Multiple sclerosis(MS) shows the pathological characteristics of "inflammatory injury of white matter" and "myelin repair disability" in the central nervous system(CNS). It is very essential for MS treatment and reduction of disease burden to strengthen repair, improve function, and reduce disability. Accordingly, different from the simple immunosuppression, we believe that key to strengthening remyelination and maintaining the "damage-repair" homeostasis of tissue is to change the current one-way immunosuppression strategy and achieve the "moderate pro-inflammation-effective inflammation removal" homeostasis. Traditional Chinese medicine shows huge potential in this strategy. Through literature research, this study summarized the research on remyelination, discussed the "mode-rate pro-inflammation-effective inflammation removal" homeostasis and the "damage-repair" homeostasis based on microglia, and summed up the key links in remyelination in MS. This review is expected to lay a theoretical basis for improving the function of MS patients and guide the application of traditional Chinese medicine.
Humans ; Multiple Sclerosis/pathology* ; Remyelination/physiology* ; Myelin Sheath/pathology* ; Inflammation/drug therapy* ; Homeostasis

The iron and inflammation homeostasis are closely coupled, forming an integrated functional unit under physiological conditions. "Iron transport balance" has become the key mechanism to maintain iron homeostasis through bidirectional regulation of iron uptake and release and dynamic management of transmembrane concentration. It is also the physiological basis for the inflammatory balance between promotion and resolution. Under pathological conditions, represented by inflammatory bowel disease (IBD), disturbed iron transportation was highly involved in almost every step of inflammatory diseases. Therefore, the iron transporting rebalancing provides the mechanistic basis and effective approach for the normalization of inflammatory microenvironment. Macrophage is the key regulator of inflammation homeostasis and determinant for iron transport balance. Unfortunately, the current clinical transformation based on iron transport balance theory has still been insufficient. Sometimes, this strategy even showed high complexity and contradiction, severely restricting its clinical application. By summarizing the theoretical research progress of iron transport balance, especially its relevance to macrophage phenotypic polarization, this review aims to explore the therapeutic value in inflammation intervention by targeting iron transporting balance. This review will provide the necessary knowledge and hints for the research and development of candidate drugs in treating inflammatory diseases.

OBJECTIVE: To evaluate the effect of the pulse width of electroacupuncture (EA) in the treatment of denervation-induced skeletal muscle atrophy in rats and examine the role of insulin-like growth factor 1 (IGF-1)/phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway during EA. METHODS: Sciatic nerve functional index (SFI), muscle wet weight and the cross-sectional area (CSA) of the gastrocnemius muscle were analyzed after treatment in model rats with EA of various pulse widths (0.5, 50, 100 and 200 ms). The apoptosis index (AI) and paired box (PAX)3 and PAX7 protein expression were also determined. Further, the mRNA and protein expressions of components of IGF-1/PI3K/Akt pathway and their downstream targets were determined, along with the inhibiting effect of the pathway with a PI3-specific inhibitor. RESULTS: EA with a pulse width of 200 ms was found to have the best effect with regard to increasing SFI, CSA and muscle weight, decreasing AI, and increasing the expression of PAX3 and PAX7. The IGF-1/PI3K/Akt pathway was found to be activated by denervation, although the downstream forkhead box O (FoxO) pathway was not suppressed by its activation. The PI3K/Akt pathway and its downstream molecule mammalian target of rapamycin (mTOR) were up-regulated further by EA to promote muscle protein synthesis. Meanwhile, the expressions of downstream FoxO and F-box protein 32 (ATROGIN-1) were down-regulated to reduce protein degradation. CONCLUSIONS EA with 200-ms pulse width was found to have a more significant effect than 0.5-ms EA. The positive effects of EA disappeared after inhibition of the PI3K/Akt pathway.

Complete healing of the intestinal mucosa is the most ideal goal in the treatment of inflammatory bowel disease (IBD). The intestinal mucosa healing not only significantly alters the course of the disease and relieves clinical symptoms, but also markedly reduces the occurrence of complications and prevents recurrence of IBD. As chronic inflammation associated with peptic ulcer damage is the main pathological feature of IBD, clinical treatment is mainly based on anti-inflammatory therapy, but such therapy cannot promote the healing of the intestinal mucosa of patients. Therefore, how to achieve long-term remission of IBD is still an urgent challenge. In the process of intestinal mucosal repair, the polarization of macrophages maintains the homeostasis of the intestinal microenvironment, which is a representative process that promotes mucosal inflammatory-repair. It is a key part of initiating tissue regeneration that should not be underestimated. In this paper, we reviewed the literature of the past decade, focusing on the promotion of intestinal mucosal healing in IBD. The discussion will highlight the importance and feasibility of regulating macrophages to promote intestinal mucosal repair. Following this thought, we discuss the shortcomings of current clinical treatments and summarize the relevant drugs which have potential to promote intestinal mucosal repair. The aim is to provide effective potential drugs and therapeutic targets for the treatment of IBD.

