Insulin has been found to enhance specific immune function in experimental animals. However, it remains hitherto unnoticed whether the antigen-presenting capability and expression of Ia antigens of the macrophage, known to be essential for the induction of both cell-mediated immunity and humoral immune response to most antigens, could also be influenced by insulin. In the present study, it was demonstrated that insulin, in a concentration of 1.03?10~(-7) mol/L, promoted the antigen-presenting capability of human monocytes significantly. Furthermore, we found that the expression of HLADQ antigen on monocytes was markedly enhanced by insulin while that of HLA-DR determinant was not affected significantly. We suggested, therefore, that the promotion of antigen-presenting capability of human monocytes by insulin may be attributed, at least in part, to its enhancing effect on the expression of HLA-DQ antigen on the monocytes.

Objective To investigate the role of N-myc downstream regulated genes 2 (NDRG2) in attenuation of focal cerebral ischemic-reperfusin injury by sevoflurane preconditioning in rats.Methods Forty-eight healthy male SD rats weighing 280-320 g were randomly divided into 3 groups ( n =16 each):sham operation group (group S),ischemia-reperfusion injury group (group I/R) and sevoflurane preconditioning group (group Sev).Focal cerebral ischemia-reperfusion injury was induced by right middle cerebral artery occlusion (MCAO)for 120 min followed by 24 h reperfusion.In group Sev,2.0％ sevoflurane was inhaled 1 h once a day for 5 consecutive days at 24 h before MCAO.The neurologic function was evaluated at 24 h of reperfusion and than the rats were sacrificed,and the brain was removed for determination of infarct volume percentage,NDRG2 and activated Caspase-3 expression in ischemic penumbra by Western Blot and NDRG2 expression and location by immunohistochemistry.Results The infarct volume percentage,NDRG2 and activated Caspase-3 expression were higher,and neurologic function score was lower in groups I/R and Sev then in group S( P ＜ 0.05).The infarct volume percentage,NDRG2 and activated Caspase-3 expression were lower,and neurologic function score was higher in group Sev then in group I/R ( P ＜ 0.05).The intranuclear NDRG2 positive staining was decreased in group Sev than in group I/R.Conclusion Sevoflurane preconditioning can reduce focal cerebral ischemia-reperfusion injury by inhibiting the expression and activity of NDRG2 and apoptosis in rats.

