Protective effects of rhu TNFR: Fc against the lipopolysaccharide induced intestinal damage of rats and its underlying mechanism / 药学学报

To investigate the protective effects of recombinant human tumor necrosis factor receptor II: IgG Fc fusion protein (rhu TNFR: Fc) against the lipopolysaccharide (LPS) induced intestinal damage of rats and its underlying mechanism. SD rats were randomly divided into four groups: control group, rhuTNFR: Fc group, LPS group and rhu TNFR: Fc + LPS group. Mean arterial pressure (MAP) was continuously monitored and the mortality rates were assessed. The levels of TNF-alpha and its bioactivity in the serum were assessed by ELISA and flow cytometry respectively. Pathologic changes of intestinal tissue were observed by HE staining. The rats of control and rhu TNFR: Fc group all survived with stable MAP, and the low level and bioactivity of TNF-alpha in the serum were maintained. While 83% of the rats in LPS group died by 6 h with the levels and bioactivity of TNF-alpha increasing significantly. In rhu TNFR: Fc + LPS group, the mortality rate of rats dropped to 33%. The TNF-alpha level increased compared with control group but its bioactivity decreased significantly compared with LPS group. The MPO activity and content of MDA decreased significantly. The status of pathological manifestation in the intestine was also ameliorated. These data suggest that rhu TNFR: Fc could protect rats from the acute intestine injury induced by LPS through ablating the rise in serum TNF-alpha level and bioactivity as well as anti-oxidation.

Effect of ryanodine receptor 2 gene silencing on ischemia-reperfusion injury of rat myocardial cells / 中华病理学杂志

<p><b>OBJECTIVES</b>To block the synthesis of ryanodine receptor 2 (RyR2) in myocardial cells by RNA interference and to investigate its biological impact on ischemia-reperfusion (I/R) in rat myocardial cells.</p><p><b>METHODS</b>Rat myocardial cells were isolated and cultured for an I/R model in vitro. RNA interference technique was used to block the synthesis of RyR2 in myocardial cells. Changes of LDH level, apoptosis, RyR2 mRNA expression and cytosolic Ca(2+) concentration were analyzed accordingly.</p><p><b>RESULTS</b>Myocardial cells after I/R manipolation were severely injuried (LDH leakage, 125 IU/L vs 12 IU/L, P < 0.05), apoptosis (60.1% vs 5.5%, P < 0.05), significant cytosolic Ca(2+) overload (21.2 vs 7.6, P < 0.05) and remarkable mitochondrial membrane potential loss (37.2 vs 85.1, P < 0.05). However, no visible change of RyR2 was observed (20.1 vs 22.7, P > 0.05). Pre-treatment with RyR2 specified siRNA demonstrated suppressed expression of RyR2 (6.8 vs 20.1, P < 0.05), increased mitochondrial membrane potential (55.8 vs 37.2, P < 0.05), attenuated cytosolic Ca(2+) overload (8.6 vs 21.2) and cellular apoptosis (31.2% vs 60.1%, P < 0.05).</p><p><b>CONCLUSION</b>RyR2 gene silencing enables to protect myocardial cells from I/R injury in vitro.</p>

Effect of high glucose on expression of MIP-2 and MCP-1 in macrophages cultured in vitro / 上海第二医科大学学报

0.05).The protein and mRNA expression of MIP-2 in high glucose group significantly increased after culture for 4 h,and guadually decreased then.The protein and mRNA expression of MCP-1 began to increase significantly after culture for 8 h,reached peak at 12 h,and slightly decreased after culture for 24 and 48 h. Conclusion High glucose promotes the protein and mRNA expression of MIP-2 and MCP-1 from mouse peritoneal macrophages cultured in vitro,which indicates that high glucose may delay the wound healing by increasing the expression of chemokines in diabetic mice.

Effect of folic acid on plasma homocysteine in patients with sudden sensorineural hearing loss / 上海第二医科大学学报

Objective To study the effect of folic acid on decreasing level of plasma total homocysteine(tHcy)in patients with sudden sensorineural hearing loss(SSHL) and the optimal dosage of folic acid. Methods Ten randomized controlled trials involving treatment data on 210 patients with SSHL were retrospectively studied.They were divided into seven groups according to the daily dosage of folic acid: group A to group G,0.2 mg,0.4 mg,0.8 mg,2.0 mg,5.0 mg,10.0 mg and 15.0 mg,respectively.Besides oral administration of folic acid,Vitamine B6 and B12were supplemented,and other routine treatment were performed.Fluorescence polarization immunoassay was employed to detect the plasma tHcy before and 3 months after the treatment.And the data of plasma tHcy of 210 patients without SSHL were collected and served as controls.The levels of plasma tHcy were statistically analysed between the SSHL group and control group and among group A to group G. Results The level of plasma tHcy in the SSHL group was significantly higher than that in the control group,(18.07?1.58)?mol/L vs(13.63?1.33) ?mol/L(P0.05). Conclusion The levels of plasma tHcy are significantly increased in SSHL.Folic acid may play an important role in decreasing the levels of tHcy in patients with SSHL,and a dosage of 10 mg/d for oral adminstration is well suggested.

Effect of Myocardial Ischemic Preconditioning on Ischemic/Reperfusion Injury in High Blood Fat Rat / 上海第二医科大学学报

Objective To study the effect of myocardial ischemic preconditioning on activity of ATPase and creatine kinase(CK) in high blood fat rat. Methods High blood fat rat mode was established from SD rats.The rats were randomly divided into three groups: ischemic preconditioning(IPC), ischemic/reperfusion(I/R) and control group.The activity of CK in coronary outflow,the activity of malonyldialdehyde(MDA),superoxide dismutase(SOD),glutathione perodxidase(GSH-Px) and ATPase in myocardium were dectected. Results CK and MDA were significantly less in IPC group than those in I/R group.In IPC group,the activity of SOD,GSH-Px,Na~(+)-K~(+)-ATPase,Ca~(2+)-ATPase and Ca~(2+)-Mg~(2+)-ATPase were much higher than those in I/R group. Conclusion Myocardial ischemic preconditioning can protect high blood fat rat from ischemic/reperfusion injury.