The effect of human complement C5b~9 complex on nitric oxide synthesis in glomerular mesangial cells of rats

AIM:To study the effect of human complement C_5b~9 complex on nitric oxide(NO) synthesis of glomerular mesangial cells (MC). METHODS: First, the human complement C_5b~9 complexes were isolated and glomerular MC of rats were cultured. Second, the MC were stimulated with C_5b~9 complex and changes of metabolism products of NO(NO₃^- and NO₂) in MC culture supernatant at 6,24 and 48 hours after C₊5b~9 stimulating were detected. Moreover, cGMP levels in cultured MC were also measured. RESULTS: NO₃^-／NO₂^- contents from culture supernatant and cGMP levels in MC were increased parallelly after C_5b~9 complex stimulation. Further, NO synthesis was inhibited by L-N^G-nitro-arginine-methylester(L-NAME). CONCLUSION: NO synthesis of rat glomerular MC was incerased by human complement C_5b~9 stimulation.     

Analysis of glomerular complement C5b-9 deposits and synthesis of NO,TNFα in the model of the rats with anti-thymocyte serum nephritis

AIM: To explore the localization and semi-quantification of the glomerular complement C5b-9 complexes and synthesis of some inflammatory mediators or cytokines such as nitric oxide (NO) and tumor necrosis factor α(TNFα) in the rats with anti-thymocyte serum nephritis(ATSN). METHODS: The animal model of rat ATSN was reproduced by a single intravenous injection of anti-thymocyte serum (ATS). Then, the deposits of glomerular C5b-9 complexes were localized and quantified by immunohistochemical staining and microscopic image scanning separately. And the glomerular mesangial cells (MC) surrounded by C5b-9 complexes were counted under microscope. In addition, the expression of glomerular MC inducible NO synthase(iNOS) mRNA and excretion of urinary NO metabolite (NO^-₂／NO^-₃) and TNF α in the rats with ATSN were detected. RESULTS: The MC in the rats with ATSN emerged necrosis followed by a rapid proliferation. In the early time of MC injury, the C5b-9 complexes were mainly seen in glomerular mesangium and MC surface. But with the progression of ATSN, the MC enclosed by C5b-9 appeared gradual decrease. Moreover, the expression of MC iNOS mRNA in early stage of ATSN obviously increased and the excretion of urinary NO^-₂／NO^-₃ and TNF α also significantly increased. However, the changes of parameters mentioned above in ATSN proliferative stage (after 7 days) alleviated gradually. CONCLUSION: The secondary lysis of MC has relation to the deposition of C5b-9 complexes and synthesis and release of NO and TNF α in rats with ATSN.     

Mechanisms of nitric oxide synthesis induced by human complement C5b-9complex in glomerular mesangial cells of rats

AIM: To explore the mechanism of the nitric oxide (NO) synthesis induced by human C5b-9 complex in glomerular mesangial cells(MC) of rats. METHODS: The MC of rats were cultured and stimulated with human complement C5b-9 complex to induce TNFα and IL-1β. At the same time, several parameters related to NO synthesis were measured at 3 h, 6 h and 24 h after C5b-9 stimulation. The effects of monoclonal antibodies against TNFα and IL-1β on NO synthesis were examined in this system. RESULTS: TNFα concentration in supernatant from MC in C5b-9 group was higher than that of control group at 6, 24 h after stimulation with C5b-9 complex and reversed by adding anti-TNFα McAb. C5b-9 complex didn't stimulate the release of IL-1β in same system. In addition, the expression of iNOS mRNA in MC was observed at 3 h after stimulation with C5b-9. Levels of iNOS mRNA expression and cGMP in MC and NO₃^-/NO₂^- in supernatant from MC in C5b-9 group were higher than those in control group at 6, 24 h after C5b-9 stimulation, these changes were also reversed by adding monoclonal antibody against TNFα. CONCLUSION: C5b-9 complex could induce iNOS mRNA expression at 3 h after C5b-9 stimulation, and the synthesis of NO at 6, 24 h was related to TNFα released from cultured MC of rats by C5b-9 complex to a certain extent.     

