Changes of plasma and myocardial calcitonin gene-related peptide in myocardial stunning rats

AIM: To investigate changes of calcitonin gene-related peptide(CGRP) in myocardial stunning rats. METHODS: Rat in vivo myocardial stunning model was used. CGRP content in plasma and myocardium were determined by radioimmunoassay. RESULTS: Plasma level of CGRP increased significantly (P＜0.01), but in left ventricular myocardium CGRP decreased obviously (P＜0.05) in myocardial stunning group compared with the control group. CONCLUSION: CGRP content in the left ventricular myocardium was negatively correlated with plasma CGRP.     

Effects of ischemic preconditioning on cardiac myocyte apoptosis and expression of bcl-2 during myocardial ischemia/reperfusion in rats

AIM:To explore the effect of ischemic preconditioning on cardiac myocyte apoptosis and the expression of bcl-2 during myocardial ischemia/reperfusion in rats. METHODS:We use TUNEL,immunohistochemical and in situ hybridization(ISH) methods to detect the cardiac myocyte apoptosis and the expression of bcl-2 during myocardial ischemia/reperfusion in rats. RESULTS:①The numbers of positive cardiac myocyte nuclear and the percentage of positive cardiac myocyte nuclear in IP+I/R_3h group decreased significantly(P<0.05,P<0.01)compared with I/R_3h group,respectively.②The numbers of bcl-2 protein positive cardiomyocyte and the percentage of bcl-2 protein positive cardiomyocyte in IP+I/R_3h group were higher(P<0.01)than that of I/R_3h group,respectively.The numbers of positive bcl-2 mRNA cardiomyocyte and the percentage of positive bcl-2 mRNA cardiomyocyte in IP+I/R_1h group were higher(P<0.01)than that of I/R_1h group,respectively.CONCLUSION:① The first window of IP's protection could reduce cardiomyocyte apoptosis significantly.② Up-regulating the protein expression of bcl-2 in cardiomyocytes during I/R may be one of the mechanisms of first window of IP's protection.     

Inhibitory effect of fructose-1, 6-diphosphate on adriamycin-induced cardiomyocyte apoptosis in rats

AIM:To study the effect of fructose-1, 6-diphosphate (FDP) on adriamycin(ADM)-induced cardiomyocyte apoptosis in rats. METHODS:Twenty-four Wistar rats were randomly divided into three groups: control group, ADM treated group and FDP intervention group. The contents of malondialdehyde (MDA) and NO₂^-/NO₃^-, the activities of glutathione peroxidase (GPx) and superoxide dismutase (SOD) were determined by colorimetric method in myocardial tissue, and the cardiomyocyte apoptosis was detected by TUNEL method in myocardial tissue, and the expression of inducible nitric oxide synthase (iNOS) mRNA, Bcl-2 mRNA and Bax mRNA in myocardial tissue were detected by in situ hybridization. RESULTS:The contents of NO₂^-/NO₃^- and MDA in myocardial tissue, the expressive levels of iNOS mRNA and Bax mRNA in cardiomyocyes and its apoptotic amounts in FDP intervention group were significantly lower than those in ADM treated group (P＜0.01). However, the activities of SOD and GPx in myocardial tissue, the expressive level of Bcl-2 mRNA of cardiomyocytes in FDP intervention group were significantly higher than those in ADM treated group (P＜0.01). CONCLUSION:FDP antagonized the reduced expression of Bcl-2 mRNA and increased expression of Bax mRNA in myocardial tissue induced by ADM, and in turn inhibited ADM-induced cardiomyocyte apoptosis.     

Changes in the expression of endothelin system in rats with chronic heart failing

AIM: To study the changes of endothelin system during chronic heart failure (CHF) and imply the relationship between endothelin system and the course of CHF by observing the mRNA expression of endothelin receptors (ET_AR and ET_BR) and PreproET₁ in early stage and later stage of CHF caused by left coronary artery ligation. METHODS: The mRNA expression of ET_A, ET_B receptors and PreproET₁ were detected by RT-PCR technique. The plasma concentrations of ET₁ and ANP were determined by RIA method. RESULTS: The plasma concentrations of ET₁ and ANP, and the mRNA expression of ET receptors and PreproET₁ in the lefe ventricle increased significantly in early stage (myocardial infarction 10 d). While the plasma concentrations of ET₁ and ANP in later stage (myocardial infarction 70 d) were higher than those in the early stage. However, the mRNA expression of ET_AR, ET_BR and PreproET₁ decreased significantly. The mRNA expression of ET_AR in myocardial infarction (MI) 70 d rats had no difference with those in sham-operated rats and the mRNA expression of ET_BR and PreproET₁ in MI 70 d rats was lower significantly than those in MI 10 d rats, but significantly higher than those in sham-operated rats. CONCLUSION: The changes of ET receptors and PreproET₁ mRNA expression are involved in the cardiac function modulation during the different stages in chronic heart failure.     

