Objective To review the application and research progress of in-situ tissue engineering technology in bone and cartilage repair. Methods The original articles about in-situ tissue engineering technology in bone and cartilage repair were extensively reviewed and analyzed. Results In-situ tissue engineering have been shown to be effective in repairing bone defects and cartilage defects, but biological mechanisms are inadequate. At present, most of researches are mainly focused on animal experiments, and the effect of clinical repair need to be further studied. Conclusion In-situ tissue engineering technology has wide application prospects in bone and cartilage tissue engineering. However, further study on the mechanism of related cytokines need to be conducted.
Abstract： Objective To investigate the acute cardioprotective effect of 17b-estradiol (17b-E2) against severe myocardial ischemia/reperfusion (I/R) injury in rabbits and the mechanism of the effect. Methods We established the model of myocardial I/R in vivo by occluding the left anterior descending coronary artery of the rabbits (who underwent coronary occlusion for 40 minutes followed by 3 hours of reperfusion). Twentyfour New Zealand white male rabbits were randomly divided into two groups with 12 in each group. Before coronary occlusion, 1 ml of ethanol or 17b-E2 at 10 μg/kg was administered intravenously to the rabbits in the control group and the experimental group respectively. The serum levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were measured by enzymelinked immunosorbent assay (ELISA) at the following time points: before occlusion, 40 minutes after occlusion, 1 hour, 2 hours and 3 hours after reperfusion. Activation of p38 mitogen activated protein kinase(MAPK) was determined by Western blotting analysis, and apoptosis of cardiocytes was identified by terminal deoxynucleotidlyl transferase mediated deoxyuridinebiotin dUTP Nick End Labeline (TdT)mediated dNTP nick end labeling (TUNEL) staining. Results During myocardial ischemia, TNF-α decreased significantly in the experimental group compared with the control group (F=0.007,P=0.001), while there was no difference in IL-6 between the two groups (F=0.616,P=0.095). During the process of reperfusion, the levels of TNF-α and IL-6 in the experimental group were significantly lower than those in the control group (Plt;0.01). Besides, the activation of p38 MAPK and apoptotic index for the experimental group were also lower (45.07%±2.73% vs. 61.25%±2.41%, t＝－15.398, P=0.000; 11.21%±3.85% vs. 22.02%±4.49%, t＝－6.332, P=0.000). Conclusion The cardioprotective effect of 17b-E2 against myocardial I/R may be attributed to its antiinflammatory and antiapoptotic properties, which is probably associated with the inhibition of 17bE2 on p38MAPK activity.
Objective To summarize the research progress on the mechanism related to traumatic brain injury (TBI) to promote fracture healing, and to provide theoretical basis for clinical treatment of fracture non-union. Methods The research literature on TBI to promote fracture healing at home and abroad was reviewed, the role of TBI in fracture healing was summarized from three aspects of nerves, body fluids, and immunity, to explore new ideas for the treatment of fracture non-union. Results Numerous studies have shown that fracture healing is faster in patients with fracture combined with TBI than in patients with simple fracture. It is found that the expression of various cytokines and hormones in the body fluids of patients with fracture and TBI is significantly higher than that of patients with simple fracture, and the neurofactors released by the nervous system reaches the fracture site through the damaged blood-brain barrier, and the chemotaxis and aggregation of inflammatory cells and inflammatory factors at the fracture end of patients with combined TBI also differs significantly from those of patients with simple fracture. A complex network of humoral, neural, and immunomodulatory networks together promote regeneration of blood vessels at the fracture site, osteoblasts differentiation, and inhibition of osteoclasts activity. Conclusion TBI promotes fracture healing through a complex network of neural, humoral, and immunomodulatory, and can treat fracture non-union by intervening in the perifracture microenvironment.
Objective To investigate the mRNA and protein expression of human β-defensin-2 (hBD-2) induced by lipopolysaccharide (LPS)，IL-1β and TNF-α in human airway primary epitheliums.Methods The bronchial primary epitheliums from human were stimulated with LPS，IL-1β and TNF-α respectively and then were harvested for hBD-2 expression detection.The mRNA expression of hBD-2 was detected by RT-PCR，and the protein expression by immunocytochemistry and western blot.Results There was a small expression of hBD-2 mRNA in human airway primary epitheliums before stimulation.The hBD-2 mRNA expression was significantly increased after 3 hours of LPS，IL-1β and TNF-α stimulation respectively and the expression increasement was in a dose dependent manner.The hBD-2 protein could be detected in cytoplasm after 4 hours of LPS (0.1 μg/mL)，IL-1β (1 ng/mL) and TNF-α (10 ng/mL) stimulation.Conclusions LPS and proinflammatory cytokines can induce the mRNA and protein expression of hBD-2 in a short time.The expression of hBD-2 may play an initial defense role against bacterial invasion.
