Objective To investigate the effects of nitric oxide precursor L-arginine on traumatic pulmonary contusion. Methods Sixty Sprague-Dawley rats were randomly divided into three groups, ie. a normal group, a model group, and a L-arginine group. The model of traumatic pulmonary contusion was established with self-made chest-impacter. Then the rats in the L-arginine group was injected intravenously with L-arginine in a dose of 250 mg/kg. All rats were sacrificed at 24 hours after these models established.Levels of TNF-α and nitric oxide ( NO2 - /NO3- ) in serum were measured by ELISA and diazo-reaction method. Lung wet/dry weight ratio, NF-κB, endothelin-1, apoptotic cell, and ICAM-1 ( intercellular adhesion molecule-1) mRNA expressions in the lung tissue were measured. Results Compared with the model group,TNF-αand lung wet/dry weight ratio decreased significantly in the L-arginine group( P lt; 0. 05) . After the L-arginine treatment, the concentration of nitric oxide, apoptotic index were significantly higher than the model group ( P lt; 0. 05) . The expressions of NF-κB, endothelin-1, and ICAM-1 mRNA in the L-arginine group were lower than those in the model group ( P lt;0. 05) . Conclusion L-arginine treatment can downregulate the expressions of NF-κB, ET-1, ICAM-1 mRNA and apoptosis obviously, and ameliorate the microcirculation of rats lung with traumatic pulmonary contusion.
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.
Objective To study the effects of L-arginine （L-Arg） on cell proliferation, inducible nitric oxide synthase (iNOS) expression and cell cycle in human colon carcinoma cell line LS174 through nitric oxide (NO) pathway. Methods LS174 cells were cultured in medium with L-Arg at different concentrations for different times. MTT method was employed to evaluate the level of the cell proliferation. The production of NO in culture supernatants of LS174 cell was detected with enzyme reduction of nitrate. The distribution of the cell cycle was detected with the flow cytometry (FCM). The expression level of iNOS in the cells was determined by Western blot and SP immunocytochemical staining method. Results The growth of LS174 was promoted by the L-Arg at low concentration (0.125 mmol/L) and inhibited at high concentrations (0.5， 2， 8 and 32 mmol/L). The level of NO was increased with the increasing concentration of L-Arg in culture medium. To compare with the control group, the ratio of cells at S phase was increased after 48 hours’ treatments with high concentrations (0.5, 2, 8 and 32 mmol/L) of L-Arg (P＜0.05, P＜0.01); while there was no obvious difference after treatments with low concentration (0.125 mmol/L) of L-Arg (Pgt;0.05). With the increase of the concentration of L-Arg, the expression of iNOS was increased as compared with control group. The higher the concentration of L-Arg was, the better the effect. Conclusion L-Arg can induce the expression of iNOS resulting in increase the production of nitric oxide (NO). Low concentration of L-Arg can promote the growth of LS174 cells, while high concentration ones can inhibit growth and proliferation. The high concentration of L-Arg could induce S phase arrestion in the cell cycle.
Objective To study the influence of hyperlipemia on rats with acute pancreatits during pregnancy and its mechanism. Methods Seventy two pregnant Sprague-Dawley rats were randomly divided into the test group and the control group， and then they were fed with high fat diet and balanced diet for 16 days separately. Pregnant rats were given intraperitoneal injection with L-arginine for 2 times (one time is 250 mg/100 g, the other is 200 mg/100 g) at an interval of 1 h. The serum triglyceride (TG), serum amylase (AMS), and lipase (LPS) from blood samples were tested just after injection, and 12 h， 18 h， 24 h， 30 h and 48 h after injection respectively, and wet/dry ratio of pancreas were measured. The histopathological score of pancreatic tissue was evaluated based on microscopic changes, and the expression of TNF-α protein was determined by SP immunohistochemical technique. Results After the last injection, the level of TG in the test group was obviously higher than that in the control group in each time (P＜0.05). The peak values of AMS and LPS in the test group appeared at 24， 18 h respectively, while the peaks appeared at 30， 24 h in the control group, respectively, which were significantly lower than those in the test group (P＜0.05). Compared with the control group, the wet/dry ratio of pancreas in the test group increased at 12, 18 and 24 h after injection (P＜0.05); The pathological changes of pancreas in test group was more serious with higher histopathological score at 0, 12, 18 and 24 h (P＜0.05), and expression of the TNF-α protein was higher at 12, 18 and 24 h (P＜0.05), too. Conclusion Hyperlipemia can make L-arginine-induced-acute-pancreatitis during pregnancy earlier occur and lead to more serious injury in pancreas. This study demonstrates that hyperlipemia may be a high risk factor for acute pancreatitis during pregnancy, making a great amount of free fatty acid released from TG and up-regulated the expression of TNF-α.
【Abstract】 Objective To investigate the effect of NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase, on the growth of colorectal cancer xenografts in vivo and on tumor-associated neovascularization. Methods Twenty BALB/c nude mice were randomly divided into control group and study group equally. Human colorectal cancer cell line SL174T was inoculated subcutaneously into nude mice to form transplantation tumors. Saline 0.2 ml was intragastric-administrated to mice in control group and L-NAME （4 mg toties guoties) was administrated orally to mice in study group three times per week for four weeks. The changes of tumors in both groups were recorded and the microvessel density (MVD) was also measured by immunohistochemistry assay. Results L-NAME significantly inhibited the growth of colorectal cancer xenografts in nude mice. The weight of transplantation tumor reduced with the inhibitory rate of 41.36%, and the inhibitory rate of tumor volume was 43.48% in study group. MVD in the study group and control group were 14.83±2.10 and 21.04±3.11, respectively, which showed that the former was significantly lower than that of the control group （P＜0.05）. Conclusion L-NAME may inhibit the growth of colorectal cancer via the suppression of tumor neovascularization.