BD针在重症急性胰腺炎急性肺损伤大鼠模型制备中的应用

Objective To investigate the improvement of BD intravenous catheters used in inducing the model of acute lung injury with severe acute pancreatitis in rats.Methods Total 40 healthy adult male SD rats were randomly assigned to 2 groups,SO group(n=10),SAP group(n=30),4% tauroeholate(0.1ml/kg)was injected via retrograde biliopancreatic ducts by using BD intravenous catheters via duodenal papilla.The serum amylase,blood gas analysis,ascites volume,lung water content and the pathological score of pancreas and lung structure under light microscope were recorded when the SAP model were induced in 3 h,6 h and 12 h.The relative data mentioned as above also detected in SO group after 12 h.Results The score of the SAP group was significantly higher than the SO group in blood amylase,ascites volume,lung water content,PaCO2,pancreas and lung histology(P＜0.05).Meanwhile,PaO2,oxygenation index were decreased significantly(P＜0.05).Conclusion It is efficient to establish simple,reproducible and stabile rat model of acute lung injury with severe acute pancreatitis by using BD intravenous catheters.     

脾切除对肝纤维化大鼠肝脏PDGF-B表达及血清PDGF-BB水平的影响

Objective To explore the effects of splenectomy on hepatic fibrosis and on the expression of PDGF-B in the liver and PDGF-BB in the serum of rats with hepatic fibrosis. Methods By hypodermic injection CCl4, we established 65 rat models with hepatic fibrosis, splenectomies were performed in the three groups at different phases: before hypodermic injection CCl4 (A group), five weeks after hypodermic injection CCl4 (B group), and ten weeks hypodermic injection CCl4 (C group). The control groups were established at the same time, with samples of the livers and serum of the rats taken in different phases. The expressions of PDGF in the liver were detected by immunohistochemistry technique and the degree of hepatic fibrosis was detected by HE staining. The serum levels of PDGF-BB were analyzed by ELISA technique. Results Absorbance values of PDGF-B in the experimental group were significantly lower than the control groups (P＜0. 05). Serum levels of PDGF-BB of the rats after splenectomy were significantly lower than those in the control groups (P＜0.05). HE and Masson's staining showed that the progression of Hepatic fibrosis was slow in the A group. Hepatic pathologic state was significantly relieved in the B group and the inflammation and fibrosis was relieved in the C group. Conclusion Earlier period splenectomy could delay the proceeding of experimental hepatic fibrosis. After splenectomy the decline in the level of PDGF may be one of the mechanisms causing the delay.     

磷脂酶A2在重症胰腺炎肾上腺损伤中的作用

Objective To investigate the role of group Ⅱ A phospholipase A2 ( sPLA2- Ⅱ A) in pancreatitis-associated adrenal injury. Methods Ninety Wistar rats were divided into sham-operation group,pancreatitis group, and pretreated pancreatitis group with sPLA2 inhibitor. The sPLA2 inhibitor was administered by intravenous injection 30 min before induction of pancreatitis. Rats were killed at 0,3,6, 12, and 24 h time points,respectively. Serum corticosterone was measured. Adrenal injury was evaluated by histological examination as well as sPLA2 activity and sPLA2- Ⅱ A protein analysis. Results After induction of pancreatitis, serum corticosterone was increased after 3 h, and declined after 6 h. Adrenal injury aggravated progressively ,and the sPLA2 activity and expression of sPLA2- Ⅱ A protein in adrenal glands were increased obviously in pancreatitis ( P < 0. 05 ). Pretreatment of sPLA2 inhibitor inhibited effectively sPLA2 activity and sPLA2- Ⅱ A expression in adrenal glands, improved 24 h serum corticosterone levels, and reduced significantly the severity of adrenal histological injury (P <0.05). Conclusion sPLA2-Ⅱ A plays crucial role in pancreatitis-associated adrenal injury.     

磷脂酶A2在重症胰腺炎肾上腺损伤中的作用

Objective To investigate the role of group Ⅱ A phospholipase A2 ( sPLA2- Ⅱ A) in pancreatitis-associated adrenal injury. Methods Ninety Wistar rats were divided into sham-operation group,pancreatitis group, and pretreated pancreatitis group with sPLA2 inhibitor. The sPLA2 inhibitor was administered by intravenous injection 30 min before induction of pancreatitis. Rats were killed at 0,3,6, 12, and 24 h time points,respectively. Serum corticosterone was measured. Adrenal injury was evaluated by histological examination as well as sPLA2 activity and sPLA2- Ⅱ A protein analysis. Results After induction of pancreatitis, serum corticosterone was increased after 3 h, and declined after 6 h. Adrenal injury aggravated progressively ,and the sPLA2 activity and expression of sPLA2- Ⅱ A protein in adrenal glands were increased obviously in pancreatitis ( P < 0. 05 ). Pretreatment of sPLA2 inhibitor inhibited effectively sPLA2 activity and sPLA2- Ⅱ A expression in adrenal glands, improved 24 h serum corticosterone levels, and reduced significantly the severity of adrenal histological injury (P <0.05). Conclusion sPLA2-Ⅱ A plays crucial role in pancreatitis-associated adrenal injury.     