Effects of ligustrazine ferulate on myocardial apoptosis and apoptosis-related protein expression in rats with myocardial ischemia-reperfusion injury

AIM:To observe the effects of ligustrazine ferulate on the apoptosis of myocardial cells in rats with myocardial ischemia-reperfusion injury, and to explore its possible mechanism. METHODS:Sixty male SD rats were randomly divided into five groups: sham-operation group, ischemia-reperfusion group, ligustrazine (4 mg/kg) group, low-dose (4 mg/kg) ligustrazine ferulate group and high-dose (8 mg/kg) ligustrazine ferulate group. The rat myocardial ischemia-reperfusion model was established by 30 min of myocardial ischemia followed by 120 min of reperfusion. Drugs were administered to the rats by jugular vein injection 10 min before reperfusion. After the reperfusion was finished, the biochemical indicators in serum and the histological indexes in myocardium were detected. RESULTS: Compared with ischemia-reperfusion group, ligustrazine ferulate lowered the serum levels of creatine kinase MB form, lactate dehydrogenase, cardiac troponin I and malondialdehyde, elevated the activity of total superoxide dismutase in serum and the expression of Bcl-2 protein in myocardium, decreased the expression of Bax protein and myocardial apoptotic index, and increased the Bcl-2/Bax ratio (all P<0.01). All the indicators in ligustrazine ferulate groups were dose-dependently superior to those in ligustrazine group (P<0.05 or P<0.01). CONCLUSION: Ligustrazine ferulate protects rats against myocardial ischemia-reperfusion injury. Its anti-apoptotic effect may be related to up-regulation of Bcl-2 and down-regulation of Bax.     

The changes in proliferation and apoptosis of macrophages in the development of pulmonary fibrosis of rats

AIM: To observe the changes in proliferation and apoptosis of macrophages in the development of pulmonary fibrosis in rats. METHODS: The number of macrophages, apoptotic cells, the proliferation index (PI) and MTT activity of macrophages were assayed on the day 14 and the day 30 after intratracheal adminstration BLMA₅ in rats. RESULTS: (1) The number of alveolar macrophages was increased in BLMA₅ 14 d group and in BLMA₅ 30 d group, compared with sham 14 d group and sham 30 d group, respectively. The number of macrophages in BLMA₅ 14 d group was higher than that in BLMA₅ 30 d group. (2) The PI of macrophages increased in BLMA₅ 14 d group, and decreased in BLMA₅ 30 d group. (3) The number of apoptotic cells increased both in BLMA₅ 14 d group and BLMA₅ 30 d group. The number of apoptotic cells in BLMA₅ 14 d group was lower than that in BLMA₅ 30 d group. (4) The MTT activity of macrophages was higher in BLMA₅ 14 d group and in BLMA₅ 30 d group than that in sham 14 d group and sham 30 d group, respectively. CONCLUSIONS: The ability of proliferation increased at first, and then decreased, but the apoptosis of macrophages increased all the time, in the development of pulmonary fibrosis. This might be partly contributed to the changes of the number and function of macrophages in lung.     

