[Effects of sodium aescinate on the apoptosis-related genes in lung injury induced by intestinal ischemia reperfusion in rats].

OBJECTIVE: To investigate the relationship between apoptosis-related genes and lung injury induced by intestinal ischemia reperfusion and to explore the effects and its possible mechanism of sodium aescinate. METHODS: Rat model of intestinal I/R injury was established with clamping of the superior mesenteric artery for 60 min and then clamping was relieved for 60 min. Twenty-four SD rats were randomly divided into three groups with eight rats in each: sham group, intestinal ischemia/reperfusion group (I/R group) and sodium aescinate group (SA + I/R group). Lung wet/dry weight ratio, lung coefficient and Superoxide dismutase (SOD), malondialdehyde (MDA) in plasma and lung tissue were measured, as well as the expression levels of Bcl-2 and Bax proteins in lung tissue were examined using immunohistochemical method. RESULTS: Compared with sham group, lung wet/dry weight ratio, lung coefficient and MDA in plasma and lung tissue were significantly increased, and while the activity of SOD in plasma and lung tissue were decreased significantly in I/R group. At the same time, the protein expression level of Bcl-2 and Bax were significantly increased. But Bax protein expression was much greater than that of Bcl-2, the ratio of Bcl-2 to Bax was decreased significantly in I/R group than that in sham group. Compared with I/R group, lung wet/dry weight ratio, lung coefficient and MDA in plasma and lung tissue were significantly decreased, and while the activity of SOD in serum and lung tissue were significantly increased in SA + I/R group. At the same time, Bax protein expression was significantly decreased, both Bcl-2 protein expression and the ratio of Bcl-2 to Bax were significantly increased in SA + I/R group than that in I/R group. CONCLUSION: Lung injury induced by intestinal ischemia reperfusion is correlated with abnormal expression levels of Bcl-2 and Bax protein which is caused by oxidative injury. Sodium aescinate can protect the lung injury induced by intestinal ischemia/reperfusion (I/R), which may be mediated by inhibiting lipid peroxidation, upregulating Bcl-2 gene protein expression, improving the ratio of Bcl-2/ Bax to inhibit lung apoptosis.

[The protective effects of ischemia preconditioning on the lung injury following with limbs ischemia/reperfusion].

OBJECTIVE: To explore the protective effects of ischemic preconditioning (IPC) on the lung injury following with limbs ischemia /reperfusion (LI/R). METHODS: The models of LI/R injury were constructed in rabbits. The blood from right external jugular vein and left common carotid artery, into and out-flowing pulmonary blood (IPB, OPB) respectively. Superoxide dismutase (SOD), malondialdehyde (MDA), nitric oxide (NO) in IPB and OPB and lung tissues were measured, as well as total nitric oxide synthase (tNOS) and inducible nitric oxide synthase (iNOS) in lung tissues were detected in different groups. The effects of IPC on the lung injury were observed. RESULTS: Compared with sham and before ischemic, the activity of SOD decreased and the content of MDA and NO increased after 4 h ischemia followed by 4 h reperfusion in IPB, OPB and lung tissues. The activity of tNOS and iNOS in lung tissues increased remarkably as well, there was statistical significance (P < 0.05, P < 0.01). SOD increased and MDA, NO, tNOS, iNOS decreased significantly by IPC before ischemia/reperfusion. The correlation analysis indicated that MDA was negatively correlated with SOD and was positively correlated with MDA, NO, iNOS (P < 0.01). CONCLUSION: Oxygen free radicals metabolic confusion of lung occurred in the course of LI/R, IPC could strengthen the resistance of peroxidation in lung and had protective effects on the lung injury following with LI/R.

[Effects of the combination of sandostatin and gardenia jasminoides ellis on pancreatic mitochondria injury in severe acute pancreatitis rats].

OBJECTIVE: To study the protective effects of the combination of sandostatin(SS) and gardenia jasminoides ellis (GJE) on pancreatic mitochondria injury in severe acute pancreatitis (SAP) rats. METHODS: SAP rat model was induced by retrograde injection of 15 g/L sodium deoxycholate into biliary tract. The rats were randomly divided into five groups: SAP group, Sham group, SS group, GJE group, as well as SS and GJE combination group. The changes of Superoxide dismutase(SOD), succinic dehydrogenase (SDH), Na+ -K+ -ATPase, Ca2+ - Mg2+ -ATPase, malondialdehyde (MDA), membrance fluidity of mitochondria in pancreatic tissue were measured. RESULTS: Compared to Sham group, the activities of SOD, SDH, Na+ -K+ -ATPase and Ca2+ -Mg2+ -ATPase in mitochondria were obviously decreased in SAP group, and MDA and microviscosity (eta) were markedly increased (P < 0.01), which were associated with the increase of serum amylase level (P < 0.01). The above-mentioned indexes of GJE group, SS group and combination group were obviously ameliorated in comparison with SAP group (P < 0.01), the improvement in combination group was the best (P < 0.05 or P < 0.01). The correlation analysis indicated that MDA was negatively correlated with SOD, membrance fluidity, as well as the activities of Na+ -K+ -ATPase and Ca2+ -Mg2- -ATPase (r = -0.857, P < 0.01; r = -0.960, P < 0.01; r = -0.966, P < 0.01; r = -0.926, P < 0.01). CONCLUSION: The combination of sandostatin and gardenia jasminoides ellis can protect pancreatic mitochondria injury in severe acute pancreatitis.