The kinetic alteration of nitric oxide formation in the lungs in the development of pulmonary fibrosis of rats

AIM: To observe the kinetic alteration of nitric oxide formation in the lungs in the development of pulmonary fibrosis in the rat. METHODS: The contents of hydroxyproline in the lungs, NO₂^-/NO₃^- (nitrite/nitrate) in out-flowing and in-flowing pulmonary blood (OPB, IPB) were assayed on the day 7, 14, 21, 30 and 70 after intratracheal administration of bleomycin A₅ . The content of NO₂^-/NO₃^- in supernatants of culture of the alveolar macrophages (AMs) and the amount of iNOS positive stain cells in lung tissue section were also observed in the rat on 14th day after-bleomycin A₅ administration. RESULTS: The content of lung hydroxyproline had no change on the 7th day, increased on the 14th day (P＜0.05), increased significantly on the 21th day, 30th day and 70th day post-bleomycin A₅ compared with control rats. On the 7th day and 14th day, the content of NO^- ₂ /NO₃^- increased in OPB and decreased in IPB (P＜0.01). On the 21th day, the content of NO₂^-/NO₃^- abated in OPB (P＞0.05) but still decreased in IPB (P＜0.01). On the 30th day and the 70th day, the NO₂^-/NO₃^- level recovered both in OPB and IPB. AMs from rats on the 14th day post-bleomycin A₅ showed significant elevation (P＜0.01) in NO₂^-/NO₃^- level. The amount of iNOS positive stain cells increased in rats on the 14th day post-bleomycin A₅. CONCLUSION: The amount of NO in the lungs was high in the initial phase of fibroproliferative reaction induced by bleomycin A₅ ,and these might be associated with the enhanced ability of AMs to release NO and the increased amount of iNOS.     

Changes of nitric oxide synthase and nitric oxide in lung of smoking rats

AIM:To observe the changes of iNOS and eNOS in lung tissue and NO in bronchoalveolar lavage fluid (BALF) in smoking rats.METHODS:80 Wistar rats were divided into control, smoking group, L-NIL group and L-NAME group (rats were exposed to smoke and injected (i.p.) with selective iNOS inhibitor L-NIL or NOS inhibitor L-NAME). iNOS and eNOS protein levels in whole lung were detected by immunohistochemical staining, and NOS mRNA was quantified using RT-PCR. In addition, NO₂^-/NO₃^- was determined using Griess assay.RESULTS:The expression of iNOS mRNA and protein in smoking rats increased, the expression of eNOS mRNA and eNOS protein decreased, and the total cell count and the level of NO₂^-/NO₃^-in BALF increased(P＜0.05). In vivo, L-NIL reduced the total cell count and NO₂^-/NO₃^- in BALF (P＜0.05), while L-NAME had no effect on them.CONCLUSION:Cigarette smoke increased expression of iNOS mRNA and protein and decreased expression of eNOS mRNA and protein. The large amount of NO generated by iNOS may amplify inflammation in lung tissue.     

Study on changes of ET、NO level and tumor weight of mice bearing S180 model and their relationships

AIM: To approach the changes of ET and NO levels of mice bearing sarcoma 180 (S₁₈₀ ) during different period(5、10 and 15 days) and the relationship between ET、NO and tumor’s development METHODS: Adopting mice bearing S₁₈₀ as the models, the levels of ET and NO₂^-/NO₃^- in serum were detected, and the weight of isolated tumors was measured On the basis of the regulation of these changes, their relationships were explored RESULTS: The levels of ET and NO₂^-/NO₃^- of mice bearing S₁₈₀ were higher than that of the control group (not bearing tumor) ( P< 0.05) Along with the development of the tumors, the levels of NO₂^-/NO₃^-and tumors weight both increased ( P< 0 05) ET also had an increasing tendency There was a positive correlation between the level of NO₂^-/NO₃^- and tumor weight ( r =0.995, P< 0.05) Ratio value of (NO₂^-/NO₃^-)/ET decreased at first and then increased CONCLUSION: ET and NO have links with the development of S₁₈₀ There may be cooperation between ET and NO during the development of tumor.     

