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C1q /TNF-related proteins (CTRPs)belong to the same category of C1q /TNF-related protein family,mainly secreted by adipose tissue and widely expressed in human and rodent.Their function turned out to be metabolic modulation,cardiovascular system protection and suppression of inflammation.But for metabolic modulation,enhancing the synthesis of glycogen,promoting fatty acid uptake and oxidation,in-creasing insulin sensitivity is the major role of CTRPs playing in governing the metabolism.Each CTRP has its own unique tissue expression profile and nonredundant function in regulating sugar and /or fat metabo-lism.In this review we focus on the recent progress about the metabolic function of CTRPs.
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Objective To compare the phenotype of myeloid derived suppressor cells (MDSCs) separated from the bone marrow of mice 3 d and 7 d after cecal ligation and puncture ( CLP) and to elucidate its potential role in the accumulation and immuno-function of MDSCs by determining the expression of microRNA-146a(miR-146a)in order to explore the effect of miR-146 a on immonosuppression of MDSCs in sepsis .Methods A septic model was prepareol by CLP in adult male C57BL/6J mice.MDSCs(expressing cell-surface CD11b and GR-1 antigens )from bone marrow were harvested 3 and 7 days after CLP and were separated with magnetic bead sorting technique .Then,cytokines secretion and arginase-I activity were detected and the T cell proliferation in vitro and the expression of miR-146a of MDSCs (3 d and 7 d after CLP)were observed.Results MDSCs secreted mostly such promoting inflammatory factors as TNF-α, IL-6 3 days after CLP, but 7 days after CLP , they primarily secreted IL-10 and TGF-βwhich were anti-inflammatory factors . MDSCs had potent immunosuppressive properties by increasing T cell suppression in a late anti-inflammatory phase ( CLP3 d vs CLP7 d, P<0.05).In the meantime,miR-146a of the MDSCs in bone marrow was overexpressed in septic mice at 7 days(P<0.05). Moreover,the expression of miR-146a of the MDSCs in bone marrow of septic mice was higher at 7 days than at 3 days after CLP(P<0.05).Conclusion The data indicate that the phenotype of MDSCs evolves through early pro -inflammatory phase into the late anti-inflammatory phase .MDSCs have potent immunosuppressive properties in the late phase of sepsis . miR-146 a might play a crucial role in the regulation of immunosuppressive activity of MDSCs in late sepsis .
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Sepsis,a complex clinical syndrome resulting from a harmful and damaging host response to infection, is the leading cause of mortality in intensive care units.Early diagnosis and appropriate intervention can improve the prognosis of patients with sepsis.Many studies have confirmed that sepsis at different stages is in different immune status.Priority used to be given to systemic inflammatory response, but immune-suppression has become the focus of study. Immune-suppression and secondary infection are the major causes of death of patients with sepsis.Study of sepsis is shifting to immune-suppression and its regulation mechanisms.
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Objective To evaluate the effects of sevoflurane preconditioning on caveolin-3 expression during myocardial ischemia-reperfusion (I/R) in rats.Methods Healthy male Wistar rats,aged 6-8 weeks,weighing 250-300 g,were anesthetized with intraperitoneal pentobarbital 30 mg/kg and heparin 1 000 IU/kg.Their hearts were excised and perfused with K-H solution in a Langendorff apparatus.Thirty isolated rat hearts were randomly assigned into 3 groups (n =10 each) using a random number table:control group (group C),I/R group and sevoflurane preconditioning group (group SP).After 30 min of equilibration,group C was continuously perfused with K-H solution for 90 min,group I/R underwent 30 min of ischemia followed by 60 min of reperfusion,and group SP was perfused with K-H solution saturated with 2％ sevoflurane for 10 min followed by 5 min washout with K-H solution,then underwent 30 min of ischemia followed by 60 min of reperfusion.HR,left ventricular enddiastolic pressure (LVEDP),+ dp/dtmax and-dp/dtmax were recorded at the end of equilibration,immediately before ischemia and at 30 and 60 min of reperfusion.Myocardial specimens were obtained from the cardiac apex for microscopic examination.Myocardial specimens were obtained from the left ventricle for determination of caveolin3 expression.Results Compared with group C,+ dp/dtmax and-dp/dtmax were significantly decreased immediately before ischemia,and HR,LVDEP,+ dp/dtmax and-dp/dtmax were decreased at 30 and 60 min of reperfusion in groups I/R and SP,and caveolin-3 expression was down-regulated in group I/R and up-regulated in group SP (P ＜ 0.05).Compared with group I/R,HR,LVDEP,+ dp/dtmax and-dp/dtmax were significantly decreased immediately before ischemia and increased at 30 and 60 min of reperfusion,and caveolin-3 expression was up-regulated in group SP (P ＜ 0.05).The pathological changes were significantly attenuated in group SP as compared with group I/R.Conclusion The mechanism by which sevoflurane preconditioning attenuates myocardial I/R injury in rats may be related to up-regulation of myocardial caveolin-3 expression.