[Protective effects and pathogenesis of complex salvin miltiorrhiza on acute mercury poisoning in rabbits].

OBJECTIVE: To study protective effect and pathogenesis of complex salvia miltiorrhiza (DanShen) on acute mercury poisoning in rabbits. METHODS: Models of acute mercury poisoning was made in rabbits. The effect of complex salvia miltiorrhiza on blood urea nitrogen (BUN), copper-protein (CP), lactate dehydrogenase (LDH), acid phosphatase (ACP) and the malondialdehyde (MDA) in plasma, superoxide dismutase (SOD) in erythrocyte and MDA, SOD in tissues homogenate were observed. RESULTS: The administration of complex salvia miltiorrhiza after mercury injection 0.5 h and 9.5 h, decreased BUN, CP, MDA, LDH and ACP, and prevented the reduction of SOD. Compared with mercury poisoning group, the difference was statistical significant (P < 0.05, P < 0.01). CONCLUSION: It is suggested that acute mercury poisoning may result in renal damage but also multiple organ tissues, and complex salvia miltiorrhiza possesses protective effect, through stabilized membranes.

[The protective effects of ischemic preconditioning on the kidney injury following with ischemia/reperfusion of limbs and the possible mechanisms].

AIM: To explore the protective effects of ischemic preconditioning on the kidney injury following with ischemia/reperfusion (I/R) of limbs. METHODS: The models of I/R injury of limbs were constructed in rabbits. The blood from right external jugular vein, renal artery and renal vein represent the peripheral blood, into and out-flowing kidney blood (IKB, OKB) respectively. Superoxide dismutase (SOD), malondialdehyde (MDA), blood uria nitrogen (BUN) in peripheral blood and SOD, MDA, nitric oxide (NO) in IKB and OKB were measured, as well as SOD, MDA, induced nitric oxide synthase (iNOS) in kidney were detected in different groups. The effects of ischemic preconditioning (IPC) on the kidney injury were observed. RESULTS: Compared with control group, the activity of SOD in peripheral blood, IKB, OKB and kidney decreased, and the content of MDA increased after 4 h ischemia followed by 4 h reperfusion. The content of BUN in peripheral blood, NO in IKB, OKB and iNOS in kidney increased remarkably as well. SOD increased and MDA, NO, BUN, iNOS decreased significantly by ischemic preconditioning (IPC) before ischemia/reperfusion. The correlation analysis indicated that MDA was negatively correlated with SOD and positively correlated with NO, BUN. CONCLUSION: Oxygen free radicals metabolic confusion of kidney occurred in the course of I/R of limbs, IPC could strengthen the resistance of peroxidation in kidney and had protective effects on the kidney injury following with ischemia/reperfusion (I/ R) of limbs

[Experimental research of prevention and therapy effect of anisodamine on acute respiratory distress syndrome (ARDS)].

AIM: To study preventive and therapeutic effect of anisodamine on acute respiratory distress syndrome(ARDS) induced by oleic acid and their mechanism of action. METHODS: Model of ARDS was made in rabbits by oleic acid (OA). The effect of anisodamine on the malondialdehyde (MDA), fibronectin (FN), lactate dehydrogenase (LDH) and acid phosphatase (ACP) in plasma, and superoxide dismutase (SOD) in erythrocyte and MDA, SOD and pulmonary surfactant (PS) in lung tissues homogenate and pathological examination of lung were observed. RESULTS: The administration of anisodamine before and after 30 minutes of injection OA decreased MDA, LDH and ACP, prevented the reduction of SOD, FN and PS. Compared with ARDS group, there was marked difference between the two, and alleviated lung injury. CONCLUSION: Anisodamine possesses preventive and therapeutic effects on ARDS by inhibiting lipid peroxidation and stabilizing membranes.

[Effects of shenmai injection on lipid peroxidation in the lung following with ischemia/ reperfusion (I/R) injury of limb].