Role of endogenous nitric oxide in apoptosis of alveolar epithelial cells in the development of pulmonary fibrosis in rats

AIM: To study the role of high level of endogenous nitric oxide (NO) in apoptosis of alveolar epithelial cells in the development of pulmonary fibrosis in rats. METHODS: The content of nitrite/nitrate (NO₂^-/NO₃^-) in out-flowing pulmonary blood (OPB) was assayed by nitric acid reduction method. The apoptosis of alveolar epithelial cells was observed by TdT-mediated dUTP nick-end labeling (TUNEL) and electron microscopy, respectively. The above indices were observed on the day 14 and the day 30 after intratracheal administration of BLMA₅ alone or along with blockade of iNOS by aminoguanidine (AG) in rats. RESULTS: (1) Both the content of NO₂^-/NO₃^- in OPB and the number of apoptotic alveolar epithelial cells in lung were increased in BLMA₅ 14 d group, compared with normal control group and BLMA₅ 30 d group, respectively (P<0.05). The high level of NO₂^-/NO₃^- in OPB and the apoptosis of alveolar epithelial cells were ameliorated by AG. CONCLUSION: The apoptosis of alveolar epithelial cell is induced by high level of endogenous NO in the development of pulmonary fibrosis.     

Changes in L-arginine/nitric oxide pathway of the aorta in septic shock rats

AIM:To observe the change of nitric oxide (NO) generation system in the vascular adventitia, media and intima in septic shock rats.METHODS:The septic shock model was made in rats by caecal ligation and puncture. The intima, media and adventitia of the rat aorta were separated. NO production (NO₂^-), nitric oxide synthase(NOS) activity and L-arginine (L-Arg) transport were measured, separately. Inducible NOS (iNOS) distribution was detected by immunohistochemistry.RESULTS:Both in early and late stage of septic shock, NO₂^- from the intima was decreased by 66.1% and 78.9%(P<0.01), while NO₂^- from the media was increased by 1.1 and 2.2 folds(P＜0.01), and the adventitia 9.6 and 18.6-fold (P＜0.01), as compared with the sham group, respectively. The changes of NOS activity and the L-arginine transport in the intima, the media layer and the adventitia of the aorta in the septic shock rat paralleled with that of NO₂^- in these tissues. The results of iNOS immunohistochemistry showed that there were obviously positive staining in the media layer and adventitia, especially the adventitia of the rat aortas in septic shock, as compared with that in the sham control.CONCLUSIONS:During septic shock, NO production in the aortic intima was progressively suppressed. However, it was progressively increased in the aortic medial layer and adventitia, especially the adventitia with shock processes. These changes result from different changes of L-arginine transport, NOS activity and its expression in three layers of the aorta from the septic shock rat.     

Protective effects of extract of Ginkgo biloba on diaphragm of diabetic rats

AIM: To investigate the effects of extract of Ginkgo biloba (EGb) on diaphragm from diabetic rats. METHODS: Sprague-Dauley rats were divided into three groups: normal control, diabetic group and EGb treatment group. The morphologic changes of diaphragm tissues were studied by light and electron microscopy, the activities of succinate dehydrogenase (SDH), superoxide dismutase (SOD), nitric oxide synthase (NOS) and contents of malondialdehyde (MDA), nitric oxide (NO₂^-/NO₃-) in the diaphragm mitochondria were assayed by spectophotometer, respectively. RESULTS: The activities of SOD, SDH decreased in diabetic diaphragm mitochondria, but the activitiy of NOS, the contents of NO₂^-/NO₃^-, MDA increased compared with control group. The activities of SOD, SDH were increased as well as NOS were decreased and the contents of NO₂^-/NO₃^-, MDA decreased in EGb treatment group compared with the diabetic group. CONCLUSION: EGb may protects the diaphragm mitochondria of diabetic rats by enhancing the function of respiratory chain, anti-oxidation and decreasing NO level.     

