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To investigate the influences of anti-ICOS antibody (anti-ICOSAb) on quantity and function of CD4(+);CD25(+);Foxp3(+);Treg cells from lymph and peripheral blood of rats with bronchial asthma.The mononuclear cells (MNC) from lymph and blood were co-cultured with anti-ICOSAb, and then the percentage of CD4(+);CD25(+);Foxp3(+);Treg cells were analyzed by flow cytometer (FCM) and the levels of IL-10 and TGF-β1 in supernatants were determined by ELISA.The MNC were collected from lymph and blood at 0, 24 and 48 h after the last challenge, respectively, and the cells were cultured for 96 h in vitro. The percentage of CD4(+);CD25(+);Foxp3(+);Treg cells in the MNC from lymph was significantly higher than that from blood in each group (P0.05); The percentage of CD4(+);CD25(+);Foxp3(+);Treg cells in the MNC from lymph and blood in asthma group was significantly lower compare with the normal control group (P0.05); The percentage of CD4(+);CD25(+);Foxp3(+);Treg cells in the MNC from lymph and blood in the anti-ICOSAb group obviously decreased compare with the asthma group (P0.05). At 0 h after the last challenge, the level of IL-10 in the supernatant of MNC from lymph and blood in the anti-ICOSAb group were significantly lower than that of the control and asthma groups (P0.05), while there were no significant differences of TGF-β1 expression in the supernatant of MNC from lymph and blood in each group at different time points.Blocking the ICOS/ICOSL signaling pathway by anti-ICOSAb could exacerbate the deficiency of CD4(+);CD25(+);Foxp3(+);Treg cells from lymph and blood in bronchial asthmatic rat, meanwhile inhibit the CD4(+);CD25(+);Foxp3(+);Treg cells secreting IL-10 at 0 h after the last challenge, but have no significant effect on the secretion of TGF-β1.

To investigate the expression of RhoA in the lung tissue of acute lung injury (ALI) rats induced by oleic acid (OA) and explore the influence of RhoA on the level of IL-8 and IL-10 in serum. Discussion RhoA and acute lung injury relationship.Establish rat oleic acid acute lung injury model, Wet/Dry weights (W/D) were detected. Pathological changes of the lung tissue were examined. The levels of IL-8 and IL-10 in serum were detected by ELISA and the expression of RhoA in homogenate of lung tissue was determined by PCR.W/D and ALI score in ALI group at 6, 12, 24 and 48 h were higher than those in control group (P0.01) and intervention group at the same time point (P0.05). The level of IL-10(ng/L) in serum in ALI group at 2, 6, 12, 24 and 48 h was remarkably higher than that in control group (P0.01), but was lower compared with intervention group at the same time point (P0.01). The level of IL-8(pg/L) in serum at 2, 6, 12, 24 and 48 h in ALI group were higher than those in control group(P0.01) and intervention group at the same time point(P0.01).Compared with that of control group, the expression of RhoA in homogenate of lung tissue in ALI group at 2, 6, 12, 24 and 48 h was higher(P0.01), but there was no difference between ALI group and intervention group at the same time point(P0.05).The expression of RhoA in lung tissue of ALI rats induced by OA is increased. RhoA expression increase that can cause lung damage degree increase in rats. RhoA can aggravate the pathology changes of ALI rats, which might be related to up regulating expression of IL-8 and down regulating expression of IL-10 by RhoA.

Hepatic stellate cells (HSCs), activated during liver injury, are defined as the most important target in the therapy of hepatic fibrosis. In the present study, we evaluated the effect of Rosmarinic acid (RosA) on the proliferation and apoptosis in activated hepatic stellate cells (HSC-T6), which is useful to decrease this cell population. The proliferation of HSC-T6 was significantly inhibited after treated with various concentrations of RosA for different times. Flow cytometric analyses and transmission electron microscope (TEM) observations revealed that HSC-T6 treated with RosA underwent apoptosis in a time dependent manner and displayed typical apoptotic features in the cells. The phosphorylation in signal transducer and activator of transcription protein-3 (STAT3), which regulates cell survival, proliferation and differentiation in a variety of tissues, was markedly decreased as the result of Western blot assay and correlated with downregulation of CyclinD1 and B cell lymphoma/leukemia-2 (Bcl-2). In conclusion, these results suggested that RosA was able to inhibit proliferation and induce apoptosis in HSC-T6, partly due to the inhibition of phosphorylation in STAT3, which contributed to the reversal of hepatic fibrosis.

To observe the expression of CD4(+) CD25(+) Foxp3(+) Treg, IL-10 and TGF-beta in lymph and blood, as well as the effect of dexamethasone on it and investigate the relationship between them.Lymph and blood samples of 0 h, 24 h, 48 h after the last challenge were collected from the rat model of asthma. The percentage of CD4(+) CD25(+) Foxp3(+) Treg were detected by flow cytometer (FCM), while the levels of IL-10 and TGF-beta were determined by ELISA.The percentage of CD4(+) CD25(+) Foxp3(+) Treg in the blood and the levels of IL-10 and TGF-beta in the plasma in cases of asthma group were significantly lower than that of the control and therapy group at different time points (P0.05); The percentage of CD4(+) CD25(+) Foxp3(+) Treg and the level of IL-10 in lymph were significantly higher than that of blood (P0.05), however, the level of TGF-beta in lymph were significantly lower than that of blood (P0.05); There were no significant differences which the percentage of CD4(+) CD25(+) Foxp3(+) Treg in the blood and the levels of IL-10 and TGF-beta in the plasma between control group and therapy group (P0.05).There is a disbalance both quantity and function of CD4(+) CD25(+) Foxp3(+) in the lymph of bronchial asthmatic rat, and the percentage of CD4(+) CD25(+) Foxp3(+) Treg in lymph are significantly higher than that of blood, which dexamethasone may effectively increase the percentage of CD4(+) CD25(+) Foxp3(+) Treg in bronchial asthmatic rat.