Role of spinal cord TNF-α in the development of bone cancer pain in mice

Objective To investigate the role of spinal cord TNF-a in the development of bone cancer pain in mice. Methods Seventy-two 4-6 week old C3H/He mice weighing 18-25 g were randomly divided into 3 groups (n = 24 each) : group I sham operation (group S) ; group II bone cancer pain (group BCP) and group Ⅲ etanercept (group E). Bone cancer pain was induced by implantation of osteosarcoma NCTC 2472 cells into the intramedullary space of right femur in group II and Ⅲ . Group Ⅲ received intraperitoneal etanercept 100 μg at 3 days before and immediately before and day 3 and 6 after tumor cell inoculation. In group S culture medium α-MEM containing no cancer cell was injected instead. The paw withdrawal threshold to mechanical stimuli (PWMT) and paw withdrawal latency to thermal stimuli ( PWTL) were measured before inoculation (baseline) and at day 3, 5,7, 10, 14 after inoculation respectively. Eight animals were killed on the 7th, 10th, and 14th day after inoculation in each group. The spinal cords were removed and TNF-α mRNA expression in the spinal cord was determined by RT-PCR. Results Cancer pain was significantly attenuated by pretreatment with etanercept. The TNF-α mRNA expression in the spinal cord was significantly increased after inoculation and was significantly attenuated by pretreatment with etanercept in group Ⅲ . Conclusion Spinal cord TNF-a is involved in the development of bone cancer pain in mice.     

磷脂酶A2在重症胰腺炎肾上腺损伤中的作用

Objective To investigate the role of group Ⅱ A phospholipase A2 ( sPLA2- Ⅱ A) in pancreatitis-associated adrenal injury. Methods Ninety Wistar rats were divided into sham-operation group,pancreatitis group, and pretreated pancreatitis group with sPLA2 inhibitor. The sPLA2 inhibitor was administered by intravenous injection 30 min before induction of pancreatitis. Rats were killed at 0,3,6, 12, and 24 h time points,respectively. Serum corticosterone was measured. Adrenal injury was evaluated by histological examination as well as sPLA2 activity and sPLA2- Ⅱ A protein analysis. Results After induction of pancreatitis, serum corticosterone was increased after 3 h, and declined after 6 h. Adrenal injury aggravated progressively ,and the sPLA2 activity and expression of sPLA2- Ⅱ A protein in adrenal glands were increased obviously in pancreatitis ( P < 0. 05 ). Pretreatment of sPLA2 inhibitor inhibited effectively sPLA2 activity and sPLA2- Ⅱ A expression in adrenal glands, improved 24 h serum corticosterone levels, and reduced significantly the severity of adrenal histological injury (P <0.05). Conclusion sPLA2-Ⅱ A plays crucial role in pancreatitis-associated adrenal injury.     

磷脂酶A2在重症胰腺炎肾上腺损伤中的作用

Objective To investigate the role of group Ⅱ A phospholipase A2 ( sPLA2- Ⅱ A) in pancreatitis-associated adrenal injury. Methods Ninety Wistar rats were divided into sham-operation group,pancreatitis group, and pretreated pancreatitis group with sPLA2 inhibitor. The sPLA2 inhibitor was administered by intravenous injection 30 min before induction of pancreatitis. Rats were killed at 0,3,6, 12, and 24 h time points,respectively. Serum corticosterone was measured. Adrenal injury was evaluated by histological examination as well as sPLA2 activity and sPLA2- Ⅱ A protein analysis. Results After induction of pancreatitis, serum corticosterone was increased after 3 h, and declined after 6 h. Adrenal injury aggravated progressively ,and the sPLA2 activity and expression of sPLA2- Ⅱ A protein in adrenal glands were increased obviously in pancreatitis ( P < 0. 05 ). Pretreatment of sPLA2 inhibitor inhibited effectively sPLA2 activity and sPLA2- Ⅱ A expression in adrenal glands, improved 24 h serum corticosterone levels, and reduced significantly the severity of adrenal histological injury (P <0.05). Conclusion sPLA2-Ⅱ A plays crucial role in pancreatitis-associated adrenal injury.     

磷脂酶A2在重症胰腺炎肾上腺损伤中的作用

Objective To investigate the role of group Ⅱ A phospholipase A2 ( sPLA2- Ⅱ A) in pancreatitis-associated adrenal injury. Methods Ninety Wistar rats were divided into sham-operation group,pancreatitis group, and pretreated pancreatitis group with sPLA2 inhibitor. The sPLA2 inhibitor was administered by intravenous injection 30 min before induction of pancreatitis. Rats were killed at 0,3,6, 12, and 24 h time points,respectively. Serum corticosterone was measured. Adrenal injury was evaluated by histological examination as well as sPLA2 activity and sPLA2- Ⅱ A protein analysis. Results After induction of pancreatitis, serum corticosterone was increased after 3 h, and declined after 6 h. Adrenal injury aggravated progressively ,and the sPLA2 activity and expression of sPLA2- Ⅱ A protein in adrenal glands were increased obviously in pancreatitis ( P < 0. 05 ). Pretreatment of sPLA2 inhibitor inhibited effectively sPLA2 activity and sPLA2- Ⅱ A expression in adrenal glands, improved 24 h serum corticosterone levels, and reduced significantly the severity of adrenal histological injury (P <0.05). Conclusion sPLA2-Ⅱ A plays crucial role in pancreatitis-associated adrenal injury.