Effects of taurine-magnesium complex on vascular endothelium and hemorheology in rats in vivo

AIM: To study the protective effects of taurine-magnesium complex (TMC) on endothelium and hemorheology in rats. METHODS: A model of the endothelial damage was made by means of giving rats an injection of adrenaline and making them swim in ice-cold water, then number of circulating endothelial cells (CEC) in whole blood, plasma ET-1 and NO₂^-/NO₃^- content, NOS activity and rheology were determined, respectively. The protective effects of TMC were also observed. RESULTS: An increase in the number of CEC accompanied by abnormal whole blood viscosity, and endothelium-derived ET-1 were observed in model rats. Both the NO₂^-/NO₃^- content and NOS activity were declined significantly in model rats. TMC reduced the number of CEC, resumed NO₂^-/NO₃^- content and NOS activity, and improved the whole blood viscosity in a dose-dependent manner in model rats. CONCLUSION: Ice-cold water bath with adrenaline causes an acute damage of vascular endothelium and abnoramal rheology. TMC protects against the injury of vascular endothelium and improves the hemorheology.     

The dynamic changes of plasma nitric oxide and endothelin-1 in prehepatic portal hypertension rats

AIM:To observe the dynamic changes of plasma levels of nitric oxide(NO) and endothelin (ET-1) in portal veins of the rats during prehepatic portal hypertension, and investigate the role of them in hyperdynamic circulation.METHODS:The models of prehepatic portal hypertension were established in Sprague-Dawley rats by means of partial portal vein ligation (PVL). The plasma levels of nitrite/nitrate (NO₂^-/NO₃^-) and ET-1 in the portal veins were detected by the method of nitric reductase and radioimmunoassay, respectively. In this study, rats were divided into normal, sham operation (SO) and PVL group. SO and PVL rats were divided into several subgroups according to different time after operations. Meanwhile, the changes of several hemodynamic indexes in these rats were also measured.RESULTS:The levels of NO₂^-/NO₃^- were significantly increased and ET-1 were significantly decreased in rats at different time after PVL compared with normal control, whereas the hemodynamic indexes changed accordingly.CONCLUSION:The portal hypertensive rats are in hyperdynamic circulatory state (HCS). NO and ET-1 may play an important role in the induction and maintenance of HCS.     

The protection of the hepatic ischemic preconditioning is concerned with the NO/ET-1 system

AIM: To study the relationship between the disturbance of nitric oxide/endothelin-1(NO/ET-1) and hepatic ischemia/reperfusion(I/R) injury as well as the regulation of NO/ET-1 system by hepatic ischemic preconditioning(IPC). METHODS: The changes of NO/ET-1 system and their relationship with hepatic I/R injury were compared between I/R group and IPC+I/R group in a rat hepatic I/R model. Two hours after reperfusion, the liver tissues were detected by RT-PCR to see whether there was inducible nitric oxide synthase (iNOS) mRNA expression. RESULTS:In the acute phase of hepatic reperfusion, the ratio of NO/ET-1 was reduced, which was due to a significant reduction of NO₂^-/NO₃^- (the metabolic product of NO) and significant elevation of ET-1 in the blood plasma. The content of ALT, AST, LDH and TNF-α in blood plasma, and of MDA in liver tissue were increased but ATP in liver tissue was reduced, the hepatic damage was deteriorated. The protection of the hepatic IPC was concerned with the elevation of the ratio of NO/ET-1 caused by the elevation of NO₂^-/NO₃^-, and reduction of ET-1 as well. There was no iNOS mRNA detected in the liver tissues.CONCLUSION: Hepatic I/R injury is related to the disturbance of NO/ET-1. The protection of the hepatic IPC in the acute phase might be conducted by its regulation of NO/ET-1 system. The cNOS rather than the iNOS generated the NO in this situation.     