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BACKGROUND:Ful-thickness articular cartilage injury is notoriously difficult to be treated in the fields of orthopedics and sports medicine. Al ogeneic bone and cartilage transplantation can offer a transparent cartilage with biological activity and biomechanical properties to repair ful-thickness articular cartilage defects. Al ogeneic osteochondral grafts from osteochondral tissue bank are adequate, and have a good prospect in the treatment of articular cartilage defects. OBJECTIVE:To summarize the drawn materials, preservation, quality control and clinical monitoring of al ogeneic osteochondral grafts supported by the osteochondral tissue bank. METHODS:The first author searched PubMed and CNKI for the relevant articles published before 2013 using the key words of“tissue bank, knee, articular cartilage, preservation, transplantation”in English and Chinese, respectively. After retrieval, we summarized the drawn materials, preservation, quality control and clinical monitoring of al ogeneic osteochondral grafts supported by the osteochondral tissue bank. RESULTS AND CONCLUSION:Nineteen of 194 retrieved articles were enrol ed according to inclusive and exclusive criteria. The results show that al ogeneic bone and cartilage transplantation is an ef ective method for the treatment of articular cartilage defects, and the establishment of the osteochondral tissue bank can provide safe and active tissues for the treatment of articular cartilage defects. Now, the osteochondral tissue bank is stil in the initial stage.
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Objective To investigate the effect of propofol on myocardial injury induced by hepatic ischemia/reperfusion (I/R) in rats and the role of PI3K/Akt signaling pathway. MethodsOne hundred and two male SD rats weighing 250-280 g were randomly divided into 5 groups:Ⅰ sham operation group (group S, n =6), ⅡI/R group ( n = 30), Ⅲ propofol group (group P, n = 30), Ⅳ propofol + LY294002 group (group P+ LY, n =18), and Ⅴ propofol + dimethylsulfoxide group (group P+ DMSO, n = 18). Hepatic I/R was produced by occlusion of hepatic pedicle for 30 min followed by reperfusion in group Ⅱ - Ⅴ. Propofol 12 mg/kg, propofol 12mg/kg + LY294002 (a specific PI3K inhibitor) 1.5 mg/kg, and propofol 12 mg/kg + DMSO 0.5 ml were injected I.v.via femoral vein at 10 min before ischemia in group Ⅲ -Ⅴ respectively, and then propofol was infused I.v. At a rate of 30 mg· kg- 1 · h - 1 and the administration was stopped before the rats were sacrificed in group Ⅲ - Ⅴ . At 0,30, 60, 120, and 240 min of reperfusion (T1-5) in group Ⅱ and Ⅲ , and at T3.5 in group Ⅳ and Ⅴ , six rata were sacrificed and myocardial tissues were taken for determination of the total Akt (t-Akt) and phosphorylated Akt (p-Akt) expression and Bcl-2 expression and apoptosis were detected at T3. The hepatic tissues were taken for microscopic examination. The rats were sacrificed at T1 and the parameters mentioned above were detected in group Ⅰ . ResultsCompared with group Ⅰ , p-Akt expression and apoptosis rate were significantly increased in the other4 groups, and Bcl-2 expression was up-regulated in group Ⅱ , Ⅲ and Ⅴ (P ＜ 0.05). Compared with group Ⅱ , p-Akt and Bcl-2 expression was up-regulated, and the apoptosis rate was significantly decreased in group Ⅲand Ⅴ ( P ＜ 0.05). Compared with group Ⅲ , p-Akt and Bcl-2 expression was down-regulated, and the apoptosis rate was significantly increased in group Ⅳ ( P ＜ 0.05). The microscopic examination showed that the injury to the hepatic tissues was less severer in group Ⅲ and Ⅴ than in group Ⅱ and Ⅳ. ConclusionPropofol can attenuate myocardial injury induced by hepatic I/R in rats by activation of PI3K/Akt signaling pathway.