Exercise-induced analgesia (EIA) refers to the elevation of pain thresholds and reduction in sensitivity to noxious stimuli achieved through exercise training. As a non-pharmacological treatment strategy, exercise therapy has demonstrated positive effects on both acute and chronic pain. Increasing evidence indicates that modulation of glial cell activity is an important mechanism underlying analgesia. Spinal glial cells contribute to the development and maintenance of pathological pain by promoting pain signal transmission through inflammatory responses and synaptic remodeling. Exercise can differentially regulate microglia and astrocyte activity, inhibiting multiple inflammatory signaling pathways, such as P2X4/P2X7 purinergic receptors, brain-derived neurotrophic factor (BDNF)/phosphatidylinositol 3-kinase (PI3K)/mammalian target of rapamycin (mTOR), interleukin (IL)-6/Janus kinase (JAK) 2/signal transducer and activator of transcription 3 (STAT3), p38-mitogen-activated protein kinases (MAPK), and Toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-κB), thereby reducing the release of pro-inflammatory cytokines, decreasing inflammatory and nociceptive hypersensitivity, and alleviating pathological pain. This review also summarized the effects of different exercise intensities, durations, and frequencies on glial cell responses in order to provide a theoretical foundation for optimizing exercise-based interventions for pathological pain conditions.
Humans ; Microglia/metabolism* ; Astrocytes/metabolism* ; Exercise/physiology* ; Signal Transduction ; Analgesia/methods* ; Spinal Cord/cytology* ; Exercise Therapy ; Pain Management/methods* ; Animals ; Brain-Derived Neurotrophic Factor/metabolism*

Objective:To investigate the changes of melanin concentration hormone receptor 1(MCHR1)in dorsal root ganglion(DRG)of mice with neuropathic pain.Methods:The expression profile of MCHR1 in the DRG of mice were observed by immunofluorescent staining.Neuropathic pain model was established by spared nerve injury(SNI)in mice.Male mice(C57BL/6)were randomly divided into 2 groups:Sham-operated group and SNI group.The paw withdrawal threshold(PWT)and paw withdrawal latency(PWL)were observed by von Frey fibers and thermal radiation stimulation.The mRNA and protein levels of MCHR1 in DRG were detected by real time RT-PCR and West-ern Blot,respectively.Results:MCHR1 was widely distributed in mouse DRG and co-labeled with small and medium-sized neuronal markers calcitonin gene-related peptide(CGRP)and isolectin B4(IB4),as well as large diameter neu-ronal marker NF200.Stable mechanical hyperalgesia and heat hyperalgesia were observed in the ipsilateral hindpaw of mice at 7 days post-SNI.Real time RT-PCR and Western Blot experiments showed that mRNA and protein expression levels in DRG were both significantly up-regulated in SNI-treated mice,as compared with Sham group.Conclusion:MCHR1 was widely distributed in large,medium and small neurons of DRG.After the SNI model mice presented a sta-ble phenomenon of hyperalgesia,the transcription and protein level of MCHR1 in DRG were significantly elevated in SNI mice.These data suggest that MCHR1 in DRG may be involved in the occurrence and development of neuropathic pain.

Objective:To investigate the changes of melanin concentration hormone receptor 1(MCHR1)in dorsal root ganglion(DRG)of mice with neuropathic pain.Methods:The expression profile of MCHR1 in the DRG of mice were observed by immunofluorescent staining.Neuropathic pain model was established by spared nerve injury(SNI)in mice.Male mice(C57BL/6)were randomly divided into 2 groups:Sham-operated group and SNI group.The paw withdrawal threshold(PWT)and paw withdrawal latency(PWL)were observed by von Frey fibers and thermal radiation stimulation.The mRNA and protein levels of MCHR1 in DRG were detected by real time RT-PCR and West-ern Blot,respectively.Results:MCHR1 was widely distributed in mouse DRG and co-labeled with small and medium-sized neuronal markers calcitonin gene-related peptide(CGRP)and isolectin B4(IB4),as well as large diameter neu-ronal marker NF200.Stable mechanical hyperalgesia and heat hyperalgesia were observed in the ipsilateral hindpaw of mice at 7 days post-SNI.Real time RT-PCR and Western Blot experiments showed that mRNA and protein expression levels in DRG were both significantly up-regulated in SNI-treated mice,as compared with Sham group.Conclusion:MCHR1 was widely distributed in large,medium and small neurons of DRG.After the SNI model mice presented a sta-ble phenomenon of hyperalgesia,the transcription and protein level of MCHR1 in DRG were significantly elevated in SNI mice.These data suggest that MCHR1 in DRG may be involved in the occurrence and development of neuropathic pain.

Objective:To summarize clinical characteristics of and treatment experience with patients with critical illnesses in a dermatological ward.Methods:All patients with serious or life-threatening conditions, who were hospitalized at the dermatological ward of the Second Xiangya Hospital of Central South University from July 9, 2011 to December 31, 2020, were collected, and their clinical data were retrospectively analyzed. Demographic characteristics, disease types and proportions, main complications, causes of serious or life-threatening conditions, important treatment measures and outcomes were summarized, and causes of death were also analyzed and discussed.Results:A total of 1 057 patients with critical illnesses were collected, with a male-to-female ratio of 1∶1.11, and 64.81% of them aged 18 to 65 years. The types of diseases mainly included drug eruptions (332 cases) , connective tissue diseases (226 cases) , bullous skin diseases (104 cases) , psoriasis (57 cases) , erythroderma (45 cases) , infectious skin diseases (67 cases) , etc. Among them, psoriasis (39 cases) and erythroderma (32 cases) mostly occurred in males, and connective tissue diseases (168 cases) mostly occurred in females. Common complications mainly involved infections, important organ damage or dysfunction, hypoalbuminemia, and fluid, electrolyte and acid-base imbalances. A total of 94 patients were diagnosed with life-threatening conditions, which were found to be mainly caused by primary skin diseases, hematologic abnormalities, respiratory failure, nervous system abnormalities, renal failure, sepsis, fluid, electrolyte and acid-base imbalances, etc. During the management of critical illnesses, 43 patients were treated with high-dose glucocorticoid pulse therapy, 264 were treated with gamma-globulin pulse therapy, 355 were transfused with other blood products, and 34 received special therapies such as hemoperfusion/immunoadsorption therapy, plasma exchange, dialysis, artificial liver support therapy; 42 patients were transferred to the intensive care unit (ICU) , 12 were transferred to the department of surgery for operations, and 12 were transferred to the department of obstetrics and gynecology for delivery or induction of labor. After treatment, 989 patients (93.57%) achieved improvement and were discharged. A total of 14 patients (1.32%) died, of whom 7 died of secondary sepsis, 2 died of severe pulmonary infections, 2 died of asphyxia caused by respiratory mucosa shedding-induced airway obstruction, the other 3 died of gastrointestinal hemorrhage, cerebral hemorrhage and neuropsychiatric systemic lupus erythematosus, respectively.Conclusions:Critical cases in the dermatological ward mainly suffered from serious skin diseases such as severe drug eruptions, connective tissue diseases and bullous skin diseases, as well as complications such as severe underlying diseases, severe organ dysfunction, sepsis or severe fluid, electrolyte and acid-base imbalances. In terms of treatment, it is of critical significance to make a clear diagnosis and assess the severity of disease as early as possible, monitor and prevent possible complications, and to consult with specialists in relevant disciplines in time.