Effects of nitric oxide on hepatic encephalopathy in cirrhotic rats induced by LPS

AIM: To investigate the effects of nitric oxide (NO) on hepatic encephalopathy in cirrhotic rats induced by LPS. METHODS: The cirrhotic model of rats was established by complex pathogeny. Since the end of the 8 th week, the rats were intragastrically-infused with 0.9% salt, L-arginine(L-arg) and LNNA respectively for 2 weeks.The hepatic encephalopathy in cirrhotic rats were induced by 3 mg/kg LPS (ip) 4 hours before the rats were sacrificed. RESULTS: The normal behaviors and electroencephalograph were appeared in L-arg group. LNNA group showed hepatic encephalopathy. The content of NO₂^-/NO₃^- of brain tissue was markedly higher in L-arg group than LNNA group(P<0.05), but the content of histamine in brain tissue was lower in L-arg group than LNNA group(P<0.05). There was a negative correlation between the content of histamine in brain tissue and the content of NO₂^-/NO₃^- of brain tissue. CONCLUSION: NO can prevent hepatic encephalopathy in cirrhotic rats induced by LPS.     

Phenytoin inhibited changes in nitric oxide of rat hippocampus induced by stress

AIM: To investigate the changes in nNOS and iNOS expression of hippocampal CA3 pyramidal neurons and NO₂^-/NO₃^- level of hippocampal homogenate of rats induced by stress, and to explore the effect of phenytoin on them. METHODS: Rats were subjected to forced-swimming stress, phenytoin was administered(ip) at 30 min before stress. Using the immunohistochemistry and the computerized image technique, the expression levels of nNOS and iNOS of rat hippocampal CA3 pyramidal neurons were assayed quantitatively, and the NO₂^-/NO₃^- level of hippocampal homogenate was also measured using nitric acid deoxidize enzyme method. RESULTS: The nNOS average grey degree of hippocampal CA3 pyramidal neurons was significantly lower in stress group (155.42±3.77)than that in control group(164.54±4.62)and in stress plus phenytoin group(164.27±2.55)(P<0.01); The iNOS relative sectional area proportion of hippocampal CA3 pyramidal neuron was significantly larger in stress group(5.87%±2.90%) than that in control group (0.90％±0.89%) and in strers plus phenytoin groups (0.90%±0.88%)(P<0.01); The NO₂^-/NO₃^- level of hippocampal homogenate was significantly higher in stress group(42.75 umol/L±14.49 umol/L)than that in control group(21.23 umol/L±6.99 umol/L)and in stress plus phenytoin group(18.40 umol/L±8.11 umol/L)(P<0.01). CONCLUSION: It is suggested that the stress could induce nNOS and iNOS expression in CA3 pyramidal neurons and excessive production of NO in hippocampus of rats, which could be inhibited by phenytoin.     

Protective effect of Ginkgo biloba extract on testicular tissue of diabetic rats

AIM: To investigate the protective effect of Ginkgo biloba extract (GBE) on diabetic testis and explore its possible mechanism. METHODS: Testicular structure of streptozotocin-induced diabetic rats was observed under light microscopy (LM) and transmission electron microscopy (TEM). Content of malondialdehyde (MDA), NO₂^-/NO₃^- and activity of superoxide dismutase (SOD), nitric oxide synthase (NOS) were determined in testicular homogenate. RESULTS: In diabetic rats, it was manifestated as deformation of seminiferous tubule, atrophy and shedding of germinal epithelium under LM, while expansion of smooth endoplasmic reticulum, formation of fatty vacuoles and decrease of lysosome obviously in the cytoplasm of sertoli cell under TEM, the injury of testicular tissue was improved by GBE. Compared with diabetic rats, activity of SOD increased while activity of tNOS and iNOS, content of MDA and NO₂^-/NO₃^- decreased in GBE-treated rats. CONCLUSION: GBE could effectively prevent the development of diabetic testis and the effect may be partly achieved by resisting lipid peroxidation,restraining the activity of testicular tissue iNOS and reducing the pathological alterations of NO.     