Role of NHE-1 in the proliferation and apoptosis of pulmonary artery smooth muscle cell in rats

AIM: To evaluate the role of Na⁺/H⁺ exchanger-1(NHE-1)in the proliferation and apoptosis of pulmonary artery smooth muscle cells in rats. METHODS: Twenty Wistar rats were equally randomized into the control group and 3-week hypoxic group. Intracellular pH (pHi) of the smooth muscle was determined with fluorescence measurement of the pH-sensitive dye BCECF-AM and the expression of NHE-1 mRNA was detected with RT-PCR. The primary culture of pulmonary artery smooth muscle cell in vitro was performed. In situ cell death detection kit (TUNEL) was used to study the effect of specific NHE-1 inhibitor, dimethyl amiloride (DMA), on the apoptosis of muscle cells which had intracellular acidification. RESULTS: pHi value and expression of NHE-1 mRNA of pulmonary artery smooth muscle cell were significantly higher respectively in the hypoxic group than those in the control group (P＜0.01). DMA elevated the apoptotic ratio significantly. The effect was enhanced when DMA concentration was augmented and the time was prolonged. CONCLUSION: With the function of adjusting pHi, NHE-1 may play an important role in the proliferation and apoptosis of pulmonary artery smooth muscle cells.     

Apoptosis and expression of apoptosis-related genes in kidneys of the rats with 5/6 nephrectomy

AIM: To establish a model of subtotal nephrectomy (SNx) and investigate the changes of apoptosis and apoptosis-related genes (Bax, bcl-2, caspase-3, caspase-8 and caspase-9) in the rat remnant kidney. METHODS: Remnant kidneys were produced in adult male SD rats by 5/6 nephrectomy. The renal function and histopathological changes were evaluated at 1, 2, 4, 8, 12, 16, 26 and 40 weeks after operation. The tissues of remnant kidneys were collected to detect apoptosis cells by in situ end-labeling of cleaved DNA (TUNEL) and proliferating cells by determining the proliferating cell nuclear antigen (PCNA). The expression of Bax, bcl-2, caspase-3, caspase-8 and caspase-9 was measured by RT-PCR and Western blotting. The proteins were detected by immunohistochemistry staining. The relation between apoptosis, proliferation, glomerulosclerosis and renal interstitial fibrosis was also observed. RESULTS: The results showed the renal pathological dynamic changes in 5/6 nephrectomy remnant kidneys were tubule-interstitial inflammation and fibrosis, as well as glomerulosclerosis. There were transient increases in both proliferating and apoptotic processes in glomerulus, tubules and interstitium. Apoptosis was increased and most of apoptotic cells were detected in tubular epithelial cells and interstitial area. The mRNA and protein expression of Bax, caspase-3, caspase-8 and caspase-9 were increased in all course, and peaked at week 4 and 40 in the SNX rats. The successive changes of these parameters were parallel to the level of focal inflammation in interstitium. Glomerulosclerosis index was related with focal inflammation cells and 24 hours urine protein (r=0.788, 0.822; P<0.01). The tubuler apoptosis index was related with Scr, BUN, 24 hours urine protein and focal inflammation cells (r=0.824, 0.794, 0.883, 0.948; P<0.01). The mRNA and protein expression of Bcl-2 was not significantly increased than those in control rats. CONCLUSION: Apoptosis may be involved in the development of chronic renal damaged in 5/6 nephrectomy and play an important role in chronic glomerulosclerosis, tubule atrophy and interstitial fibrosis. The renal interstitial inflammation may promote the apoptosis in the remnant kidney.     

Role of 17-AAG in inducing apoptosis and cell cycle arrest of HCT-15 cells

AIM: To investigate the effects of 17-AAG on apoptosis and cell cycle of HCT-15 cells and to clarify the related mechanisms. METHODS: MTT method was employed to evaluate the inhibitory effects of 17-AAG with Aifferent time and different doses on the proliferation of HCT-15 cells. The cells were stained with Annexin V-FITC/propidiumiodide and measured by flow cytometry. The expression of STAT3, cyclin D1, Cyt C, caspase 9 and caspase 3 at mRNA and protein levels was determined by RT-PCR and Western blotting. RESULTS: Treatment with 17-AAG at concentration of 1.25~20 mg/L for 24 h and 48 h significantly inhibited the activity of HCT-15 cells at both time-and concentration-dependent manners. Treatment with 17-AAG at concentrations of 0.425, 0.85 and 1.7 mg/L for 48 h significantly induced apoptosis and cell cycle arrest of HCT-15 cells. The exposure of 17-AAG at concentrations of 0.425, 0.85 and 1.7 mg/L for 48 h to the HCT-15 cells significantly down-regulated the expression of STAT3 and cyclin D1 at mRNA and protein levels, but up-regulated Cyt C, caspase 9 and caspase 3 mRNA and protein in a concentration-dependent manner. CONCLUSION: 17-AAG inhibits the cell activity, induces apoptosis and G₁ arrest by down-regulating the expression of cyclin D1, and promoting the mitochondria apoptosis through STAT3 pathway.     

