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Objective To study the protective effect of shenfu injection on cerebral ischemia reperfusion injury in rats.Methods 120 male Sprague Dawley (SD) rats(320-350 g) were randomly divided into sham operation group,model control group,Nimodipine injection group,low,medium and high dose group of shenfu injection according to gender weight.20 males in each group were given medicine once a day for 7 days before operation.The cerebral ischemia model was established by thread embolization after 5 days of administration.In the sham operation group,the other operations were the same as those in the model group except for carotid artery ligation and thread insertion.After 24 hours of perfusion,the neurological score,abdominal aorta blood flow,malondialdehyde (MDA),superoxide dismutase (SOD) and glutathione (GHS) levels in brain tissues were measured.Triphenyltetrazolium chloride (TTC) staining was used to calculate the area of cerebral infarction and pathological examination of brain tissues.Results Compared with the model control group,the middle and high dosage of shenfu injection could obviously improve the nerve function and increase the percentage of cerebral infarction area (P ＜ 0.05);the high dosage group of shenfu injection could obviously decrease the whole blood viscosity (P ＜ 0.01);the middle and high dosage of shenfu injection could obviously reduce the level of MDA in rat brain tissue (P ＜ 0.01) while increasing the levels of SOD and GSH (P ＜0.01),finally could significantly improve the pathological changes of brain tissues such as mild swelling of nerve fibers,mild neuronal degeneration,inflammatory interstitial edema and inflammation.Conclusions Shenfu injection has obvious protective effect on cerebral ischemia reperfusion model in rats.
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Objective To study the protective effect of total trans retinoic acid (ATRA) on renal injury induced by ischemia-reperfusion in rats.Methods 24 Sprague Dawley (SD) rats were divided into 4 groups of (1) Normal control group,(2) Sham operation group,(3) Model group:the model of renal ischemia-reperfusion was established.(4) Retinoic acid treatment Group:ATRA were given by gavage for 7 consecutive days.The rats were killed 24 hours after the model,and the serum and renal tissue were collected.Serum creatinine,tumor necrosis factor-α (TNF-αx) and interferon-γ (IFN-γ) levels,kidney biopsy,renal tubular score,renal damage and renal tissue apoptosis were detected.Results Compared with the model group,the serum creatinine level decreased and the creatinine clearance rate increased in ATRA treated group (P ＜ 0.05);the damage of renal tubular epithelial cells was alleviated in the pathological slices;and the apoptosis rate of renal tubular epithelial cells was decreased (P ＜ 0.05).Serum levels of TNF-α and IFN-γ decreased (P ＜ 0.05).Conclusions ATRA can protect the renal ischemia-reperfusion injury through inhibiting inflammatory reaction and apoptosis.
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Objective To explore effects of dizocilpine (MK-801) preconditioning on excitatory amino acids and inflammatory response in rats induced by cardiac arrest-cardiopulmonary resuscitation (CACPR).Methods 18 male Sprague Dawley (SD) rats were randomly divided into three groups:control group,CA group and CA + MK-801 group.To establish rat models of CA-CPR and keep samples of serum and specimens of brain tissues for following detection.The injury of neurons was observed by HE staining and expression of N-methyl-D-aspartic acid receptor (NMDAR) in brain tissues was detected by Western blot.The concentrations of interleukin 1 beta (IL-1 β) and tumor necrosis factor (TNF)-α in serum were detected by enzyme linked immunosorbent assay (ELISA).Results Neurons in CA group were disorganized,cells shrank,nuclei pyknosis,and cytoplasmic eosinophilia,accompanied by inflammatory cell infiltration.Preconditioning with MK-801 reduced the pathological damage of neuron and degree of macrophage infiltration.The relative expression of NMDAR protein in CA group were significantly higher than that in control group (907.9 ±24.9 vs 321.6 ± 18.4,P ＜0.001).Preconditioning with MK-801 significantly decreased the expression of NMDAR in CA + MK-801 group compared with that in CA group (512.4 ± 21.1 vs 907.9 ± 24.9).The CA group showed significantly increased concentrations of IL-1 β and TNF-α than that in control group (P ＜ 0.001),and this effect was abolished by preconditioning with MK-801.CA rats treated with MK-801 showed higher concentrations of IL-1 β and TNF-α than the control group.Conclusions Cardiac arrest causes pathological injury of neurons,up-regulates expression of NMDAR and aggravates inflammatory response.These results induce the apoptosis of nerve cells.Blocking glutamate receptor with MK-801 can inhibit expression of NMDAR,decrease level of cytokines,down-regulate inflammatory reaction degree therefore to protect the brain.