Effects of NG-nitro-L-arginine on LPS-induced lung injury in rats

AIM: To investigate the effects of nitric oxide (NO) and NO synthase (NOS) inhibitor N^G-nitro-L arginine (L-NA) on LPS induced-lung injury in rats. METHODS: Forty healthy male SD rats, weighing 300±20 g, were used. The animals were anesthetized with 20% urethane 1 g·kg^-1. Common carotid artery (CAA) and jugular vein were exposed through a median incision in the neck. Mean arterial pressure (MAP) was measured through a pressure transducer connected with intubation of CAA. The animals were randomly divided into five groups: group 1: control; group 2: LPS (5 mg·kg^-1, iv); group 3: high dose L-NA (20 mg·kg^-1 intraperitoneal injection, ip); gropu 4: middle dose L-NA (10 mg·kg^-1, ip); group 5: low dose L-NA (5 mg·kg^-1, ip). Group1 : 0.9% saline solution was given and the animals were killed 6 h after the saline solution. Gruop 2: saline solution was given 3 h after LPS and the animals were killed 3 h after administration. Group 3, 4 and 5: L-NA was given 3 h after LPS iv and the animals were killed 3 h after administration, respectively. The pulmonary was removed immediately. The pulmonary coefficient and water content in pulmonary tissue were calculated (%). The NO₂^-/NO₃^- content in plasma, MDA content and NOS, SOD activity in the pulmonary tissue were measured. RESULTS: L-NA significantly decreased pulmonary coefficient and water content in pulmonary tissue and ameliorated LPS induced lung injury. The effect in high dose group was better than that in low dose group. L-NA significantly decreased NO₂^-/NO₃^- content in plasm, decreased MDA content and inhibited NOS activity and enhanced SOD activity in the pulmonary tissue. CONCLUSION: It may be concluded that L-NA has a beneficial effect on lung injury induced by LPS.     

Effect of nitric oxide and peroxynitrite on lung injury induced by ischemia-reperfusion of hind limbs in rats

AIM:To observe the changes in nitric oxide(NO) and peroxynitrite anion (ONOO^- ) in the injuried lung following the ischemia-reperfusion of hind limbs and evaluate the contribution of NO and ONOO^- to tissue injury.METHODS:A model of hind limbs ischemia was made by clamping infrarenal aorta with a microvascular clip and lung injury occurring after reperfusion.Lung t issue was obtained from the animals received sham operation(group 1),4 hours ischemia without reperfusion(group2),1 hour reperfusion following 4 hours ischemia(group3)and 4 hours reperfusion fol owing 4 hours ischemia(group4).The contents of MDA,NO₂^-/NO₃^- and the activities of SOD in the lung were examined.Immunohistochemical echnique was used to determine the immunoreactivity to iNOS and nitrotyrosine(NT)-a specific "footprint" of peroxynitrite.RESULTS:Compared with group1 and group2,the contents of MDA and NO₂^-/NO₃^- increased significantly (P<0.05) and the activities of SOD decreased markedly(P＜0.05) in group3 and group4.Immunohistochemical examination demonstrated intense staining for iNOS and NT throughout the lung in group3 and group4.CONCLUSION:NO and ONOO^- are involved in oxidant-mediated lung injury following reperfusion of ischemic hind limbs.     