Effects of propofol on levels of amino acid and neuronal apoptosis of hippocampus after global ischemia-reperfusion in rats

AIM:To investigate the effects of propofol on levels of amino acid and neuronal apoptosis of hippocampus after global ischemia-reperfusion in rats．METHODS:60 male Wistar rats were randomly assigned to five groups ( twelve animals each)．After global cerebral ischemia for 10 min then reperfusion for 60 min and 72 h,the animals were decapitated and the brains were removed respectively．HPLC was adopted to measure the contents of amino acids in hippocampus．The density of apoptosis neurons in the hippocampal CA1 subfield was evaluate with light microscope．Flow cytometry technique was applied to detect the neuronal apoptosis index in the hippocampus．RESULTS:The contents of Glu and Asp increased markedly and the levels of GABA and Gly decreased obviously in hippocampus after ischemia-reperfusion. The levels of Glu and Asp were lower in propofol group than those in control group (P<0.05 or P<0.01),and the contents of GABA and Gly were higher in propofol group than those in control group (P<0.05 or P<0.01). Apoptosis index and density of apoptosis neurons in the hippocampus were higher in control group than those in propofol group. CONCLUSION:Propofol inhibits neuronal apoptosis of hippocampus after global ischemia-reperfusion,and suppresses the excessive release of excitory amino acids and the exhaustion of inhibitory amino acids in hippocampus after ischemia-reperfusion. Its mechanism may be related with decreasing the neuronal apoptosis.     

Effects of fluctuant high blood glucose on apoptosis in glomerular endothelial cells and renal tubular epithelial cells in diabetic rats

AIM:To explore the effects of fluctuant high blood glucose and stable high blood glucose on apoptosis and the expression of Bax and Bcl-2 in glomerular endothelial cells and renal tubular epithelial cells in diabetic rats. METHODS: 24 SD rats were divided into 3 groups: control group, stable high blood glucose group and fluctuant high blood glucose group. Diabetic rats were induced by intraperitoneal injection of STZ, and the fluctuant high blood glucose animal model was induced by intraperitoneal injection of aspart and glucose at different time points every day. Apoptosis was assessed by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling (TUNEL), and immunohistochemistry was used to detect apoptosis associated gene bax and bcl-2 expression in kidney. RESULTS:After 4 experimental weeks, a significant increase in cell apoptosis, up-regulation of Bax protein expression in kidney tubular epithelial cell and down-regulation of Bcl-2 in glomerular endothelial cell in fluctuant high blood glucose rats were observed compared with stable high blood glucose rats.CONCLUSION: Fluctuant high blood glucose induces more apoptosis in renal tubular epithelial cells than that in stable high blood glucose diabetic rats.     

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 of pro-inflammatory cytokines in serum and lung of rats with oleic acid-induced acute respiratory distress syndrome and the effect of anisodamine

AIM: To observe the changes of interleukin-6(IL-6), IL-8 and tumor necrosis factor-α(TNF-α) in serum and lung at different time, and the effects of anisodamine (654-2) treatment in rats with oleic acid-induced ARDS. METHODS: The ARDS model induced by intravenous injection of oleic acid in the rat was used and levels of IL-6, IL-8, TNF-α in serum and lung tissue supernatant were measured using enzyme linked immunosorbent assay (ELISA). RESULTS: Levels of serum and lung tissue IL-6, IL-8, TNF-α in oleic acid type ARDS 4 h group were increased significantly. These cytokines in oleic acid type ARDS 8 h group were lower than that of ARDS 4 h group, but serum IL-6, TNF-α and lung tissue IL-6 were still higher than that of control group . In oleic acid type ARDS 16 h group, serum IL-6, TNF-α were lower than that of the ARDS 8 h group and serum TNF-α and lung tissue IL-6 were higher than that of control group. After 654-2 treatment, the levels of serum and lung tissue IL-6, TNF-α were decreased significantly. CONCLUSION: IL-6, IL-8 and TNF- α might play important roles in the oleic acid-induced ARDS in the rat. 654-2 might alleviate ARDS by inhibiting excess production of IL-6 and TNF-α.     