AIM: To explore the effects of shenmai (Chinese transitional medicine) injection on lipid peroxidation in the lung following with ischemia/reperfusion (I/R) injury of limb. METHODS: The models of I/R injury of limb were constructed in rabbits. Superoxide dismutase (SOD) and malondialdehyde (MDA) in into and out-flowing pulmonary blood (IPB, OPB) and lung tissue were measured, as well as the effects of shenmai injection were observed. RESULTS: Compared with sham group, the activity of SOD in IPB, OPB and lung tissue were decreased, and the content of MDA was increased after 4 h ischemia followed by 4 h reperfusion. SOD increased and MDA decreased significantly by icy shenmai injection 30 min before reperfusion. The correlation analysis indicated that MDA was negatively correlated with SOD . CONCLUSION: Oxygen free radicals metabolic confusion of lung occurred in the course of I/R, shenmai injection can alleviate lipid peroxidation, get rid of free radicals and inhibit the damage of lung.

[Therapeutic effect of zinc sulfate on lung injury during superior mesenteric artery occlusion(SMAO) shock].

AIM: To study preventive and therapeutic effect of zinc sulfate on lung injury during superior mesenteric artery occlusion (SMAO) shock and their mechanism of action. METHODS: Model of rabbit SMAO shock was made. The effect of zinc sulfate on the malondialdehyde (MDA) in erythrocyte membrane and plasma, oxidase (XOD) in plasma, superoxide dismutase (SOD) in erythrocyte and MDA, SOD and pulmonary surfactant (PS) in lung tissues homogenate were observed. RESULTS: The administration of zinc sulfate decreased MDA and XOD, prevented the reduction of SOD and PS, and alleviated lung injury. CONCLUSION: It is suggested that lung is injured during SMAO shock and zinc sulfate possesses preventive and therapeutic effect, through stabilized membrane.

[Function of endothelin-1 in neurogenic pulmonary edema].

AIM: To investigate the role of endothelin-1 in the pathogenesis of neurogenetic pulmonary edema. METHODS: The levels of endothelin-1 in plasma and lung were measured in rats which suffered from diffuse brain injury on Marmarous' model. The changes of endothelin-1 in the lungs were also detected using an immunohistochemical method. RESULTS: After heavy diffuse brain injury in rats, the levels of endothelin-1 in plasma and lung began increasing at 1 hour, and peaked at 6 hour. Though a little declining at 24 hour, it maintained a higher level within 48 hours (P < 0.05). Pulmonary pathology showed that after brain injury there were congestion, swelling in pulmonary microvessels with broadened pulmonary interstitial tissue, and leucocyte infiltration was dominated by neutrophils and monocytes from 1 hour on, which peaked at 6 hour. More serious congestion, swelling and protein effusion in pulmonary alveoli were observed at both 24 h and 48 h. Immunohistochemically, endothelin-1 had more significant expression and higher levels of OD in the experimental groups than that in the control's, the most significance of which was at 6 hour. CONCLUSION: The inflammatory injury mechanism caused by endothelin-1 may play an important role in neurogenic pulmonary edema.

[Influence of astragalus and zinc sulfate on the viscosity in erythrocyte membrane during intestinal ischemia - reperfusion(I/R) injury].

AIM: To study the influence of astragalus and zinc sulfate on the viscosity in erythrocyte membrane during intestinal I/R and their mechanism of action. METHODS: Models of rabbits intestinal I/R injury were made. The effect of astragalus and zinc sulfate on the viscosity and malondialdehyde (MDA) in erythrocyte membrane, superoxide dismutase (SOD) in erythrocyte, oxidase (XO) in plasma and MDA tissues homogenate were observed. RESULTS: The administration of astragalus and zinc sulfate decreased viscosity and MDA and XO, prevented the reduction of SOD, and alleviated I/R injury. CONCLUSION: Lipid peroxidation injury of the erythrocyte membrane was one of the pathogenesis of I/R injury, and astragalus and the zinc sulfate possessed effects of anti-lipid peroxide, stabilized erythrocyte membrane, increased red blood cell deform ability and raised microcircular perfusion.

[The effect of nitric oxide on acute lung injury following ischemia/reperfusion of hind limbs in the rat].

On a model of reperfusion after ischemia in the hind limbs (LIR) of rats, we used aminoguanidine (AG) which inhibits nitric oxide synthase (NOS) and L-arginine (L-Arg), one of the substrates in the process of nitric oxide synthesis, to observe the changes in NO, NOS, malondialdehyde (MDA), myeloperoxidase (MPO) and wet/dry ratio (W/D) in both skeletal muscles and the lung as well as the changes in phosphatidyl choline (PC) of lung surfactant. The morphologic changes were observed with microscopy. It was observed that the values of NOS, MPO, MDA of the muscle and lung in LIR group increased significantly and the content of PC decreased obviously compared with those of the normal control. Pulmonary observation revealed that after LIR leucocyte assembling and infiltration took place, which was dominated by polymorphocytes with broadened pulmonary interstitial tissue. In LIR+L-Arg group the above changes were reversed, and in LIR+AG group the injuries became more serious. The results obtained suggest that the activity of NOS and the production of NO following ischemia/reperfusion of hind limbs increased significantly, and that the endogenous NO may play a protective role during the early stage of acute lung injury after LIR.