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To observe the effects of Shenmai injection(SM) on p38MAPK and the apoptosis-related genes in lung injury induced by intestinal ischemia reperfusion (I/R) in rats and to investigate the protective mechanism of SM.Rat model of intestinal I/R injury was established with clamping of the superior mesenteric artery (SMA) for 60 min and then clamping was relieved for 60 min. Twenty-four SD rats were randomly divided into three groups with eight rats in each: control group, intestinal ischemia/reperfusion group(I/R group), Shenmai injection treated group (SM+I/R group). Lung wet/dry weight ratio(W/D), the contents of phosphatidylcholine (PC) and total phospholipid(TPL) which are the major ingredients of pulmonary surfactant were measured, as well as the expression levels of p38MAPK, Bcl-2 and Bax proteins in lung tissue were examined by using immunohistochemical method.Compared with control group, lung W/D was significantly increased, the contents of PC and TPL were significantly decreased, the protein expression levels of p38MAPK, Bcl-2 and Bax were significantly increased in I/R group (all P＜0.01). But Bax protein expression was much greater than Bcl-2 protein expression, the ratio of Bcl-2 to Bax were significantly decreased in I/R group than that in control group (P＜0.01). Compared with I/R group, lung W/D was significantly decreased, while the contents of PC and TPL were significantly increased, the p38MAPK and Bax protein expression levels were significantly decreased in SM+I/R group (all P＜0.01); both Bcl-2 protein expression and the ratio of Bcl-2 to Bax were significantly increased in SM+I/R group than those in I/R group (P＜0.01). The correlation analysis indicated that the expression level of p38MAPK protein in lung tissue was negatively correlated with the contents of PC and the ratio of Bcl-2 to Bax (r is -0.787 and -0.731, all P＜0.01).SM can protect the lung injury induced by intestinal I/R injury, which may be mediated by inhibiting the activation of p38MAPK, improving the ratio of Bcl-2 to Bax to inhibit lung apoptosis.

The up-regulation of HER2/neu is associated with human malignancies and is a useful target for developing anticancer drugs. Overexpression of human manganese superoxide dismutase (MnSOD) has been demonstrated to effectively suppress various carcinoma cells, including breast carcinomas, in vitro and in vivo. This study demonstrates that MnSOD effectively suppresses HER2/neu oncogene expression at the transcriptional level. Additionally, stable transfection was used and the MnSOD-transfected human breast cancer clones were found to be able to down-regulate the endogenous production of p185HER2/neu. Furthermore, the MnSOD-overexpressing stable transfectants exhibited reduced soft-agarose colony-forming ability and metastatic properties, unlike control cell lines. These data suggest that MnSOD may be useful in treating HER2/neu-mediated human breast tumor malignancy.

To explore the morphological and expressional changes of Th1 cells and Th2 cells in retina of a rat model of glaucoma vaccinated by Cop-1 (Copolymer-1) and elucidate the possible neuroprotection roles played by Th1/Th2.After modeling, the aqueous outflow from the right eyes was blocked by a ligation of three of four episcleral veins. There were 48 rats with elevated IOP (intraocular pressure) immunized by Cop-1 (Cop-1 group), 48 rats with elevated IOP immunized by PBS (phosphate-buffered saline) (PBS group) and 10 rats without any treatment (normal group). The experimental rats were immunized with Cop-1/PBS emulsified in a total volume of 0.4 ml complete Freund's adjuvant. The immunization was administered subcutaneously at the base of tail. Immunofluorescence was employed to test the distribution and activation of Th1 and Th2 cells in retina at Days 3, 7, 10, 17, 24 and 31 post-immunization respectively for each group. Western blot was selectively performed according to the results of immunofluorescence to verify if there was a similar variation of the retinal expression of IL-4 protein.The results of immunofluorescence showed the numbers of Th1 cells peaked at Day 7 in both Cop-1 ((216 ± 21)/mm(2)) and PBS groups ((194 ± 27)/mm(2)). And no statistical significance existed between two groups (P0.05). The numbers of Th2 cells in the experimental groups peaked at Day 7 with statistical significance (Cop-1 group: 300 ± 28/mm(2) vs PBS group: 129 ± 27/mm(2)) (P0.01). With the prolongation of experimental period, the number of Th2 cells decreased gradually in the Cop-1 group but remained greater than that of the PBS group afterward (P0.05). The Western blot results showed that the expression of IL-4 in the Cop-1 group (1.91 ± 0.05) was significantly higher than that of the PBS group (0.51 ± 0.04) from Day 3 and peaked at Day 7 (2.11 ± 0.06 vs 0.57 ± 0.05). Then the IL-4 expression decreased gradually in the COP-1 group but still represented statistical significance versus the PBS group until Day 31 post-immunization (P0.001).The retinal activation and accumulation of IL-4 are found in a rat model of chronic glaucoma immunized by Cop-1. Thus Th2 cells may play vital roles in the Cop-1-induced neuroprotective autoimmune responses.