Myocardial remodeling is a common pathological physiology change for a variety of heart diseases under stimulation such as stress or ischemia. The engine body will release a lot of cytokines to promote the change of myocardial structure and ultimately lead to heart failure. Myocardial remodeling includes myocardial cells remodeling and the extracellular matrix remodeling. In recent years, we find that the function of adipose tissue is not only about energy storage, buffering to protect, supporting and filling, but also has a powerful function of secretion. Adipose tissue can secrete various adipocytokines, such as leptin, adiponectin, visfatin, omentin, angiotensin Ⅱ, and so on. Current studies have shown that adipocytokines and myocardial remodeling are intimated. And this article will summarize the function of adipocytokines on myocardial remodeling.
Objective To evaluate the effect of hemoperfusion for absorption of inflammatory cytokines on sepsis . Method A prospective randomized controlled study was carried out to collect 60 sepsis patients admitted to the Department of Critical Care Medicine of this hospital from June 2019 to December 2021. They were randomly divided into a study group (30 cases) and a control group (30 cases) by using the random number table method. Both groups of patients received routine treatment according to the guidelines, including fluid resuscitation, mechanical ventilation, antibiotic and vasoactive agents. For the patients with renal failure, renal replacement therapy (RRT) was used. Routine vital sign monitoring and serum procalcitonin (PCT) and interleukin-6 (IL-6) determination were recorded. The study group received two times of hemoperfusion to absorb inflammatory cytokines at 0 h and 24 h after enrollment. At 24 h and 48 h after treatment, the vital signs and related physical and chemical indexes of patients were recorded again, including norepinephrine dose, oxygenation index, PCT, IL-6 and blood lactic acid. The changes of physical and chemical indexes and the 28-day survival rate of the two groups were compared. Results There was no difference in the general situation of the two groups when they were enrolled (P>0.05). The dosage of norepinephrine [(0.77±0.48)μg·kg–1·min–1 vs. (0.92±0.62) μg·kg–1·min–1, P=0.030] and the level of blood lactic acid [(2.70±1.43)mmol/L vs. (4.05±2.60)mmol/L, P=0.001] in the study group were significantly lower than those in the control group 24 h and 48 h after treatment. The oxygenation index in the study group was higher than that of the control group 24 h after treatment (212±68)mm Hg vs. (197±42)mm Hg, P=0.042). The inflammation related indexes PCT [(17±24)ng/mL vs. (32±36)ng/mL, P=0.013] and IL-6 [299 (102, 853)pg/mL vs. 937 (247, 2230)pg/mL, P=0.026] in the study group were significantly lower than those in the control group 48 h after treatment. The dosage of noradrenaline, oxygenation index, PCT, IL-6 and blood lactate level in the study group after treatment were improved compared with those before treatment (P<0.05), while those in the control group were not significantly improved after treatment (P>0.05), and oxygenation index in the two groups had no significant difference before and after treatment (P>0.05). There was no significant difference in the 28-day survival rate between the two groups (χ2=0.211, P=0.646). Conclusion Although the hemoperfusion for absorption of inflammatory cytokine factors can not reduce the 28-day mortality of sepsis, it can significantly improve the early physical and chemical indicators of patients, and provide opportunities for follow-up treatment.
ObjectiveTo investigate the effect of etomidate and propofol on inflammatory cytokines and cortisol for patients with lung adenocarcinoma. MethodSixty patients scheduled for lung cancer surgery under general anesthesia were studied. All patients were randomly divided into an etomidate total intravenous anesthesia group (group E, 30 patients, 16 males and 14 females at age of 58.0±5.0 years) and a propofol total intravenous anesthesia group (group P, 30 patients, 17 males and 13 females at age of 55.0±5.0 years), with 30 patients in each group. ResultsThe concentration of IL-6 in serum of patients in the two groups at time points T1, T2 and T3 was significantly higher than those at time point T0 (P < 0.01). The concentration of IL-10 and TNF-α in serum of patients at time points T1 and T2 was significantly higher than those at time point T0 (P < 0.01). And the difference of the concentration of TNF-α in serum of patients at time points T0 and T3 was not statistically significant (P > 0.05). The level of Cor of patients in the group E at time point T0 was slightly higher than those at time point T1, but lower than that at time points T2 and T3. There was no statistical difference in the concentration of IL-6 and TNF-α in serum of patients between the two groups. The level of IL-10 of patients in the group E at time points T2 and T3 was lower than those in the group P (P < 0.05), but no significant difference was observed at the other time points. The concentration of Cor in the patients in the group E at time point T1 was lower than that in the group P (P < 0.01), but no significant difference was observed either at the other time points. ConclusionThe effect of etomidate used for maintenance of general anesthesia on the inflammatory factors is essentially similar to that of propofol.