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Objective To investigate the effect and its mechanism of diazoxide on the blood-brain barrier (BBB) of rats after cerebral ischemia/reperfusion (I/R) injury.Methods Sixty Wistar rats were randomly divided into sham operation group,I/R group,and diazoxide pretreatment groups of low,middle,large dose (5,10,20 mg/kg).The I/R models of rats were performed to undergo middle cerebral artery embolism by thread.BBB permeability was estimated by Evans blue (EB) dyeing,transmission electron microscope (TEM) was used to observe the modification of interendothelial tight junction (TJ) of capillaries.The expression of aquaporin-4 (AQP4) in every rat brain tissues was detected by immunity histochemistry technique.Results (1) Compared to sham operation group,the permeability extent of EB were significantly increased by I/R,which was distinctly attenuated in middle and large dose of diazoxide pretreatment rats,while no obvious changes were found between I/R and low dose groups.(2) TEM showed that TJ of the brain tissue opened after I/R injury and no significant opening of TJ was observed in middle and large dose of diazoxide preconditioning groups.(3) Compared to sham operation group,the expression of AQP4 in the brain tissue of the I/R group was apparently increased (P ＜0.01).Compared to I/R group,the expression of AQP4 was apparently increased in middle and large dose pretreatment groups (P ＜ 0.01),and there were no obvious difference between low dose group and the I/R group.Conclusions Preconditioning of ischemia/reperfusion injury with diazoxide protects the blood-brain barrier,which may due to keep the TJ closed and decrease expression of AQP4 protein.
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Objective To investigate the effect of fluvastatin on the expressions of caspase-12,CCAAT/enhancer-binding protein homologous protein(CHOP), and c-Jun N-terminal kinases (JNK) in ischemia-reperfusion brain injury in rats.Methods Forty two rats were randomly divided into sham operation group (6 rats), ischemia-reperfusion (I/R) group (18 rats), and fluvastatin (Flu) group (18 rats).The rats of I/R and Flu groups were molded by modified Longa intraluminal thread, then put to death at 2 h occlusion and 24 h reperfusion point.Expressions of caspase-12, CHOP, and JNK were detected with immunohistochemistry and Western blot.Results Immunohistochemistry and Western blot showed that the expressions of caspase-12, CHOP, and JNK were increased at 24 h reperfusion.Compared to I/R group, the expressions of caspase-12 and CHOP in Flu group were decreased significantly (all P ＜0.01);and the expression of JNK had no difference between I/R and Flu groups(P ＞ 0.05).Conclusions The increased expression of caspase-12, CHOP, and JNK showed that endoplasmic reticulum stress was involved in the pathological process of ischemia-reperfusion brain injury.Fluvastatin could inhibit the expression of caspase12 and CHOP, and could delete endoplasmic reticulum stress (ERS) in ischemia-reperfusion brain injury.
