Objective To study the effect and intrinsic mechanism of acute suppurative peritonitis associated ascitic fluid (ASPAAF) on experimental liver injury of rats. Methods Thirty-two male or female Sprague-Dawley (SD) rats were randomly divided into two groups: ASPAAF group (n=16) and control group (n=16), in which 8 ml ASPAAF or normal saline (NS) were injected into the peritoneal cavity, respectively. The rats were killed at each time intervals after peritoneal cavity injection (6 h and 12 h) respectively in two groups and specimens were made to detect the levels of serum TNF-α, endotoxin and liver function (AST, ALT and STB). The level of TNF-α in liver tissues was measured. The pathological change of liver was observed by microscope. Results The levels of TNF-α, endotoxin, ALT, AST and STB in serum and the levels of TNF-α in liver tissues at different time points were markedly higher in ASPAAF group compared with those in control group (P＜0.05), and these indexes increased with increasing time in ASPAAF group (P＜0.05). In ASPAAF group, hepatic tissue appeared hydrops, even spotty necrosis and the changes at 6 h and 12 h were not obvious different. No abnormal pathological change of hepatic tissue was found in control group. Conclusion ASPAAF can induce the injury of the liver in rats, which may involved in TNF-α and endotoxin.
ObjectiveTo discuss the changes of myelin basic protein (MBP), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) in serum and cerebrospinal fluid of experimental pancreatic encephalopathy rat model, analyze the relationship between each factor and the occurrence and development of pancreatic encephalopathy, and to provide the experimental basis for clinical diagnosis and treatment of pancreatic encephalopathy.
MethodsSelecting 40 SD rats were randomly divided into sham operation group (SO group, n=10) and pancreatic encephalopathy group (PE group, n=30), respectively by the duodenal papilla retrograde pancreatic puncture injection of saline solution or 5% sodium taurocholic acid induced rat pancreatic encephalopathy model were set up. The rats in SO group were sacrificed on 1 d, and the PE group were sacrificed ten rats on 1 d, 3 d, and 7 d, respectively after surgery. The brain and pancreatic tissues of rats in each group were taken to observe the pathological changes of the rats and the brain white blood cells within microvessels gathered and coanda phenomenon. The water content of brain tissues, and the contents of MBP, TNF-α and TL-6 in serum and cerebrospinal fluid were detected.
ResultsThe changes of brain nerve cell edema and nerve fiber demyelination were obvious in PE group rats after surgery with the extension of time. The contents of MBP, TNF-α and TL-6 in serum and cerebrospinal fluid on 1 d, 3 d, and 7 d after surgery in PE group were significantly higher than that SO group (P<0.05), and gradually increased with the extension of time. But by two two compared, the change trend of the above three indicators were different.
ConclusionsMBP, TNF, and IL-6 on the occurrence and development of brain damage of pancreatic encephalopathy play a synergistic effect. To detecte the MBP, TNF-a, and IL-6 content in blood and cerebrospinal fluid could be diagnosed and evaluated the pancreatic encephalopathy.
Objective To study the effects of malondialdehyde (MDA), superoxide dismutase (SOD) and tumor necrosis factor-α (TNF-α) on brain tissue in rats with pancreatic encephalopathy (PE). Methods Thirty-six Wistar rats were randomly divided into control group (n=6) and PE model group (n=30). In control group, rats were injected with normal saline by internal carotid artery (0.1 ml/100 g) and were killed on the first day after the injection. In PE model group, rats were injected with phospholipases A2 (0.1 ml/100 g, 1 000 U/0.1 ml) by internal carotid artery, to establish animal model of PE in rat and 10 rats were killed on day 1, 3, 7 respectively after the injection. The changes of water content in the brain were measured. Leucocytes aggregation and margination in the microvessels, and the changes of cerebral cells and nerve fibers were observed. The levels of MDA, TNF-α and the activity of SOD were tested in the brain homogenate in rats. Results In PE model group, water contents of brain increased; The phenomena of leucocytes accumulation and margination, cellular edema of neurons and demyelination of nerve fibers became more obvious; The levels of MDA and TNF-α increased significantly than those in the control group, while the activity of SOD reduced (P＜0．05， P＜0.01)． Conclusion Inthe rat model of PE, MDA, SOD, and TNF-α play important roles on the occurrence and development of brain injury.
ObjectiveTo investigate the protective mechanism of prostaglandin E1 against hepatic ischemia reperfusion injury.MethodsUsing 45minute ischemiareperfusion rat model in normal temperature, PGE1 was injected into portal vein before ischemia. An hour later blood was taken from portal vein to examine the enzyme levels, including GOT, GPT, LDH and TNFα, ET1. The alteration of pathological morphology of the ischemia lobe was observed.ResultsThe three enzemes, TNFα, ET1 levels of ischemiareperfusion group were significantly higher than those of the control group (P＜0.01). The indices of the PGE1 group were much lower than those of the ischemiareperfusion group (P＜0.01), but little higher than those of the control group (P＞0.05). The control group had obvious alteration in pathological morphology, but only slight alteration in PGE1 group, compared with the control group. ConclusionPGE1 protects against ischemiareperfusion injury of the liver.