Osteochondral defects is a common clinical joint disease. The complexity of cartilage-bone interface and the poor self-repair capacity of cartilage are both reasons for current relatively limited clinical treatments. The introduction of tissue engineering provides a new treatment method for osteochondral repair. This paper reviews three main elements of cartilage-bone tissue engineering: seed cell source and culture method, cytokines regulation and synergistic effect, and scaffold components and type. We mainly focused on current status quo and future progress of cartilage-bone repair scaffolds. This paper provides some reference for the further development of osteochondral tissue engineering.
ObjectiveTo summarize the research status and progress of interleukin-6 (IL-6) in Takayasu arteritis (TAK). MethodRecent literature published at home and abroad about the study of IL-6 in the TAK was reviewed and analyzed. ResultsIL-6 was a pro-inflammatory cytokine secreted by a variety of cells, which participated in a variety of inflammatory and immune reactions, and played an important role in the progress of TAK. The expression levels of IL-6 in the peripheral blood and vascular wall tissues of patients with TAK were increased. The gene polymorphism of IL-6 might be related to the occurrence of TAK. Tocilizumab, an IL-6 receptor antagonist, was effective and safe in the treatment of TAK. ConclusionsIL-6 can be used as one of the monitoring indicators for the active phase and recurrence of TAK. IL-6 receptor antagonist can be used as the treatment choice of TAK, but the application results in different stages of TAK are still worth expecting.
ObjectiveTo investigate the expression of α7 nicotinic acetylcholine receptor (α7 nAChR) in thymocytes of patients with myasthenia gravis (MG) and its effect on cytokine secretion and T cell proliferation. MethodsPatients with MG who underwent expanded thoracoscopic thymectomy in the Comprehensive Diagnosis and Treatment Center of the Henan Provincial People’s Hospital from June 2021 to June 2022 were selected and allocated to a MG group. Patients who underwent partial thymectomy to expose the surgical field during the cardiac disease surgery from June 2021 to September 2022 in the Department of Adult Cardiac Surgery of Fuwai Huazhong Cardiovascular Hospital were selected as the control group. Thymic single cell suspensions were prepared from MG and control groups, and the expression of α7 nAChR in thymocytes of the two groups was detected by real-time polymerase chain reaction and Western blotting. Then CD3/CD28 monoclonal antibody coupled with magnetic beads was used to induce T cell activation, and the levels of cytokines interferon-gamma (IFN-γ), tumor necrosis factor-α (TNF-α), interleukin-4 (IL-4), IL-6, IL-10, IL-17, and IL-21 in thymocytes of the two groups were detected by enzyme-linked immunosorbent assay (ELISA). The activated T cells of the MG group were divided into a blank control group, an α7 nAChR antagonist group, and an α7 nAChR agonist group according to different treatment methods. After 72 hours of culture, IFN-γ, TNF-α, IL-4, IL-6, IL-10, IL-17, and IL-21 expression levels in the culture supernatant were measured by ELISA. Afterwards, CD4-PE and CD8-APC antibodies were added, and the proliferation of T cell subsets was detected by flow cytometry. ResultsA total of 10 MG patients were collected, including 3 males and 7 females with an average age of 19.25±6.28 years; and 15 control patients were collected, including 6 males and 9 females with an average age of 26.18±6.77 years. Compared with the control group, the mRNA and protein levels of α7 nAChR in the thymocytes of MG group were decreased, and the expression levels of IFN-γ, TNF-α, IL-4, IL-6 and IL-21 in the supernatant were increased (P<0.05), but there was no statistical difference in the expression of IL-10 and IL-17 (P>0.05). The cell-culture experiment showed that compared with the blank control group, the levels of IFN-γ, TNF-α, IL-6 and IL-21 secreted by T cells in the α7 nAChR antagonist group were increased (P<0.05), while they were decreased in the α7 nAChR agonist group (P<0.05). There was no statistical difference in the secretion levels of IL-4, IL-10 or IL-17 among the three groups (P>0.05). CD4+ T and CD8+ T cells in the α7 nAChR agonist group were significantly less than those in the blank control group and α7 nAChR antagonist group (P<0.001), while they were significantly more in the α7 nAChR antagonist group than those in the blank control group (P<0.001).ConclusionThe expression of α7 nAChR in thymocytes of MG patients is decreased, and α7 nAChR may be involved in the inflammatory response in thymocytes and thus in thymic function.