Effect of hydrogen molecule on apoptosis-related proteins and Nrf2 signaling pathway in glomerular mesangial cells cultured with high glucose

AIM: To investigate the role of hydrogen molecule on apoptosis-related proteins in glomerular mesangial cells cultured with high glucose and to explore its possible mechanism. METHODS: Mouse glomerular mesangial cells cultured in vitro were divided into 4 groups:normal control group (C group, 5.5 mmol/L glucose), mannitol group (G group, 5.5 mmol/L glucose+19.5 mmol/L mannitol), high glucose group (H group, 25 mmol/L glucose), high glucose+hydrogen-rich water group (HH group, 25 mmol/L glucose+hydrogen-rich water), and cultured for 48 h. The protein levels of Bax, Bcl-2, cleaved caspase-3, nuclear factor E2-related factor-2 (Nrf2), heme oxygenase-1 (HO-1) and NAD(P)H:quinone oxidoreductase-1 (NQO-1) were determined by Western blot, and the mRNA expression of HO-1 and NQO-1 was determined by RT-PCR. The level of intracellular reactive oxygen species (ROS) was detected by dihydroethidium method, and the activity of superoxide dismutase (SOD) was measured by WST-8 assay. RESULTS: Compared with C group, the protein levels of Bax and cleaved caspase-3 were up-regulated, and Bcl-2 was down-regulated in H group (P <0.05). No significantly difference of the protein levels mentioned above between C and HH group was observed. Compared with H group, the protein levels of Bax and cleaved caspase-3 were down-regulated, and Bcl-2 was up-regulated in HH group (P <0.05). The level of intracellular ROS was higher and the activity of SOD was lower in H group than those in C group (P<0.05). However, there was no difference of the SOD activity between C group and HH group. The level of intracellular ROS decreased and the activity of SOD increased in HH group as compared with H group (P<0.05). Compared with C group, clearly reduced protein expression of Nrf2, HO-1 and NQO-1, and decreased mRNA expression of HO-1 and NQO-1 in H group were observed (P<0.05). Compared with H group, the protein levels of Nrf2, HO-1 and NQO-1 as well as the mRNA levels of HO-1 and NQO-1 were obviously increased in HH group (P<0.05).CONCLUSION: Hydrogen molecule inhibits the expression of pro-apoptotic proteins and induces the expression of anti-apoptotic proteins in glomerular mesangial cells cultured with high glucose. The mechanism may be related to activation of Nrf2 signaling pathway.     

Effect of Chinese herbs 9602 on the alterations of evoking population spike and morphology in hippocampal CA1 region after ischemia/reperfusion in rats

AIM:To explore the relationship between dynamic changes of population spike (PS) and morphologic alterations in hippocampal CA1 region and morphology after transient ischemia/reperfusion and the improving effects of Chinese herbs 9602.METHODS:Changes of evoking population spike ware investigated by electrical stimulating Schaf er collateral in CA1 region of hippocampal slice after ischemia/reperfusion in vivo.Apoptosis and morphologic alterations at different time points after cerebral ischemia/reperfusion were detected by using TUNEL and Nissl staining.RESULTS:The threshold voltage of CA1 region in evoking population spike increased markedly as compared with sham control. The enhancement of wave amplitude was reduced significantly after tetanic stimulation. The duration of enhancement in amplitude decreased with the passage of reperfusion. Above all were observed from 8 h after ischemia/reperfusion. They became remarkable and got to its top at 7 day after ischemia/reperfusion treatment. TUNEL positive cells were observed in hippocampal CA1 region at 8 h, got to the top at 24 h and then gradually reduced after ischemia/reperfusion. A lot of abnormal cells in CA1 region was found, and the number of pyramidal cell reduced progressively by Nissl staining after ischemia/reperfusion. Chinese herbs 9602 reduced the threshold voltage of CA1 region in evoking population spike remarkably, enhanced the wave amplitude and prolonged the duration of PS enhancement; decreased the number of TUNEL positive cell, prevented the reduction of pyramidal cell in CA1 region. CONCLUSIONS:The excitability and reactivity were decreased and there was a gradual functional disturbance of synaptic transmission in CA1 pyramidal cell and most notable changes happened at 7 d ischemia/reperfusion, suggesting that was partly due to delayed neuronal death induced by ischemia/reperfusion. Apoptosis plays an important role in the functional deficiency of CA1 region of hippocampus induced by cerebral ischemia/reperfusion. The effects of 9602 on ameliorating the excitability and reactivity of CA1 pyramidal cells relate to inhibiting apoptosis, attanuating delayed neuron death induced by ischemia/reperfusion.     