ObjectiveTo investigate the expression of tumor necrosis factor α(TNF-α ) in isolated rat heart at different time points after myocardial hypoxia/reoxygenation.
MethodsThe isolated langendorff perfused rat heart model was established. Forty-eight SD rats were randomly divided into four groups: a sham group, hypoxia/reoxygenation groups including a H/R 0.5 h group, a 1 h group and a 2 h group. The heart rate(HR), the 1eft ventricular development pressure(LVDP), maximal rates of increase/decrease of the left ventricular pressure(±dp/dtmax) were continuously recorded. The concentrations of TNF-α and creatine kinase-MB(CK-MB) in myocardium, mRNA expression of TNF-α in myocardium were tested. Ultra structure of myocardium was observed under electron microscope.
ResultsThe levels of LVDP, ±dp/dtmax, and HR of hypoxia/reoxygenation group were significantly lower than those in the sham group(P<0.05).The levels of TNF-α and CK-MB and the expressions of TNF-α at mRNA level in the hypoxia/reoxygenation group were higher than those in the sham group(P<0.05).There were significant differences in the above parameters among the H/R 0.5 h group, the 1 h group, the 2 h group(P<0.05).The concentrations of TNF-α and CK-MB, the mRNA expression of TNF-α were higher in the I/R 2 h group than those in the other two groups.
ConclusionThe high expression of TNF-α in myocardium after myocardial hypoxia/reoxygenation in rats is related to the degree of myocardium damage and may lead to myocardial injury.
【Abstract】ObjectiveTo explore the effect of glutamine on immune function of rat with obstructive jaundice and its possible mechanism. MethodsFifty male Wistar rats were randomly divided into three groups: Control group (n=10)， obstructive jaundice group (n=20) and glutamine treatment group (n=20). The serum concentration of TNF-α, IL-10 was detected by using radioimmune method. Liver function was measured through automated biochemistry analyzer. The animal model of obstructive jaundice was established by ligating the rat’s common bile duct. Bacteria cultures were performed with the rat’s tissues of lung, spleen, liver and kidney respectively. ResultsCompared with control group, obstructive jaundice group showed statistically lower serum level of TNF-α, and statistically higher serum level of IL-10, TBIL, ALT and AST during the first and the second week after ligation of common bile duct. During the first and second week after administration of glutamine, the serum TNF-α of glutamine treatment group was statistically higher than that in control group and obstructive jaundice group. Meanwhile, glutamine treatment group showed statistically lower serum level of IL-10, TBIL, ALT and AST than obstructive jaundice group. There were statistically less bacteria translocations in glutamine treatment group than those in obstructive jaundice group. Conclusion Glutamine can increase the immune function by changing serum concentration of TNF-α, IL-10 and decrease the bacteria translocation.
ObjectiveTo investigate the inhibitory effects of L arginine (L arg) on systemic inflammatory response after cardiopulmonary bypass(CPB).MethodsFifty one patients with rheumatic heart disease were randomly divided into two groups: L arg group ( n =25) and control group ( n =26). For L arg group, L arg at 300mg/kg was given during operation. Plasma levels of tumor necrosis factor α(TNF α),interleukin 1β(IL 1β)and interleukin 10(IL 10) were measured by enzyme linked immunosorbent assay technique at baseline(before operation) and at 2,4,8,24 and 48 h after CPB termination.ResultsTNF α,IL 1β and IL 10 levels were increased in both groups after CPB ( P lt;0.05); levels of TNF α, IL 1β returned to normal at 48 h after CPB; In L arg group, TNF α and IL 1β levels were significantly lower than those in control group at 4,8 and 24 h after CPB ( P lt; 0 05). No significant difference were detected in IL 10 between groups( P gt;0.05).ConclusionL arg may decrease plasma levels of TNF α and IL 1β after CPB, it implies L arg may inhibit inflammation induced by CPB.
ObjectiveTo investigate the anti-inflammatory mechanism of sodium aescinate in preventing postoperative intestinal adhesion in rats.
MethodsThe SD rats were subjected to operation for establishing intestinal adhesion models, then randomly divided into model group, dexamethasone group(dexamethasone, i.v. 5 mg/kg), and sodium aescinate group(sodium aescinate, i.v. 2 mg/kg), 10 rats in each group. Another ten normal rats were selected as sham operation group. One times administration was administered on day 1 before establishing adhesion model, and administration for 3 d after modeling, once a day. On day 7 after operation, all of the rats were killed. The intestinal adhesion was graded and the adhesive tissues were taken for hydroxyproline determination. The levels of tumor necrosis factor(TNF)-α, interleukin(IL)-1β, and IL-6 in the serum were detected by ELISA.
