lncRNA MIAT levels were quantified, macrophage polarization was detected via immunofluorescence. Interventions included local lentiviral lncRNA MIAT overexpression (LV-MIAT), adeno-associated virus-mediated lncRNA MIAT knockdown (AAV-siMIAT), and GW4869 (exosome inhibitor) injection. Neuronal cells were transfected with miR-130a-3p mimics/inhibitors or LV-MIAT, and lncRNA MIAT/miR-130a-3p/KLF7 interactions were confirmed via dual-luciferase assays. Results: EA intervention promotes peripheral nerve functional recovery in PNI rats, enhances axonal density, increases M2 macrophage number, and exosomal lncRNA MIAT level. M2-Exo administration in neuron promoted nerve cells viability and neurite length, while siMIAT/GW4869 partially reversed these effects. More, lncRNA MIAT acted as a miR-130a-3p sponge, relieving its repression of KLF mRNA and protein levels. Overexpressing lncRNA MIAT or silencing miR-130a-3p activated KLF7 expression, enhancing neuronal survival and axon regeneration. Conclusion: EA intervention improved PNI, restored neuronal function, increased PNI area M2 macrophage polarization and regulated lnc MIAT/miR-130a-3p/KLF7 axis expression.