The augmentative effect of inducible nitric oxide synthase on pulmonary fibrosis progression

AIM: To study the up-regulation of inducible nitric oxide synthase (iNOS) in lung of pulmonary fibrosis and its relationship with fibrosis. METHODS: The changes of amount of iNOS positive stain cells and type Ⅰ?Ⅲ collagen were examined on the day 7, 14 and 30 after intratracheal administration of bleomycin A₅. The contents of NO₂^-/NO₃^- (nitrite/nitrate) in out-flowing pulmonary blood (OPB), hydroxyproline in lung and the histological changes were detected after iNOS was blocked by aminoguanidine (AG). RESULTS: (1) The number of iNOS-positive stain cells increased significantly in BLMA₅ 7 d, 14 d and 30 d groups compared with that in control group (P<0.01). Furthermore, the increment of the number of iNOS-positive stain cells in BLMA₅ 7 d, 14 d groups was more than that in BLMA₅ 30 d group. There was an increment of collagen in BLMA₅ 14 d group and in BLMA₅ 30 d group , with an increase in type Ⅲ collagen in BLMA₅ 14 d group and an increase in type Ⅰcollagen in BLMA₅ 30 d group. (2) The high level of NO₂^-/NO₃^- in OPB and hydroxyproline level in lung could be reversed by AG, a selective inhibitor of iNOS. Large amount of fibroblasts and macrophages were also abated by AG. CONCLUSION: In the development of pulmonary fibrosis, the expression of iNOS is up-regulated, which induces nitric oxide (NO) production and promotes propagation of pulmonary fibrosis.     

Effect of Xin-Tong capsule on nitric oxide production and cGMP content of ventricular myocardium in rats with experimental myocardial ischemia

AIM:To study the effect of xin-tong capsule on nitric oxide production and cGMP content of ventricular myocardium in rats with experimental myocardial ischemia. METHODS:Rat model of acute myocardial ischemia induced by pituitrin was used in this study, and the lift of ST segment in ECG was used as the index of myocardial ischemia. The NO₂^-/NO₃^- and cGMP contents of ventricular myocardium in rats with myocardial ischemia were determined.RESULTS: NO₂^-/NO₃^- and cGMP contents in ventricular myocardium of myocardial ischemia were (486±59) nmol/g protein and (0.38±0.08) nmol/g protein, respectively, and markedly lower than those of control (P＜0.01). After administration of Xin-Tong capsule, contents of NO₂^-/NO₃^- and cGMP in ventricular myocardium of rats with myocardial ischemia were obviously elevated . In comparison with control, ST segment of ECG in rats with myocardial ischemia was lifted, and the lift peak of ST segment occur in 45 min after myocardial ischemia (P＜0.01). Pretreatment of Xin-Tong capsule can improve conditions of myocardial ischemia . CONCLUSION:Xin-Tong capsule can elevate the contents of nitric oxide and cGMP, and attenuate myocardial ischemia injury in rats.     

Relationship between levels of IL-2, TNF-α and nitric oxide in aqueous humor after intraocular lens implantation

AIM: To investigate the relationship between the level of interleukin-2 (IL-2), tumour necrosis factor-α (TNF-α) and nitric oxide (NO) in aqueous humor after intraocular lens implantation. METHODS: New Zealand rabbits were divided randomly into three groups: (1) control group; (2) extracapsular cataract extraction group (ECCE); (3) extracapsular cataract extraction and posterior chamber intraocular lens implantation group (ECCE+IOL). The inflammation in all experimental rabbit eyes was observed via zoom-photo slit-lamp microscope on 1, 3, 7, 14 d and 30 d postoperation. Meanwhile, aqueous humor was drawn for white blood cell (WBC) counting and classifying and for determining IL-2, TNF-α and NO₂^-/NO₃^- contents. RESULTS: (1) The level of IL-2 and TNF-α and NO₂^-/ NO₃^- in aqueous humor of ECCE+IOL group were higher than that in ECCE and control at 1 to 14 days postoperation, respectively, it increased to peak value at 3 to 7 days postoperation and decreased gradually two weeks postoperation; (2) The changes in IL-2, TNF-α and NO₂^-/NO₃^- in each group were basically similer; (3) The changes of IL-2 and TNF-α level were closely related with NO content in aqueous humor (r=0.69, P<0.01 and r=0.98, P<0.01). CONCLUSION: IL-2, TNF-α and NO play an important role in intraocular inflammation intraocular lens implantation.