Effect of NAC on oxidant stress and apoptosis in the hippocampal CA1 region of rats exposured to chronic intermittent hypoxia

AIM: To investigate the effect of N-acetylcystein (NAC) on oxidant stress, neuron apoptosis in the hippocampal CA1 region of rats exposured to chronic intermittent hypoxia (CIH). METHODS: 30 healthy male Wistar rats were randomly divided into three groups of 10 each, a CIH group, a NAC therapeutic group and a control group. The levels of MDA and SOD were detected by colorimetric method. Immunohistochemistry was used to examine the expression of p-JNK and TUNEL was used to detect the neuron apoptosis in the hippocampal CA1 region. RESULTS: The level of MDA in NAC group were lower than that in CIH group［(1.71±0.43) μmol/g protein vs （1.37±0.26) μmol/g protein, P<0.05)］. The activity of SOD in NAC group was higher than that in CIH group［(44.94±14.01) 103 NU/g protein vs(57.66±14.07) 103 NU/g protein, P<0.05)］. The expression of p-JNK protein and the apoptotic indices ［(0.39±0.16), (0.20±0.11)］ in NAC group were significantly lower than those in CIH group ［(0.53±0.10), (0.32±0.18), all P<0.05］. CONCLUSION: NAC protects hippocampal neuron from apoptosis by suppressing the oxidant stress in the hippocampal CA1 region and inhibiting the activation of JNK signaling pathway.     

Effects of propofol on expression of AIF and cell apoptosis in brain tissues of the rats with LPS-induced brain injury

AIM: To investigate the effects of propofol on the expression of apoptosis-inducing factor (AIF) and cell apoptosis in brain tissues of rats with lipopolysaccharide(LPS)-induced brain injury. METHODS: Seventy-two male and female SD rats weighing 220~250 g were randomly divided into 3 groups (n=24 each). Cerebral edema was induced by injection of LPS at 1 mg/kg via left internal carotid artery in LPS group and LPS+propofol group. In control group, equal volume of normal saline was administered instead of LPS. The rats in LPS+propofol group received intraperitoneal injection of propofol at 100 mg/kg immediately after LPS administration. Six rats in each group were decapitated 6 h, 12 h, 24 h or 48 h after operation and the frontal lobe cortex were immediately removed for determination of the water content. The apoptotic neurons were detected by Annexin V-PI staining. The protein levels of AIF, NF-κB and caspase-3 were measured by immunohistochemistry. The protein expression of AIF was detected by Western blotting analysis. RESULTS: Compared with control group, the brain water content, the number of neuronal apoptosis and the protein expression levels of AIF, NF-κB and caspase-3 were significantly increased in LPS group and LPS+propofol group. Compared with LPS group, the results mentioned above were markedly reduced in LPS+propofol group. CONCLUSION: Propofol attenuates LPS-induced brain injury by decreasing AIF protein expression and inhibiting apoptosis.     

Relationship between airway inflammation and bronchial hyperreactivity in rats and the effect of theophylline

AIM: To determine the relationship between antigen-induced airway inflammation characterized by pulmonary eosinophilia and bronchial hyperreactivity in rats, and to evaluate the effect of theophylline at different doses. METHODS: In ovalbumin (OA)-sensitized rats, bronchiole wall area, eosinophils around bronchi, and the responses to methacholine (MCh) aerosol were measured after 1% OA aerosol challenge with computer-assisted techniques. RESULTS: OA challenge caused both inflammation and airway hyperreactivity, and there was a significantly positive correlation between them. Oral theophylline (1-12.5 mg/kg, bid for 7 days) attenuated antigen-induced inflammation (swelling of bronchiole walls and pulmonary eosinophilia) and bronchial hyperreactivity. CONCLUSION: These findings confirm that bronchial hyperreactivity positively correlates to airway inflammation in the rat, and suggest that theophylline at relatively lower doses has anti-inflammatory effect in airway allergic reaction.