Objective:To explore the changes of estrogen, androgen and progesterone in serum of male patients with primary gouty arthritis (pGA) and their possible role in the pathogenesis of gout.Methods:The serum, clinical data and laboratory parameters of 266 patients with PGA [including 93 patients with acute gout (AG), 118 patients with intermittent gout (IG), 55 patients with chronic gout (CG)] and 129 healthy controls (HC) were collected. The serum estradiol (E 2), progesterone (P), testosterone (T) and E 2/T were detected by CMIA Expression level. SPSS 17.0 statistical software was used for analysis, Wilcoxon rank sum test was used for comparison of measurement data between groups, and Spearman correlation analysis was used for correlation analysis between variables. Results:① The level of E 2 and T level in the serum of PGA, AG, IG and CG group was lower than that of the HC group [(30±8) pg/ml, (27±7) pg/ml, (31±8) pg/ml, (34±7) pg/ml, (35±10) pg/ml; F=17.770, P<0.05] and [(4.4±1.6) ng/ml, (3.8±1.4) ng/ml, (4.6±1.4) ng/ml, (5.1±2.0) ng/ml, (5.8±1.9) ng/ml; F=23.314, P<0.05], but there was no significant difference between HC group and CG group ( P>0.05), The serum E 2 and T levels in AG group were lower than those in IG and CG groups [(27±7) pg/ml, (31±8) pg/ml, (34±7) pg/ml; F=17.770, P<0.05] and [(3.8±1.4) ng/ml, (4.6±1.4) ng/ml, (5.1±2.0) ng/ml; F=23.314, P<0.05], andthe serum E 2 level in IG group was lower than that in CG group [(31±8) pg/ml, (34±7) pg/ml; F=17.770, P<0.05). The levels of P and E 2/T in HC group were lower than those in pGA and AG group [(0.24±0.10) ng/ml, (0.27±0.11)ng/ml, (0.30±0.15) ng/ml; F=5.124, P<0.05] and [(0.006 6±0.002 2) ng/ml, (0.007 6±0.003 2) ng/ml, (0.008 0±0.003 8) ng/ml; F=3.787, P<0.05), while those in IG and CG group were lower than those in AG group [(0.25±0.09) ng/ml, (0.26±0.08) ng/ml, (0.30±0.15) ng/ml; F=5.124, P<0.05]; ② Spearman correlation analysis showed that E 2 level in pGA group was positively correlated with T and CysC( r=0.310, P<0.01; r=0.164, P=0.008), negatively correlated with MO ( r=-0.133, P=0.030), P level was positively correlated with MO ( r=0.139, P=0.023), T level was positively correlated with Crea and CysC ( r=0.179, P=0.003; r=0.162, P=0.008), negatively correlated with WBC, GR and MO ( r=-0.140, P=0.022; r=-0.173, P=0.005; r=-0.149, P=0.015), E 2/T was positively correlated with apob1 and Glu ( r=0.131, P=0.032; r=0.140, P=0.023). In AG group, E 2 level was positively correlated with T and Crea ( r=0.234, P=0.024; r=0.245, P=0.018), T level was positively correlated with Crea ( r=0.349, P=0.001), and negatively correlated with apob1 ( r=-0.250, P=0.016), and E 2/T was positively correlated with apob1 ( r=0.276, P=0.007). In IG group, E 2 level was positively correlated with T ( r=0.269, P=0.003), and negatively correlated with MO ( r=-0.183, P=0.048), while P level was positively correlated with MO( r=0.204, P=0.027). Conclusion:The expression of E 2 and T in the peripheral blood serum of gout patients decreases significantly, the expression of P and E 2/T increases significantly, and there is a positive correlation between E 2 and T, as well as the inflammatory and glycolipid metabolism indexes of gout patients, suggesting that estrogen, androgen and progesterone may participate in the pathogenesis of gout by regulating the inflammation and metabolism of gout.

We have previously reported that Cystatin C (CysC) is a pivotal mediator in the neuroprotection induced by hyperbaric oxygen (HBO) preconditioning; however, the underlying mechanism and how CysC changes after stroke are not clear. In the present study, we demonstrated that CysC expression was elevated as early as 3 h after reperfusion, and this was further enhanced by HBO preconditioning. Concurrently, LC3-II and Beclin-1, two positive-markers for autophagy induction, exhibited increases similar to CysC, while knockdown of CysC blocked these elevations. As a marker of autophagy inhibition, p62 was downregulated by HBO preconditioning and this was blocked by CysC knockdown. Besides, the beneficial effects of preserving lysosomal membrane integrity and enhancing autolysosome formation induced by HBO preconditioning were abolished in CysC rats. Furthermore, we demonstrated that exogenous CysC reduced the neurological deficits and infarct volume after brain ischemic injury, while 3-methyladenine partially reversed this neuroprotection. In the present study, we showed that CysC is biochemically and morphologically essential for promoting autophagic flux, and highlighted the translational potential of HBO preconditioning and CysC for stroke treatment.
Animals ; Autophagy ; physiology ; Beclin-1 ; metabolism ; Brain ; metabolism ; pathology ; Brain Ischemia ; metabolism ; pathology ; therapy ; Cystatin C ; genetics ; metabolism ; Disease Models, Animal ; Gene Expression ; Gene Knockdown Techniques ; Hyperbaric Oxygenation ; Lysosomes ; metabolism ; pathology ; Male ; Microtubule-Associated Proteins ; metabolism ; Neurons ; metabolism ; pathology ; Neuroprotection ; physiology ; Oxygen ; therapeutic use ; Random Allocation ; Rats, Sprague-Dawley ; Rats, Transgenic ; Reperfusion Injury ; metabolism ; pathology ; therapy