ResultsCompared with the model group, sodium aescinate could obviously improve the severity of postoperative adhesion, markedly decrease hydroxyproline content in the adhesive tissues(P < 0.01), and significantly inhibit the levels of TNF-α, IL-1β, and IL-6 in the serum(P < 0.01).
ConclusionSodium aescinate could effectively prevent the formation of postoperative intestinal adhesion by inhibiting the expressions of inflammatory cytokines and decreasing the inflammatory response.
Objective To investigate the changes and significance of intercellular adhesion molecule-1 (ICAM-1) and tumor necrosis factor-α (TNF-α) in intestinal mucosa in rats with obstructive jaundice. MethodsTwenty-four SD rats were randomly divided into sham operation (SO) group and bile duct ligation (BDL) group, and each group were randomly divided into the day 7 and day 14 subgroup. The expression of ICAM-1 was assayed by immunohistochemistry. The level of TNF-α was determined by ELISA. The activity of myeloperoxidase (MPO) and diamine oxidase (DAO) was determined as well.ResultsOn the day 7 and 14, in the bile duct ligation group, the ICAM-1 protein was mainly expressed in the intestinal epithelia and increased with the time on (P＜0.05); the level of TNFα increased from （14.25±1.01） ng/g to （23.83±1.43） ng/g （P＜0.01）； the intestinal DAO activity decreased from （1.70±0.36） U/mg to （1.22±0.41） U/mg （P＜0.01），and plasma DAO activity increased from （6.44±1.74）U/ml to （8.93±1.29） U/ml （P＜0.01）; the MPO activity increased from （2.85±1.22 ） U/mg to （4.93±1.37） U/mg （P＜0.01）. ConclusionThe ICAM-1 expression is significantly upregulated and the level of TNFα significantly increases after bile duct ligation, which may be involved in the PMNmediated injury to intestinal mucosa.
Objective
To explore the mechanism of Liuhedan in promoting wound healing through applying Liuhedan to the infective wounds of New Zealand white rabbits.
Methods
A total of forty New Zealand white rabbit models of infective wounds were established after anesthesia. Five circular infective incisions were generated on the back of each rabbit, with a diameter of 2 cm. Five wounds of each rabbit were assigned respectively to the control group, model group, traditional Chinese medicine (TCM) group (Oleum Lithospermum), Western medicine group (calcium alginat), and treatment group (Liuhedan). Wound dressings were performed every day since postoperative day 1. Ten rabbits were selected randomly to be euthanized on postoperative day 3, 7, 14 and 21, respectively. Each specimen was divided into two parts. One was used for detecting interleukin-1β (IL-1β) by enzyme-linked immunosorbent assay, and the other was used for detecting tumor necrosis factor-α (TNF-α) by immunocytochemistry.
Results
On postoperative day 3 and 7, groups with the expression of IL-1β from low to high were respectively the control group, the treatment group, the Western medicine group, the TCM group, and the model group [postoperative day 3: (680.81±185.53), (1 028.67±205.57), (1 278.67±251.15), (1 449.86±230.74), (1 544.62±371.77) pg/mL; postoperative day 7: (1 024.43±239.94), (1 333.57±257.31), (1 635.14±222.40), (1 784.71±323.85), (1 953.29±324.78) pg/mL], and all the differences among the groups were significant (P<0.05); On postoperative day 14, groups with the expression of IL-1β from low to high were respectively the treatment group, the control group, the Western medicine group, the TCM group, and the model group [(908.71±108.61), (978.57±161.75), (1 120.43±265.39), (1 129.71±298.06), (1 191.14±234.92) pg/mL], and all the differences among groups were significant (P<0.05) except the difference between the Western medicine group and the TCM group (P>0.05); On postoperative day 21, the expression of IL-1β in the control group, the model group, the TCM group, and the Western medicine group was (487.19±121.80), (496.35±102.15), (500.31±139.34), (499.08±120.67) pg/mL, respectively, with no significant differences among the groups (P>0.05), which were all higher than that in the treatment group [(398.62±102.93) pg/mL] with significant difference (P<0.05). The expression of TNF-α in the model group was significantly greater than those in the other groups. The expression of TNF-α in the treatment group and Western medicine group was significantly lower compared with the model group. The expression of TNF-α in the TCM group was stronger compared with those in the treatment group and the Western medicine group.
Conclusion
Liuhedan can specifically suppress the expressions of IL-1β and TNF-α in the treatment of infective wounds, decrease the release of inflammatory factor and promote the healing.