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Objective To investigate the protective effect of meglumine adenosine cyclosphosp (MAC) on the cerebral ischemia-reperfusion (I/R) injury in rabbits.Methods Twenty four healthy rabbits were randomly divided into control group (n =6),I/R group (n =6),MAC pretreated group (n =6),and MAC treated group (n =6).Cerebral ischemia-reperfusion injury model was made by separating and electrocoagulating vertebral arteries and clipping common carotid arteries in the latter 3 groups after anesthesia.The sham-operated group underwent vessel separation without clipping.L/R group was administered with nothing,while MAC pretreated group with MAC before ischemia,and MAC treated group with MAC just after ischemia.Blood was gathered from jugular vein before ischemia,and 30 min,1 h,and 2 h after reperfusion for testing IL-8,superoxide dismutase (SOD) and malondialdehyde (MDA).The brain tissue slice was observed by optical microscope.Results Compared to control group and before ischemia,the levels of IL-8 and SOD in serum were significantly increased and decreased,and the levels of MDA was significantly increased at 30 min after reperfusion in I/R group; the levels of IL-8 and MDA in serum were significantly increased,and the levels of SOD in serum was significantly decreased at 1 h and 2 h after reperfusion in I/R group.The levels of IL-8 in serum was less at 30 min and 1 h and 2 h after reperfusion in MAC pretreated group than in I/R group.At 1 h and 2 h after reperfusion,the levels of MDA in serum was less and the levels of SOD in serum was higher in MAC pretreated group than in I/R group.At 1 h and 2 h after reperfusion,the levels of IL-8 in serum were less and the levels of SOD in serum were higher in MAC treated group than in I/R group.The levels of MDA in serum were less at 2 h after reperfusion in MAC treated group than in I/R group.Compared to I/R group,pathological change was lighter in the MAC pretreated and MAC treated group.Conclusions MAC has a fine cerebral-protective effect and has no side effect.
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Objective To research the effect of octreotide on the lung injury of far place organ after ischemia-reperfusion in rabbit liver.Methods Prings maneuver rabbit hepatic ischemia-reperfusion models were established. 24 adult New Zealand rabbits were random divided into three groups: group Ⅰ (sham operative group) , group Ⅱ (ischemia-reperfusion by physiological saline group) and group Ⅲ (octreotide preconditioning group). To group Ⅲ, we injected octreotide of 20μg/kg to abdominal cavity and octreotide of 30(μg/kg to skin following, and octreotide was dissolved into 2ml with 0. 9% physiological saline. To group Ⅰ and Ⅱ, octreotide were replaced with the same amount of physiological saline. The changes of MAP, HR in every group were recorded at the time before ischemia (T1 ) , 30min (T2) after ischemia, 30min(T3) , 60min(T4) , 120min(T5) , 240min(T6) after reperfusion. The tumor necrosis factor-alpha (TNF-a) and interleukin-lbeta (IL-1β) in the plasma in every group at T1, T2, T3, T4 , T5, T6 were detected. These rabbits were killed 240 min after reperfusion, then the lung's hepatocellular ultrastructures of every group were observed under electromicroscope, and the apoptosis of lung was detected by TUNEL. Results The MAP, HR of group Ⅱ and group Ⅲ were lower than that of group Ⅰ at T2 to T4. Moreover, group Ⅱ were lower than that of group Ⅲ (P <0.05). The TNF-a, IL-1β of group Ⅱ (fromT2) and group Ⅲ ( from T3) were higher than that of group Ⅰ ( P < 0.05) , and group Ⅲ were lower than group Ⅱ after ischemia (P <0. 01). Through electromicroscope, we found that the injury of the lungs hepatocellular ultrastructure in group Ⅲ was slighter than that in group Ⅱ . We detected the apoptosis of the lung organizes by TUNEL under 5 fields of light microscopes, and found that the apoptosis counts of group Ⅱ (55. 82 ±4. 19) and group Ⅲ (32. 17 ±3. 10) were more than that of group Ⅰ (3. 96 ±0. 87), and group Ⅲ were less than thatof group Ⅱ (P < 0. 01). Conclusion Octreotide can protect the lung injury of far place organ after ische-mia-reperfusion in rabbit liver.
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Objective To explore the protective mechanisms of Buyanghuanwu decoction (BHD) on heart function by observing its effect on MIRI rabbits. Methods The rabbits were randomly divided into three groups, including sham group, model group, and BHD group. After pretreatment for one week, the model of myocardial ischemia reperfusion injury was established by ligating the branch of left coronary arter-y. The changes of electrocardiography were observed, and the values of LVSP, + dp/dtmax, - dp/dtmax were recorded and compared. Results Compared with the model group, the values of LVSP, + dp/dtmax, - dp/dtmax in BHD group were significantly increased (P<0.01 ). Conclusion BHD can improve heart function of MIRI rabbits.