Aortic Valve/surgery* ; Aortic Valve Stenosis/surgery* ; China/epidemiology* ; Heart Valve Prosthesis Implantation ; Humans ; Severity of Illness Index ; Treatment Outcome

Respiratory infectious diseases are important diseases causing major public safety events, posing a great threat to life, health, and social development. Effective control and scientific treatment of the diseases is the key basis for ensuring the stability and long-term development of the community of a shared future for human health. Although the pathogens of respiratory viral infectious diseases are diverse and the process is complex, the common pathological basis of their pathogenesis is characterized by the "damage-repair" functional imbalance of the immune microenvironment of the lesions, which leads to the subsequent structural and functional destruction of important organs. Therefore, the treatment should focus on antivirus and immunological regulation, strengthen the protection against immune injury, and promote the functional repair of damaged tissues. The above conclusions are the scientific core of host-directed therapies(HDT), which coincides with "human-disease co-treatment and healthy qi and pathogen interaction" in traditional Chinese medicine(TCM) theories. Under the support of TCM and western medicine theories, the complete pathological chain "infection-immunity-injury" of respiratory viral infectious diseases is integrated with dynamic change in "healthy qi-pathogen" in TCM to transform the treatment focus from the diseases to the patients. It is possible to fundamentally correct the "damage-repair" imbalance in the disease state, change the environment for disease development, and bring benefits to patients by strengthening human intervention, maintaining immune homeostasis, enhancing the protection of tissues and organs, and promoting the repair and regeneration of damaged tissues. This study focused on the common and key pathological processes of respiratory infectious diseases, especially the immune damage caused by the viral infection, to seek effective prevention and treatment strategies, review relevant theoretical progress, summarize effective drug candidates, prospect future research and development, and highlight the therapeutic characteristics of TCM.
Drugs, Chinese Herbal/therapeutic use* ; Humans ; Medicine, Chinese Traditional ; Respiratory Tract Infections/therapy*

The normal immune system has the ability to distinguish between "self" and "non-self". Because of its dynamic balance of "immune activity-immune tolerance", it will produce immune response to the non-self antigen, but with no response or weak response to the self-antigen. However, if the balance was broken, T cell in the abnormal immune activation state will respond continually to the self-antigen, with an abnormal immune response, which caused autoimmune disease. Pathologically, "invalid" immune recognition and immune response become the main causes for autoimmune diseases. Co-stimulatory molecule is an important link between Attach antigen presenting cells（APC） and immune cells (T cell and B cell). Studies have proved that excessive co-stimulation and/or insufficient co-inhibition could cause detect of self-tolerance and induce autoimmunity. Although co-stimulatory and co-inhibitory pathways have a significant impact on all ADS, this paper focuses on their effect on two systemic autoimmune diseases [systemic lupus erythematosus （SLE） and rheumatoid arthritis（RA）] and two organ-specific autoimmune diseases [multiple sclerosis （MS） and type 1 diabetes （T1DM）], in order to discuss the pathogenesis and relationship between co-stimulatory molecules and autoimmune diseases.

Objective:To study the protective effect and mechanism of artemisinin on systemic inflammatory response syndrome （SIRS）mice using endotoxin （LPS）-induced SIRS mouse model. Method:Male BALB/c mice aged 5-7 weeks were randomly divided into normal group， LPS model group， low， medium and high-dose artemisinin groups （25， 50， 100 mg·kg^-1） and ibuprofen group （39 mg·kg^-1）. LPS （10 mg·kg^-1） was intraperitoneally injected at the 7^th day after the prophylaxis. According to the SIRS clinical diagnostic criteria， the respiratory rate， rectal temperature， lung index， spleen index， glycolipid metabolism， brain tissue inflammatory factors， and phosphorylation of lung tissue inflammation-related proteins were measured. Result:Intraperitoneal injection of LPS significantly reduced the respiratory rate of mice （P<0.05）， body temperature decreased significantly （P<0.01）， spleen index increased significantly （P<0.01）， peripheral blood neutrophil percentage increased significantly （P<0.05）， percentage of monocytes decreased significantly （P<0.01）， thrombocyte decreased （P<0.01）， platelet specific ratio decreased （P<0.01）， total cholesterol content in plasma decreased （P<0.01）， plasma glucose content decreased （P<0.01）. The expression of interleukin-1β increased in hippocampus and cortex of brain tissue （P<0.01）， and the secretion of tumor necrosis factor-α increased in hippocampus and cortex of brain tissue （P<0.01）. The expression of phosphorylated protein STAT1 was increased （P<0.01）， and the expression of phosphorylated protein c-Jun was increased （P<0.01）. After the administration of artemisinin， the body temperature and the respiratory rate of mice induced by LPS were significantly increased， the pathological changes of various organs induced by LPS were alleviated， the hypoglycemia induced by LPS was significantly increased （P<0.05）， the levels of inflammatory factors in hippocampus and cortex was significantly reduced， and the expressions of phosphorylated proteins STAT1 and c-Jun in lung tissue were significantly reduced （P<0.05， P<0.01）. Conclusion:Artemisinin has a significantly protective effect on SIRS mice induced by intraperitoneal injection of LPS possibly by reducing the secretion of inflammatory factors TNF-α and IL-1β.